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blood circulation
Blood circulation mind map, the content includes the bioelectrical phenomena and physiological characteristics of myocardial cells, the pumping function of the heart, vascular physiology, the regulation of cardiovascular activity, etc. Don't miss it if you are a related major~
Edited at 2023-03-02 20:22:14
- cáncer de pulmón
El cáncer de pulmón es un tumor maligno que se origina en la mucosa bronquial o las glándulas de los pulmones. Es uno de los tumores malignos con mayor morbilidad y mortalidad y mayor amenaza para la salud y la vida humana.
- diabetes
La diabetes es una enfermedad crónica con hiperglucemia como signo principal. Es causada principalmente por una disminución en la secreción de insulina causada por una disfunción de las células de los islotes pancreáticos, o porque el cuerpo es insensible a la acción de la insulina (es decir, resistencia a la insulina), o ambas cosas. la glucosa en la sangre es ineficaz para ser utilizada y almacenada.
- sistema digestivo
El sistema digestivo es uno de los nueve sistemas principales del cuerpo humano y es el principal responsable de la ingesta, digestión, absorción y excreción de los alimentos. Consta de dos partes principales: el tracto digestivo y las glándulas digestivas.
blood circulation
- cáncer de pulmón
El cáncer de pulmón es un tumor maligno que se origina en la mucosa bronquial o las glándulas de los pulmones. Es uno de los tumores malignos con mayor morbilidad y mortalidad y mayor amenaza para la salud y la vida humana.
- diabetes
La diabetes es una enfermedad crónica con hiperglucemia como signo principal. Es causada principalmente por una disminución en la secreción de insulina causada por una disfunción de las células de los islotes pancreáticos, o porque el cuerpo es insensible a la acción de la insulina (es decir, resistencia a la insulina), o ambas cosas. la glucosa en la sangre es ineficaz para ser utilizada y almacenada.
- sistema digestivo
El sistema digestivo es uno de los nueve sistemas principales del cuerpo humano y es el principal responsable de la ingesta, digestión, absorción y excreción de los alimentos. Consta de dos partes principales: el tracto digestivo y las glándulas digestivas.
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- Outline
blood circulation
Bioelectrical phenomena and physiological characteristics of cardiomyocytes
Bioelectrical phenomena of cardiomyocytes
Classification of cardiomyocytes
Working cells (ordinary cardiomyocytes, non-autonomous cells)
Atrial myocardium, ventricular myocytes
Function
The power of the heart's pumping function
It has excitability and conductivity, but does not have the ability to automatically generate rhythmic excitement.
Specially differentiated cardiomyocytes (autonomous cells)
Sinoatrial node, atrioventricular junction, atrioventricular bundle, left and right bundle branches, Purkinje fibers
Function
Together they form the heart's specialized conduction system.
It has excitability and conductivity, but no contractile ability
Except for the nodal area cells of the atrioventricular bundle, all others have the function of automatically generating rhythmic excitation.
Transmembrane potential of cardiomyocytes (taking ventricular muscle as an example) Compared with ventricular myocytes, atrial myocytes do not have an obvious plateau.
Transmembrane potential of working cells and its ionic basis
resting potential
Resting potential is -80~-90mv
Resting Potential Ionic Basics: Potassium Ion Equilibrium Potential
Inward rectification: IK1 channels are highly permeable to potassium ions at rest but become less permeable to potassium ions during depolarization.
Action potential
Period 0 (depolarization period, 1-2ms)
The membrane potential increased from -80~90mV to 30mV
Superjection(n)
Action potential amplitude (n)
Formation mechanism
Voltage-dependent fast sodium channels that can be blocked by tetrodotoxin
Repolarization (200~300ms)
Phase 1 (initial stage of rapid repolarization, 10ms)
The membrane potential dropped from 30mV to about 0mV
Ionic basics
The transient outward ion flow of potassium ion load, that is, potassium ion efflux, can be blocked by tetraethylamine and 4-aminopyridine
Phase 2 (slow repolarization phase, plateau phase, 100~150ms)
The membrane potential is stable at 0mV for 100ms-150ms. This is the main reason why the action potential lasts longer and is the main difference between the action potentials of ventricular myocytes and other cells.
