Blood Pressure Homeostasis: Learning Objectives: • Explain how and why blood pressure varies throughout the circulation

• Describe the factors that determine arterial blood pressure • Explain how arterial blood pressure is regulated acutely by the baroreflex • Explain how the kidneys regulate arterial blood pressure, with reference to the reninangiotensin system • Explain how salt intake influences blood pressure Blood Pressures throughout circulation: The heart pumps blood continually into the aorta. The wall of the aorta is compliant it accommodates the blood forced into it from the contracting left ventricle by stretching outwards and because the wall is also highly elastic it readily springs back into place. In this way the elasticity of the aorta allows it to store energy that is then imparted to the blood so forcing it further along the vessel. Pulse pressure is the difference between peak (systolic) and minimum (diastolic) pressures in the arterial circulation. As the arteries are distensible, they buffer the pressure wave from the left ventricle. Thus pulse pressure is a function of stroke volume and arterial distensibility. The arterial pressure alternates between a systolic pressure (peak arterial pressure) level of 120 mm Hg and a diastolic pressure (minimum arterial pressure) level of 80 mm Hg. Mean arterial pressure is the average arterial pressure throughout a cardiac cycle and it is approximately 90mm Hg as the heart spend more time in diastolic.

At any level of the circulatory system blood flow will be the same (i.e. approx 5L/min at rest). As diameter of vessels decreases, the total cross-sectional area increases and velocity of blood flow decreases. There is only one aorta with a cross-sectional area of 5 cm2 but the total cross-sectional area of the millions of capillaries is 2500 cm2. This situation is much like a river that flows rapidly through a narrow gorge but flows slowly through a broad plane. (Circulation time approx. 1 minute.) Blood pressure averages 100 mm Hg in aorta and drops to ~0 mm Hg by the time the blood gets to the right atrium. Greatest drop in pressure occurs in arterioles which regulate blood flow through tissues. This is because as cross-sectional area of vessels increases the pressure decreases (P = Force/Area).There are no large fluctuations in capillaries and veins. Muscular arteries and arterioles are capable of constricting or dilating in response to autonomic and hormonal stimulation. Muscular arteries regulate flow into a region of the body; arterioles regulate flow into a specific tissue.

by relaxing. When applied pressure exceeds systolic (peak) pressure. Factors that determine Arterial Blood Pressure: 1. CARDIAC OUTPUT: back to Ohm’s law. The artery is now always open. BLOOD VOLUME: via increased cardiac output 2. Korotkoff sounds disappear. thus having the capability of vastly altering blood flow in each tissue bed in response to the need of the tissue. but still compressed. Measuring Blood Pressure (Auscultatory Method): 1.The arterioles are the last small branches of the arterial system. P = F (CO) × R. Sounds are emitted due to turbulence created in blood as it passes through the lumen of blood vessels (or through the heart). Cuff pressure continues to fall. ***It is important to note that this is just a good estimation of blood pressure but for accurate measure need to sample pressure from a vessel. Korotkoff sounds become muffled 6. Stroke Volume: is the volume of blood ejected at each beat of the heart. they act as control conduits through which blood is released into the capillaries. Cuff pressure drops below diastolic pressure. when cardiac . As long as applied pressure is greater than diastolic pressure there will be Korotkoff sounds. the artery is closed off 3. Thus. 4. It depends on: a. 5. This causes the Korotkoff sounds. The arteriole has a strong muscular wall that can close the arteriole completely or can. blood spurts through compressed artery as arterial pressure transiently exceeds applied pressure. As cuff pressure is released. Applied pressure drops to the point where the artery is practically unaffected. dilate it several fold. Cuff applies pressure to antecubital artery 2. Stroke volume is directly related to the force of ventricular contraction.

