Physiological Regulation of Arterial Blood Pressure
Physiological Regulation of Arterial Blood Pressure Dr Khwaja Amir Assistant Professor Objectives By the end of this session, the student should be able to: a) Outline the different mechanisms involved in regulation of ABP. b) Discuss the role of reflexes especially
baroreceptor reflex in regulation of ABP. c) Discuss the role of renin-angiotensin system in regulation of ABP. d) Discuss the role of renal-body fluid in longterm regulation of ABP. Mechanisms Involved for Regulation of Arterial Blood Pressure Changes in mean arterial pressure after rapid
hemorrhage A-return of MAP to normal by compensatory mechanism B-failure of compensatory mechanism leading to hypovolemic shock and death
Mechanisms Involved for Regulation of Arterial Blood Pressure Rapidly acting mechanism for regulation of blood pressure Mostly the nervous control mechanism Baro receptor feed back mechanism Central nervous system ischemic mechanism Chemoreceptor mechanism Intermediate acting mechanism for control of blood pressure Renin angiotensin vasoconstrictor mechanism
Stress relaxation of vasculature Fluid shift across the capillary for adjustment of blood volume Long term mechanism for control of blood pressure Sympathetic nervous control of circulation The baroreceptor
system for controlling arterial pressure Role of the Nervous System in Rapid Control of Arterial Pressure Nervous control of arterial pressure is by far the most rapid of all our mechanisms for pressure control. When there is drop in arterial blood pressure there are three major changes that occur simultaneously, each of which helps to increase arterial pressure. They are as
follows 1. Most arterioles of the systemic circulation are constricted. 2. The veins especially (but the other large vessels of the circulation as well) are strongly constricted. This displaces blood out of the large peripheral blood vessels toward the heart, thus increasing the volume of blood in the heart chambers. 3. Finally, the heart itself is directly stimulated by the Reflex Mechanisms for Maintaining Normal
Arterial Pressure Reflex Mechanisms for Maintaining Normal Arterial Pressure Baroreceptor reflex It is the baroreceptor arterial pressure control system and it is the best known nervous mechanism for control of arterial pressure. Basically, this reflex is initiated by stretch receptors,
called either baroreceptors or pressoreceptors, located at specific points in the walls of several large systemic arteries. Baroreceptors are spray-type nerve endings that lie in the walls of the arteries; they are stimulated when stretched. They are extremely abundant in (1) the wall of each internal carotid artery slightly above the carotid bifurcation, an area known as the carotid sinus, and (2) The baroreceptors respond much more to a rapidly changing pressure than to a stationary pressure.
Because the baroreceptor system opposes either increases or decreases in arterial pressure, it is called a pressure buffer system and the nerves from the baroreceptors are called buffer nerves. The long-term regulation of mean arterial pressure by the Changes in mean aortic pressure in response to 8% blood loss in three groups of individual (2) Control of Arterial Pressure by the Carotid and Aortic Chemoreceptors-chemoreceptor reflex
Whenever the arterial pressure falls below a critical level, the chemoreceptors become stimulated because diminished blood flow causes decreased oxygen, as well as excess buildup of carbon dioxide and hydrogen ions that are not removed by the slowly flowing blood. The signals transmitted from the chemoreceptors excite the vasomotor center, and this elevates the arterial pressure back toward normal. However, this chemoreceptor reflex is not a powerful arterial pressure controller until the arterial pressure falls below 80 mm Hg. Therefore, it is at the lower
pressures that this reflex becomes important to help prevent further decreases in arterial pressure and Pulmonary Artery Reflexes Regulate Arterial Pres Both the atria and the pulmonary arteries have in their walls stretch receptors called low-pressure receptors These low-pressure receptors play an important role, especially in minimizing arterial pressure changes in response to changes in blood volume They do detect simultaneous increases in pressure in the low-pressure areas of the circulation caused by
increase in volume, and they elicit reflexes parallel to the baroreceptor reflexes to make the total reflex system more potent for control of arterial pressure Atrial Reflexes That Activate the Kidneys-The "Volume Reflex." Stretch of the atria also causes significant reflex dilation of the afferent arterioles in the kidneys. Signals are also transmitted simultaneously from the atria to the hypothalamus to decrease secretion of antidiuretic hormone (ADH). Combination of these two
effects-increase in glomerular filtration and decrease in reabsorption of the fluid-increases fluid loss by the kidneys and reduces an increased blood volume back toward normal Atrial stretch caused by increased blood volume also elicits a hormonal effect on the kidneys-release of atrial natriuretic peptide-that adds still further to the excretion of fluid in the urine and return of blood volume toward normal rial Reflex Control of Heart Rate (the Bainbridge Reflex)
An increase in atrial pressure also causes an increase in heart rate, sometimes increasing the heart rate as much as 75 percent The stretch receptors of the atria that elicit the Bainbridge reflex transmit their afferent signals through the vagus nerves to the medulla of the brain. Then efferent signals are transmitted back through vagal and sympathetic nerves to increase heart rate and strength of heart contraction. Thus, this reflex helps prevent Central Nervous Ischemic
damming of bloodSystem in the veins, atria, and pulmonary Response circulation This arterial pressure elevation in response to cerebral ischemia is known as the central nervous system (CNS) ischemic response. It is one of the most powerful of all the activators of the sympathetic vasoconstrictor system
The Renin-Angiotensin System: Its Role in Arterial Pressure Control Components of the Renin-Angiotensin System Renin is synthesized and stored in an inactive form called prorenin in the juxtaglomerular cells (JG cells) of the kidneys. The JG cells are modified smooth muscle cells located in the walls of the afferent arterioles immediately proximal to the glomeruli.