Ionic basics
It is composed of inward ion flow calcium ions and outward ion flow potassium ions.
The inward ion flow of calcium ions is mediated by a voltage-dependent L-type slow channel. This channel opens when the membrane potential is depolarized to -40mV and can be blocked by manganese ions and dihydropyridines.
Phase 3 (end of rapid repolarization, 100~150ms)
The membrane potential quickly recovers from 0mV to -90mV
Ionic basics
The inward electron flow channel is closed and the outward electron flow potassium ions further increases.
Action potential duration (n)
Phase 4 (recovery period)
In phase 4, the membrane potential has recovered and stabilized, but the electron distribution inside and outside the membrane has not yet recovered. There are more potassium ions outside the membrane, and more sodium ions and calcium ions inside the membrane. For every molecule of ATP consumed by the sodium-potassium pump, 3 sodium ions are reversibly transported outside the membrane and 2 potassium ions are transported into the membrane. The transport of calcium ions is mainly carried out by sodium ion calcium ion exchanger and calcium pump. For every 3 sodium ions transported into the membrane along the concentration, one calcium ion will be transported out of the cell. This method of calcium ion transport belongs to Secondary active transport. Digitalis drugs block the activity of the sodium-potassium pump.
Transmembrane potential of autonomous cells and its ionic basis
Overview
Maximum diastolic potential (maximum repolarization potential n)
Phase 4 automatic depolarization is the basis for the rhythmic excitation of myocardial autonomic cells.
Purkinje cells
The action potential is basically the same as that of ventricular myocytes, but its phase 4 membrane potential is unstable. When the phase 3 membrane potential repolarizes to -90mV, an inward ion flow is generated. The enhancement of the inward ion flow is the reason why Purkinje cells generate rhythm. the basis of sex
inward ion flow sodium ion membrane channel
When the membrane potential reaches -60mV in phase 3, the calcium channel opens. When the membrane potential reaches -100mV, it is completely opened. When the membrane potential reaches -50mV, the channel closes.
Calcium channels can be blocked by cesium and are not sensitive to tetrodotoxin. They are slow channels, so the phase 4 automatic depolarization of Purkinje cells is slow and the automatic rhythm is low.
premature ventricular contractions
Pacing current (n)
sinoatrial node P cells
Compared with Purkinje cells, it has the following characteristics
There are periods 0, 3, and 4, but no obvious periods 1 and 2.
The absolute values of the maximum diastolic potential (-70mV) and threshold potential (-40mV) are smaller than those of Purkinje cells
Phase 0 depolarization is slow and action potential amplitude is small
Phase 4 depolarization is fast, significantly faster than Purkinje cells
Action potential
Period 0 (depolarization period)
When the membrane potential automatically depolarizes from the maximum diastolic potential to -40mV, the L-type calcium ion channel opens and calcium ions flow in. Because it is a slow channel, the P cell phase 0 depolarization rate is slow.
Phase 3 (repolarization phase)
Calcium channels close, potassium channels open, and potassium ions flow out
4 periods of automatic depolarization
A weakening of the inward ion current
When P cells repolarize to -50mV in phase 3, Ik channels are inactivated in a time-dependent manner. Progressive attenuation of potassium efflux underlies phase 4 P cell automatic depolarization
Two types of outward ion current enhancement
If channel-mediated sodium ion influx
The membrane potential at which calcium channels are fully activated is -100mV, but the maximum diastolic potential of P cells is -70mV. Therefore, calcium channel activation is very slow and only causes a small amount of sodium ion inflow. Therefore, the inflow of sodium ions automatically depolarizes P cells in the fourth phase. The effect of potassium ion outflow attenuation is much smaller than that of potassium ion outflow attenuation.
Calcium ion influx
When the membrane potential automatically depolarizes to -50mV, T-type calcium ions are heard to open, and a small amount of calcium ions flow in, forming part of the 4th phase of automatic depolarization.