Any increase in venous return will cause an increase in cardiac output via the Frank Starling mechanism (to be covered later). The central venous pressure (CVP) is the venous pressure measured at the entrance to the right atrium. increasing venous return boosting cardiac output via the Frank Starling mechanism 5. thus DP increases more than SP and PP falls accordingly. IX and X. pliable walls. This is HYDROSTATIC PRESSURE. Afferents from the aortic baroreceptors run in the vagus nerve (X). Thus in accordance with Ohm’s law. an acute increase in venous blood volume (via infusion) or in venous return (due to a selective vasoconstriction) will secondarily increase ABP due to an increase in FLOW.output is increased exclusively through an increase in stroke volume. even a slight change in pressure causes a strong change in the baroreflex signal to re-adjust arterial pressure back toward normal. Locations rich in baroreceptors include the aortic arch and the carotid sinus. The efferent pathways involve thoracic sympathetic nerves that innervate the heart (SA node and muscle) and the smooth muscle of blood vessels. The contraction of the leg muscles expels blood from the microvasculature. Because of the muscle pump. 4. The full effect of hydrostatic pressure is not normally exerted because of the VENOUS VALVES. veins above the heart simply collapse so that lumen pressures remain essentially atmospheric. 3. the baroreceptor feedback mechanism functions most effectively in the pressure range where it is most needed. When standing upright CVP remains unchanged although the venous pressure in the brain should fall to -10 mmHg (or 10 mmHg below atmospheric). Output from the CVC is relayed to sympathetic motor neurons via inhibitory inter neurones. This is due to the fact that the brain is above RA. Heart Rate: A large increase in heart rate (HR) is associated with a decrease in filling time for the ventricle and a decreased ‘run off’ time for the arterial circulation. PERIPHERAL RESISTANCE: Ohm’s law again. they are stimulated when stretched. In health CVP is 0-2 mmHg (i. When resistance in the circulation downstream from the major arteries increases. while afferents from the carotid sinus run in the glossopharyngeal nerve (IX). hydrostatic pressure only increases venous pressure by ~20 mm Hg in a walking adult. Baroreceptors are spray-type nerve endings that lie in the walls of the arteries. Thus. Thus. because veins have thin. GRAVITY: Hydrostatic pressure The effect of gravity means that blood pressure in the feet should be approximately 90 mmHg grater than at the heart.e. especially that in the normal operating range of arterial pressure. Note. SP rises more than DP. VENOUS CAPACITANCE: A reduction in venous capacitance ‘frees up’ venous blood. thus causing an increase in PP. combined with the venous valves this system is called the MUSCLE PUMP. Short Term Control of ABP: Baroreflex: Short term control of ABP relies on the presence of baroreceptors that monitor the degree of stretch (hence pressure) applied to artery walls. very close to atmospheric pressure). Afferent pathways from the carotid sinus and aortic arch pass via cranial n. if cardiac output is raised exclusively through increased HR. DP rises more than SP and PP falls. b. It is the sum of the resistances offered by the rest of the vascular system. These inputs are integrated within the nucleus solitarius located in the medulla. . this is reflected more in the DP than in the SP. In actual fact.

CNS ischemic response: when blood flow to the vasomotor centre in the lower brain stem becomes decreased severely enough to cause nutritional deficiency—that is. The net effects are (1) vasodilation of the veins and arterioles throughout the peripheral circulatory system and (2) decreased heart rate and strength of heart contraction. secondary signals inhibit the vasoconstrictor centre of the medulla and excite the vagal parasympathetic centre. . reflex causing the pressure to rise back toward normal. Control of blood volume is carried out by the kidneys. Conversely. to cause cerebral ischemia—the vasoconstrictor and cardioaccelerator neurons in the vasomotor centre respond directly to the ischemia and become strongly excited. An additional layer of control occurs via the hormonal pathway known as the Renin-Angiotensin System (RAS). Chemoreceptor reflex: a drop in arterial PO2 sensed by the carotid and aortic bodies and leads to the activation of the SNS. low pressure has opposite effects. excitation of the baroreceptors by high pressure in the arteries reflex causes the arterial pressure to decrease because of both a decrease in peripheral resistance and a decrease in cardiac output. The CNS ischemic response is one of the most powerful of all the activators of the sympathetic vasoconstrictor system.After the baroreceptor signals have entered the nucleus solitarius (CVC) of the medulla. Long Term control of ABP: Long-term control of arterial blood pressure is achieved by regulation of blood volume. Therefore.

the secondary increase in total peripheral resistance that results from the autoregulation mechanism helps greatly in increasing the arterial pressure. thus returning the pressure back toward normal. which (5) increases cardiac output. so that this autoregulation mechanism constricts blood vessels all over the body. because arterial pressure is equal to cardiac output times total peripheral resistance. The rising pressure in turn has a direct effect to cause the kidneys to excrete the excess extracellular fluid. Renin combines with angiotensinogen . It also causes an increase in sodium output (pressure natiuresis). which (6) increases arterial pressure. Long-term arterial blood pressure is SOLELY DETERMINED BY FLUID BALANCE. the blood volume and arterial pressure rise. When increased blood volume increases the cardiac output. Long-term ABP is at the ‘balance point’ between fluid intake and renal output. Finally. This in turn increases the total peripheral resistance. The Renin-Angiotensin System (RAS): Renin is an enzyme produced (from prorenin in the juxtaglomerular cells) and released by the kidneys under conditions of reduced ABP. Chronic intake of water and salt 2. which (3) increases the mean circulatory filling pressure. Most of the renin enters the renal blood and then passes out of the kidneys to circulate throughout the entire body. Thus two factors account for the long-term ABP: 1. The left-right shift of the renal function curve Changes in peripheral resistance will only change arterial blood pressure acutely. The overall mechanism by which increased extracellular fluid volume elevates arterial pressure follows the sequential events: (1) increased extracellular fluid volume (2) increases the blood volume. When the body contains too much extracellular fluid. There are two ways in which an increase in cardiac output can increase the arterial pressure. changes in vascular function may impact the renal circulation and thus indirectly alter blood volume (and thus long-term ABP) by shifting the renal function curve. but is the first step in the RAS cascade.Increasing arterial pressure causes a corresponding rise in renal urinary output (pressure diuresis). However. One of these is the direct effect of increased cardiac output to increase the pressure. and the other is an indirect effect to raise total peripheral vascular resistance through autoregulation of blood flow. the blood flow increases in all tissues of the body. which (4) increases venous return of blood to the heart. Renin itself has no direct effect on ABP. However. small amounts of the renin do remain in the local fluids of the kidney and initiate several intrarenal functions.