When the arterial pressure falls, intrinsic reactions in the kidneys themselves cause many of the prorenin molecules in the JG cells to split and release renin. Most of the renin enters the renal blood and then passes out of the kidneys to circulate throughout the entire body Renin-angiotensin vasoconstrictor mechanism for arterial pressure
control Angiotensin II is an extremely powerful vasoconstrictor, and it also affects circulatory function in other ways as well. During its persistence in the blood, angiotensin II has two principal effects that can elevate arterial pressure. i. The first of these, vasoconstriction in many areas of the body, occurs rapidly. Vasoconstriction occurs intensely in the arterioles and much less so in the veins. Constriction of the arterioles increases the
total peripheral resistance, thereby raising the arterial pressure. ii. The second principal means by which angiotensin II increases the arterial pressure is to decrease excretion of both salt and water by the kidneys. This long-term effect, acting through the extracellular fluid volume mechanism, is even more powerful than the acute vasoconstrictor mechanism in Angiotensin II causes the kidneys to retain both salt and water in two major ways:
1. Angiotensin II acts directly on the kidneys to cause salt and water retention. 2. Angiotensin II causes the adrenal glands to secrete aldosterone, and the aldosterone in turn increases salt and water reabsorption by the kidney tubules. Thus both the direct effect of angiotensin on the kidney and its effect acting through aldosterone are important in long-term arterial pressure control. However, research has suggested that the direct effect of angiotensin on the kidneys is perhaps three or more times as potent as the indirect effect acting
through aldosterone-even though the indirect effect is the one most widely known. Stress Relaxation ofVasculature Delayed Compliance in a Venous Segment Delayed compliance (Stress relaxation) of vessels The principle of delayed compliance is the mechanism by which a blood vessels attempts to return back to its
original pressure when it is loaded with blood or blood is withdrawn from it , this is a property of smooth muscles and is exhibited by blood vessels as well as hollow viscera like urinary bladder When a segment of a vein is exposed to increased volume , then immediately its pressure increases but after some time the pressure returns back to normal due to stretching of the vessel wall, similarly after drop in original volume due to any fluid loss the blood pressure decreases for some time and then it returns back to normal due to changes in the arrangement of
smooth muscle. Similar phenomenon can be seen in urinary bladder. Fluid shift across the capillary for adjustment of blood volume The arterial hypotension, arteriolar constriction, and reduced venous pressure during hemorrhagic hypotension lower hydrostatic pressure in the capillaries. The balance of these forces promotes the net reabsorption of interstitial fluid into the vascular
compartment Considerable quantities of fluid may thus be drawn into the circulation during hemorrhage. About 0.25 mL of fluid per minute per kilogram of body weight may be reabsorbed by the capillaries. Thus, approximately 1 L of fluid per hour might be autoinfused from the interstitial spaces into the circulatory system of an average individual after acute blood loss Substantial intracellular exchange is
quantities of fluid may shift slowly from the to the extracellular space. This fluid probably mediated by secretion of cortisol Role of renal-body fluid control mechanism in long-term regulation of ABP An increase in arterial pressure in the human of only a few mm Hg can double renal output of water, which is
called pressure diuresis, as well as double the output of salt, which is called pressure natriuresis. Control of renal NaCl and water excretion Renal Sympathetic Nerves ( Activity: NaCl Excretion) GFR Renin secretion Na+ reabsorption along the nephron Renin-Angiotensin-Aldosterone ( Secretion: NaCl Excretion) Angiotensin II stimulates reabsorption of Na+ along the nephron
Aldosterone stimulates Na+ reabsorption in the thick ascending limb of Henle's loop, distal tubule, and collecting duct Angiotensin II stimulates secretion of ADH Natriuretic Peptides: ANP, BNP, and Urodilatin ( Secretion: NaCl Excretion) GFR Renin secretion Aldosterone secretion (indirect via in angiotensin II and direct on the adrenal gland) NaCl and water reabsorption by the collecting duct ADH secretion and inhibition of ADH action on the distal tubule and
collecting duct enal Urinary Output Curve The approximate average effect of different arterial pressure levels on urinary volume output by an isolated kidney, demonstrating markedly increased urine volume output as the pressure
rises. This increased urinary output is the phenomenon of pressure diuresis. Not only does increasing the arterial pressure increase urine volume output, but it causes Increases in cardiac output, urinary output, and arterial
pressure caused by increased blood volume in dogs whose nervous pressure control mechanisms had been blocked. This figure shows return of arterial pressure to normal after about an hour of fluid loss into the
urine Near infinite feedback gain This return of the arterial pressure always back to the equilibrium point is the near infinite feedback gain principle for control of arterial pressure by the renal-body fluid
mechanism. Two ways in which the arterial pressure can be increased: A, by shifting the renal output curve in the right-hand direction toward a higher pressure level or B, by increasing the
intake level of salt and water Summary a) Outline the different mechanisms involved in regulation of ABP. b) Discuss the role of reflexes especially baroreceptor reflex in regulation of ABP. c) Discuss the role of renin-angiotensin system in regulation of ABP.
d) Discuss the role of renal-body fluid in long-term regulation of ABP. thanks
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