When the membrane potential automatically depolarizes to -40mV, the L-type calcium ion channel opens and forms a new rising branch of the action potential.
Action potentials of other autonomous cells
Similar to P cells, but phase 4 depolarization is slower than P cells
Electrophysiological types of cardiomyocytes
The speed of depolarization in phase 0
fast response cells
slow responding cells
Physiological properties of cardiomyocytes
Electrophysiological properties
self-discipline(n)
Normal pacemaker point of the heart and sinus heart rate
The excitability of P cells in the sinoatrial node is the highest, followed by the atrioventricular junction, and Purkinje fibers are the lowest.
Normal pacemaker: sinoatrial node, sinus rhythm (n)
Secondary pacemaker point: atrioventricular junction, junctional rhythm (n)
Third-level pacemaker points: atrioventricular bundle, left and right bundle branches, Purkinje fibers, ventricular rhythm (n)
Potential pacemaker (n)
Arrhythmia
Ectopic pacemaker (n)
Ectopic rhythm (n)
How the sinoatrial node controls potential pacemakers
Be the first to occupy (obtain n more)
Overdrive suppression (n)
Factors that determine and influence self-discipline
The speed of automatic depolarization in phase 4
The distance between the maximum diastolic potential and the threshold potential
Excitability
Factors that determine and influence excitability
The distance between the maximum diastolic potential and the threshold
state of ion channels
Periodic changes in excitability (taking ventricular muscle as an example) It does not undergo a complete tonic contraction like skeletal muscle, but a rhythmic activity of alternating contraction and relaxation. This is an important prerequisite for the heart to pump blood.
Valid refractory period (refractory n)
Absolute refractory period (n) (repolarization to -55mV from period 0 to period 3)
Effective refractory period (n) (3rd phase repolarization to -55mV to 3rd phase repolarization to -60mV)
Relative refractory period (n)
Membrane potential repolarizes from -60mV to -80mV
supernormal period
Membrane potential repolarizes from -80mV to -90mV
Premature contractions (premature contractions n) and compensatory intervals (n)
A large threshold means low excitability; a small threshold means high excitability. Purkinje cells are the most excitable, followed by atrial and ventricular myocardium, and the atrioventricular junction is the lowest.
Conductivity (n)
The pathways and characteristics of excitement propagation in the heart
Special conduction system of the heart
Has the function of pacing and conducting excitation
Conduction pathways: sinoatrial node, atrial myocardium (predominant conduction pathway), atrioventricular junction, atrioventricular bundle, left and right bundle branches, Purkinje fiber network, ventricular myocardium
Characteristics of excitation conduction in the heart
Chamber delay (n) and its significance
Arrhythmia
Factors affecting myocardial conduction
structural factors
The main structural factor is the diameter of the cardiomyocyte, and the cell diameter has an inverse relationship with the intracellular resistance. That is, the larger the cell diameter, the smaller the intracellular resistance, and the faster the excitation conduction speed, and vice versa. Purkinje cells have the largest diameter and therefore spread the fastest
physiological factors The main physiological factor is the electrophysiological properties of cardiomyocytes
The speed and amplitude of action potential phase 0 depolarization
membrane potential level
Excitability of neighboring unexcited cells
Mechanical properties
Contractibility
Characteristics of myocardial contraction
Synchronized shrinking (all or no shrinking)
Complete tetanic contraction does not occur
Dependence on extracellular calcium ions
Within a certain range, the higher the calcium ion concentration in the extracellular fluid, the more calcium ions will flow in during excitement, and the stronger myocardial contractility will be.