Vasoconstriction occurs intensely in the arterioles and much less so in the veins. Angiotensin causes the kidneys to retain both salt and water in two major ways: 1. . vasoconstriction in many areas of the body. it also stimulates release of ADH from the pituitary. the entire long-term renal– body fluid mechanism for arterial pressure control automatically becomes set to a higher arterial pressure level than normal. Angiotensin II is an extremely powerful vasoconstrictor. Angiotensin acts directly on the kidneys to cause salt and water retention. whenever excess amounts of angiotensin circulate in the blood. Also. salt and ADH: Aldosterone (secreted by the adrenal glands) acts on the kidneys to increase Na+ reabsorption. 2. This slowly increases the extracellular fluid volume. the mild constriction of the veins promotes increased venous return of blood to the heart. Aldosterone. acting through the extracellular fluid volume mechanism. Remember: “Where sodium goes. thereby raising the arterial pressure. occurs rapidly. water follows”. Angiotensin causes the adrenal glands to secrete aldosterone. The second principal means by which angiotensin II increases the arterial pressure is to decrease excretion of both salt and water by the kidneys. Angiotensin II has two principal effects that can elevate arterial pressure. and the aldosterone in turn increases salt and water reabsorption by the kidney tubules. ADH strongly stimulates water reabsorption by the kidneys. Ang I is then converted to ang II in the pulmonary circulation by angiotensin converting enzyme (ACE) present in the endothelium of the lung vessels. This long-term effect. Constriction of the arterioles increases the total peripheral resistance. which then increases the arterial pressure. thereby helping the heart pump against the increasing pressure. The first of these.(from the liver) to form angiotensin I. Na+ stimulates thirst centres and causes increased fluid ingestion. is even more powerful than the acute vasoconstrictor mechanism in eventually raising the arterial pressure. Thus. Angiotensin I has a mild vasoconstrictor properties but not enough to cause significant changes in circulatory function.

. but salt is not excreted so easily. Role of atrial natriuretic hormone (ANH) in the control of blood pressure: Stretching of the wall of the right atrium. making the person drink extra amounts of water to return the extracellular salt concentration to normal. Thus. This increases the extracellular fluid volume. This leads to reduction in ECF volume and hence also blood pressure. As salt accumulates in the body. The antidiuretic hormone then causes the kidneys to reabsorb greatly increased quantities of water from the renal tubular fluid. for these important reasons. The increase in osmolality caused by the excess salt in the extracellular fluid also stimulates the hypothalamic-posterior pituitary gland secretory mechanism to secrete increased quantities of antidiuretic hormone. causes the release of ANH from atrial cells.Salt Intake and ABP: Experimental studies have shown that an increase in salt intake is far more likely to elevate the arterial pressure than is an increase in water intake. accumulation of even a small amount of extra salt in the body can lead to considerable elevation of arterial pressure. the amount of salt that accumulates in the body is the main determinant of the extracellular fluid volume. as occurs with an increase in ECF volume. it also indirectly increases the extracellular fluid volume for two basic reasons: 1. When there is excess salt in the extracellular fluid. thereby diminishing the excreted volume of urine but increasing the extracellular fluid volume. leading to loss of Na+ from the kidney. Because only small increases in extracellular fluid and blood volume can often increase the arterial pressure greatly. 2. the osmolality of the fluid increases. ANH acts on the adrenal cortex to inhibit the release of aldosterone. The reason for this is that pure water is normally excreted by the kidneys almost as rapidly as it is ingested. and this in turn stimulates the thirst centre in the brain. The Na+ is accompanied by water.

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