Factors affecting myocardial contraction
Calcium ion concentration in plasma
Hypoxia and acidosis
Both hypoxia and acidosis can increase the concentration of hydrogen ions. Both hydrogen ions and calcium ions can bind to troponin. The two are competitively inhibited. The increase in hydrogen ion concentration leads to a decrease in the binding of calcium ions to troponin. Myocardial contraction depends on calcium ions, so myocardial contractility is weakened
Hypoxia leads to reduced ATP synthesis and weakened myocardial contractility
Sympathetic nerves and catecholamines
Sympathetic nerve excitement or increased catecholamine concentration can increase the permeability of myocardial cell membranes to calcium ions, promote the influx of calcium ions, and increase myocardial contractility.
heart pumping function
Cardiac cycle and heart rate
Cardiac cycle (n0.8s)
atrium
Systole period 0.1s
Diastolic period 0.7s
ventricle
Systole period 0.3s
Diastolic period 0.5s
Heart rate (n75 beats/min)
heart pumping process
Overview
Factors affecting the completion of the heart's pumping function
The rhythmic relaxation and contraction of the heart causes pressure differences between the ventricles and atria, ventricles and arteries, forming a driving force for blood flow.
Four sets of valves in the heart control the direction of blood flow
Ventricular systole—ejection process
Isovolumic contraction period (maximum pressure increase at 0.05s)
Rapid ejection period (maximum volume reduction in 0.10s)
Slow down the ejection period (ventricular volume shrinks to minimum in 0.15s)
Ventricular diastole—filling process
Isovolumic diastole period (maximum pressure reduction at 0.07s)
Rapid filling period (maximum volume increase in 0.11s)
Slow down filling period (0.22s)
Atrial systole (0.1s)
The role of the atria in the heart's pumping process
initial pumping action of atrial contraction
Heart sounds (n) and phonocardiogram
first heart sound
A sign of the beginning of ventricular contraction, shock caused by ventricular muscle contraction, sudden closure of the atrioventricular valve, and blood flowing into the artery.
second heart sound
A sign of the onset of ventricular diastole, a shock caused by closure of the arterial valves, deceleration of blood in the large arteries, and rapid decrease in intraventricular pressure.
third heart sound
At the end of the rapid filling phase, blood flows from the atria into the ventricles, causing vibrations in the ventricular walls and papillary muscles.
Fourth heart sound (atrial sound)
At the end of ventricular diastole, atrial contraction causes ventricular filling
Evaluation of heart pumping function
The amount of blood output by the heart
Stroke volume (n70ml) and ejection fraction (n)
Output per minute (n cardiac output) and cardiac index (n)
heart work capacity
Stroke work (n) and work per minute (n)
heart function reserve
mental reserve (n)
Heart rate reserve (n)
Stroke volume reserve (n)
Factors affecting cardiac output
stroke volume
When the heart rate remains constant, cardiac output increases or decreases with the increase or decrease in stroke volume.
ventricular filling (preload)
Arterial blood pressure (afterload)
Ventricular hypertrophy, ventricular enlargement
Ventricular muscle contractility (n)
Isometric adjustment (n)
Effect of heart rate
40~180 beats/min. When stroke volume remains unchanged, cardiac output increases or decreases with the increase or decrease of heart rate.
Above 180 beats/min, the cardiac filling period is significantly shortened and the filling volume is obviously insufficient, so the stroke volume and cardiac output are reduced.
Below 40 beats/min, because the diastolic period is too long and close to the limit of ventricular filling, the stroke volume remains unchanged, so the cardiac output decreases significantly.
Vascular Physiology
Structural and functional characteristics of various types of blood vessels
elastic reservoir vessel
The aorta, pulmonary artery and their largest branches have thick walls, are rich in elastic fibers, and have obvious elasticity and expansibility.
Has the function of buffering systolic blood pressure and maintaining diastolic blood pressure
distribute blood vessels
Located between large arteries and small arteries, the wall is mainly composed of smooth muscle and has strong contractility.
It has the function of transporting blood to various tissues and organs and distributing blood flow.
precapillary resistance vessels
Arterioles and arterioles have smaller diameters, accelerated blood flow, and great resistance to blood flow. The walls of the arteries are rich in smooth muscle and have strong contractility.
Important for maintaining arterial blood pressure
exchange blood vessels
capillaries
A place where blood and tissue fluid exchange substances.
postcapillary resistance vessels
venule
The relaxation and contraction of venular smooth muscle can affect the ratio of front and rear resistance of capillaries, thereby changing capillary pressure and the distribution of body fluids inside and outside blood vessels.
volumetric vessels
The entire venous system has thin walls, is easy to expand, and has a large capacity.
Serves as a blood reservoir
short circuit blood vessel
Direct anastomotic branches between arterioles and venules, mainly distributed in fingers, toes, auricles, etc.
related to body temperature regulation
Hemodynamics
Blood flow and blood flow velocity
blood flow (n volume velocity)
Influencing factors: the pressure at both ends of the blood vessel and the resistance of the blood vessel to blood flow
Blood flow velocity (n)
The blood flow velocity of various types of blood vessels is inversely proportional to the total cross-sectional area of similar blood vessels
blood flow pattern
Laminar flow
Turbulence
Blood flow resistance (n)
source
friction between blood
Friction between blood and blood vessel walls
Poiseuille's law
blood pressure (n)
Formative factors
Average filling pressure of circulatory system (n)
heart ejection
peripheral resistance
Retraction of elastic reservoir vessels
Arterial blood pressure (n) and arterial pulse
Arterial blood pressure and its normal values
Systolic blood pressure (n)
Diastolic blood pressure (n)
Pulse pressure (n)
mean arterial pressure (n)
Factors affecting arterial blood pressure
stroke volume
When the heart rate and peripheral resistance are relatively stable, the stroke volume increases, the ejected blood volume increases, the pressure on the arterial wall increases, the systolic blood pressure increases, the diastolic blood pressure remains basically unchanged, and the pulse pressure increases. On the contrary, the pulse pressure decreases.
heart rate
Within a certain range, heart rate increases, cardiac output increases, arterial blood pressure increases, and vice versa
When the stroke volume and peripheral resistance are relatively stable, the heart rate increases, the diastolic period shortens, the blood volume remaining in the arteries increases, and the diastolic blood pressure rises. Due to the increase in arterial blood pressure, a large amount of blood flows to the periphery during systole. , so the increase in systolic blood pressure is not as good as the increase in diastolic blood pressure, and the pulse pressure decreases
peripheral resistance
When cardiac output and heart rate are relatively stable and peripheral resistance changes, it will have an impact on both diastolic and systolic blood pressure, but the impact on diastolic blood pressure will be greater, because during diastole, the speed of blood flow to the periphery is mainly determined by peripheral resistance, and peripheral resistance Increase, the amount of blood remaining in the arteries at the end of diastole increases, and diastolic blood pressure increases, and vice versa. Therefore, diastolic blood pressure reflects the amount of peripheral resistance.
elasticity of aortic wall
The relationship between circulating blood volume and blood vessel volume
Venous blood pressure and venous blood return volume
venous blood pressure
Peripheral venous pressure (n)
Low blood pressure and low blood flow resistance
Helps veins store blood and return it to the heart
Largely affected by body position and gravity
Hydrostatic pressure (n)
Venous filling is greatly affected by transmural pressure
Transmural pressure (n)
Central venous pressure (n)
Influencing factors
cardiac ejection capacity
The heart's ejection ability is good, and blood can be taken into the aorta in a timely manner. The central venous pressure is low, and vice versa.
venous blood return velocity
Venous blood return speed increases and central venous pressure increases
effect
Effect on ventricular filling
If central venous pressure is too low, ventricular filling will be insufficient and cardiac output will decrease. If central venous pressure is too high, it is not conducive to venous blood return
In clinical practice, venous pressure is often used as an indicator of the speed and volume of fluid replacement.
Central venous elevation
Too much fluid, too fast, or cardiac ejection insufficiency
low central venous pressure
Reduced blood volume or impaired venous return
Venous blood return to the heart and its influencing factors
Venous return to the heart (n is usually equal to cardiac output)
Factors affecting the amount of venous blood returned to the heart
average filling pressure of circulatory system
When blood volume increases or volume vasoconstriction, the average filling pressure of the circulatory system increases, and the venous return blood volume increases, and vice versa.
myocardial contractility
The myocardial contractility is strong, the ejection speed is accelerated, the ejection volume is increased, and the ventricular emptying is relatively complete. During diastole, the ventricular pressure is low, the suction force of the blood in the atrium and large veins is greater, and the venous return blood volume increases.
Left heart failure, pulmonary circulation venous congestion. Right heart failure, systemic venous congestion
Effects of gravity and body position
skeletal muscle compression
respiratory movements
Microcirculation
Microcirculation components and blood flow pathways
Typical microcirculation composition
Arterioles, posterior arterioles, precapillary sphincter, true capillaries, permeating capillaries, arteriovenous anastomoses, venules
roundabout pathway (nutritional pathway)
No blood capillaries and arteriovenous anastomotic branches
It is a place where blood and tissues exchange substances.
direct access road
No precapillary sphincter, true capillaries, arteriovenous anastomotic branches
Promote the rapid return of blood to the heart through capillaries
Arteriovenous short circuit
arteriole, arteriovenous anastomosis, venule
Regulates body temperature and promotes heat dissipation. It is usually in a closed state and is mainly located on the palms, toes, auricles, etc.
Physiological characteristics of microcirculation
Regulation of microcirculatory blood flow
exchange of substances between blood and tissue fluid
Way
Diffusion (main method)
Small portions of fat-soluble substances and small-molecule water-soluble substances with diameters smaller than the pores of capillary walls
swallow
Filtration (n) and reabsorption (n)
Tissue fluid and lymph fluid
Generation of interstitial fluid (n) and reflux (n)
Effective filtration pressure = (capillary blood pressure interstitial fluid colloid osmotic pressure) - (plasma colloid osmotic pressure interstitial fluid hydrostatic pressure)
Factors affecting tissue fluid production and reflux
capillary blood pressure
Depends on the ratio of capillary front resistance to rear resistance. As the ratio increases, capillary blood pressure decreases and tissue fluid production decreases. As the ratio decreases, capillary blood pressure increases and tissue fluid production increases.
plasma colloid osmotic pressure
permeability of capillary walls
lymphatic drainage
The meaning of lymphatic drainage
Recovery of proteins from tissue fluid
Transport fats and other nutrients
Regulate the balance between plasma and tissue fluid
Immune barrier function of lymph nodes
Regulation of cardiovascular activity
neuromodulation
Heart innervation and its functions
cardiac sympathetic nerve
Preganglionic nerve fibers are cholinergic neurons, and their terminals release acetylcholine (ACh), which binds to the cholinergic N1 receptor on the cell membrane of postganglionic neurons, causing excitation of postganglionic neurons.
Postganglionic neurons are adrenergic neurons. Their terminals release norepinephrine (NE), which binds to β1 receptors on the myocardial cell membrane and causes positive myocardial inotropic effects.
Increased heart rate - positive chronotropic effect
Increased cardiac contraction - positive inotropic effect
Accelerated conduction at the atrioventricular junction - positive conduction change
cardiac vagus nerve
Preganglionic and postganglionic neurons are all cholinergic neurons, and their terminals release acetylcholine (ACh), which interacts with the M-type receptors on the myocardial cell membrane postganglionic to weaken cardiac activity and exhibit a negative inotropic effect.
Innervation of blood vessels and their functions
vasomotor nerve fibers
sympathetic vasoconstrictor nerve
Preganglionic neurons are cholinergic neurons that release acetylcholine (ACh)
Postganglionic neurons are adrenergic neurons that release norepinephrine (NE), which binds to the a receptor on the vascular smooth muscle, causing smooth muscle contraction, and binds to the β2 receptor on it, causing its relaxation, but NE and a Receptor binding capacity is stronger than β2 receptors
vasodilatory nerves
sympathetic vasodilatory nerves
Postganglionic fibers release acetylcholine, which binds to vascular smooth muscle M receptors and causes vasodilation.
It is of great significance to the defense response and the redistribution of blood flow during exercise.
parasympathetic vasodilatory nerve
Postganglionic fibers release acetylcholine, which binds to vascular smooth muscle M receptors and causes vasodilation.
cardiovascular center(n)
spinal cord
Medulla oblongata
Function overview
The basic center that regulates cardiovascular activity. Many basic cardiovascular reflexes are intersected in the medulla oblongata. The functions of high-level centers also exert effects through the medulla oblongata center down to the cardiovascular neurons of the spinal cord.
Functional partitions of different parts
rostral ventrolateral part of medulla oblongata
Location of cardiac sympathetic center and sympathetic vasoconstrictor center
Dorsal and nucleus ambiguus of the vagus nerve in the medulla oblongata
The location of the cardiac vagal center and vagal preganglionic neurons
nucleus of solitary tract
The neuron here is the first-level substitution station for incoming neurons.
caudal ventrolateral part of medulla oblongata
Excitation of neurons here can inhibit the tonic activity of sympathetic vasoconstrictor nerves in the ventrolateral part of the rostral medulla oblongata, causing vasodilation.
hypothalamus
Important integration center through which cardiovascular activity becomes an integral component of thermoregulation and defense responses
Reflexive regulation of cardiovascular activity
Baroreceptor reflex (depressor reflex) of the carotid sinus and aortic arch
carotid sinus baroreceptor
The afferent nerve is the sinus nerve, which merges with the glossopharyngeal nerve and enters the medulla oblongata.
aortic arch baroreceptor
The afferent nerve is the aortic nerve, which travels along the vagus nerve and then enters the medulla oblongata.
Mechanism of action (highest sensitivity at 60-180mmHg)
When arterial blood pressure suddenly increases, the carotid sinus and aortic arch baroreceptors are strengthened by mechanical stretch stimulation, causing their firing frequency to increase. The afferent through the carotid sinus and aortic arch nerves respectively increases and reaches the nucleus of the solitary tract of the medulla oblongata. Acts through 3 ways
Inhibits the neurons in the ventrolateral part of the rostral medulla oblongata, inhibiting the tonic activity of the cardiac sympathetic center and sympathetic vasoconstrictor center
Exciting the dorsal vagal nucleus and nucleus ambiguus in the medulla oblongata, increasing vagal activity
Inhibits the release of vasopressin in the supraoptic and paraoptic nuclei of the hypothalamus
Chemoreceptive reflex (pressor reflex) of the carotid body and aortic body
Particularly sensitive to changes in the chemical composition of the blood, such as low oxygen, increased partial pressure of carbon dioxide, and increased hydrogen ion concentration
The afferent impulses are transmitted to the nucleus of the solitary tract of the medulla oblongata via the sinus nerve and the vagus nerve respectively, which reflexively triggers the excitement of the respiratory center, deepens and accelerates breathing, and thereby indirectly causes changes in cardiovascular activity: increased heart rate, increased cardiac output, heart and brain blood flow increases, but blood flow to abdominal viscera and kidneys decreases, and blood pressure increases
Features
Normally, chemoreceptive reflexes do not significantly regulate cardiovascular activity.
When the blood pressure is reduced to 40-80mmHg, there are few incoming impulses from the baroreceptor reflex, but the chemoreceptor reflex is significantly enhanced. This is due to chemical stimulation such as local hypoxia, increased carbon dioxide partial pressure, and high concentration of hydrogen ions caused by reduced local blood flow. for the sake of enhancement
The chemoreceptor reflex first causes changes in respiratory movements, which indirectly causes an increase in blood pressure.
physiological significance
In cases of hypoxia, asphyxia, acidosis, blood loss, hypotension, or insufficient blood supply to the brain, increase peripheral resistance, redistribute blood flow, and ensure blood flow supply to the heart and brain.
body fluid regulation
Epinephrine (E) and norepinephrine (NE)
E (a, beta receptor) (cardiac emergency drug)
Heart (binds to β1 receptors)
The heart rate is accelerated, the conduction at the atrioventricular junction is accelerated, the myocardial contractility is strengthened, and the cardiac output is increased.
Blood vessels (depending on the distribution of a receptors and β2 receptors on vascular smooth muscle)
Skin, kidneys, gastrointestinal tract (binds with a receptor)
vasoconstriction
Skeletal muscle, liver, coronary blood vessels (binds with β2 receptors)
vasodilation
Intravenous injection E
In small doses, it mainly stimulates β2 receptors and produces vasodilation.
In large doses, it also excites α receptors, causing a vasoconstrictor effect.
NE (vasopressors)
It mainly binds to α and β1 receptors, but less to β2 receptors. Therefore, NE has the effect of directly exciting the heart and has a strong contraction effect on most blood vessels, increasing peripheral resistance and significantly increasing blood pressure.
Reasons why blood pressure increases and heart rate decreases after intravenous injection of NE
The increase in blood pressure strengthens the blood pressure receptor reflex activity, and its inhibitory effect on the heart is stronger than the excitatory effect of NE on the heart, so the heart rate decreases.
renin-angiotensin system
An important body fluid regulation system in the human body, which plays an important role in regulating the body's blood pressure, water and electrolyte balance, and the homeostasis of the internal environment.
Physiological effects (exerting physiological effects by binding to angiotensin receptors on the cell membrane surface)
Directly constricts the arterioles throughout the body, increases blood pressure, constricts the venules throughout the body, and increases the amount of blood returned to the heart.
Promote the release of NE from sympathetic vasoconstrictor nerve fiber terminals
Effects on the central nervous system
Reduce the sensitivity of the central nervous system to the baroreceptor reflex and increase the tone in the sympathetic vasoconstrictor
Promote the release of vasopressin and oxytocin from the adenohypophysis
Promotes the action of adrenocorticotropin-releasing hormone
Produce or enhance thirst, leading to drinking behavior
Stimulates the release of aldosterone from the zona glomerulosa of the adrenal cortex, increases the reabsorption of sodium ions and water by the renal tubules, and increases circulating blood volume
antihypertensive drugs
ACE inhibitor (captopril) AT receptor antagonist (losartan)
Kallikrein-kinin system
Bradykinin and vasodilator are strong vasodilator substances that can relax vascular smooth muscles, increase capillary permeability, and lower blood pressure, but they have a contractile effect on other parts of smooth muscles.
The kinin system and RAS have close functions. Plasma kallikrein can convert prorenin into renin under isolated conditions, and ACE can degrade kinin into inactive fragments, thereby reducing the vasodilation effect of kinin. role
Vasopressin (VP)
Vascular smooth muscle V1 receptor
Cause strong vasoconstriction and increase blood pressure
V2 receptors on the peritubular membrane of renal distal tubules and collecting ducts (main site of action)
Promotes the reabsorption of water by renal tubules and collecting ducts, so it is also called antidiuretic hormone
VP does not often regulate blood pressure. Only under conditions of water deprivation, blood loss or dehydration, VP secretion increases and plays an important role in maintaining fluid volume in the body and maintaining arterial blood pressure.
atrial natriuretic peptide
Important humoral factors that regulate water and salt balance in the body
Has a strong diuretic and natriuretic effect
Contract vascular smooth muscle, reduce peripheral resistance, slow heart rate, reduce stroke volume, reduce cardiac output, and reduce blood pressure
Inhibits the renin-angiotensin-aldosterone system, indirectly promotes the excretion of sodium ions and inhibits the effect of VP
Vasoactive substances produced by vascular endothelial cells
endothelial relaxing factor
Nitric oxide can reduce the concentration of calcium ions in smooth muscle cells and relax blood vessels. At the same time, it can work with prostacycline and other vasodilator substances to counteract the effects of NE and other vasoconstrictor substances released by sympathetic nerve endings.
endothelial vasoconstrictor
Endothelin is the strongest vasoconstrictor substance currently known among vasoactive substances. Its mechanism of action is to bind to specific receptors on smooth muscle cells and promote the release of calcium ions from the sarcoplasmic reticulum, thereby enhancing the contraction of vascular smooth muscles.
Other regulatory substances
histamine
It has a strong vasodilatory effect, which can enhance the permeability of capillary and venous walls, increase the production of tissue fluid, and cause tissue edema.
prostaglandins
Opioid peptides
self-regulation