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The aortic and carotid bodies are densely vascularized groups of specialized cells found in the proximity ofthe arterial baroreceptors. Although they are more importantin regulation of respiration (see Section 4), they respond toreduced arterial PO2, and to a lesser extent to elevated PCO2and H+ concentration, by initiating a neural reflex that produces arterial and venous constriction.The Peripheral CirculationREGULATION OF ARTERIAL BLOOD PRESSUREFrom the foregoing, it should be clear that local, intrinsicmechanisms for vascular regulation are mainly aimed at regulation of regional blood flow, whereas neural and humoralmechanisms are often aimed at regulation of arterial bloodpressure. The maintenance of mean arterial pressure (MAP)near its normal level is necessary for adequate perfusion oftissues throughout the systemic circulation.
Rearranging theflow equation (Q = ΔP/R), the relationship ΔP = R × Q results,where ΔP is the pressure gradient, R is resistance, and Q isflow. The pressure gradient is the difference between arterialand central venous pressure. For the overall systemic circulation, Q is equal to cardiac output and R is total peripheralresistance (TPR), yieldingΔP = CO × TPRBecause venous pressure is very low, this equation can beessentially reduced to:MAP = CO × TPRThus, regulation of arterial blood pressure involves regulationof cardiac output and systemic resistance, through the variousmechanisms already described. Blood pressure is monitoredat several points in the system (Fig.
12.6):■■■aortic arch and carotid sinus baroreceptorsrenal juxtaglomerular apparatuslow-pressure (cardiopulmonary) baroreceptorsShort-Term Regulation of Blood Pressure byArterial BaroreceptorsThe high-pressure arterial baroreceptors of the aortic archand carotid sinus and the associated baroreceptor reflexes aremost important for moment-to-moment regulation of arterial pressure.
During normal, quiet daily activities, an inverserelationship is usually observed between changes in bloodpressure and heart rate, reflecting this role of the baroreceptorreflex in maintaining pressure: when pressure falls, heart raterises; when pressures rises, heart rate falls. These fluctuationsin heart rate reflect changes in sympathetic and parasympathetic outflow from the medullary cardiovascular centers, inresponse to the degree of baroreceptor stretch.Efferent sympathetic nerve activity is inversely related to MAPbetween the range of 60 to 160 mm Hg in a normal individual(see Fig. 11.2). At pressures below 60 mm Hg, sympatheticnerve activity is maximal.
In addition to MAP, baroreceptorsare also sensitive to pulse pressure. If pulse pressure is dampened while MAP is held constant, afferent nerve impulsesfrom the baroreceptors to the cardiovascular center will beless frequent, and sympathetic efferent activity and thus arterial blood pressure will be elevated.The arterioles of the juxtaglomerular apparatus of the kidneysalso contain high-pressure baroreceptors; in this case, stretch131“Resetting” of arterial baroreceptor sensitivity occurswhen blood pressure is chronically elevated.
In a healthyperson with normal blood pressure, baroreceptors function toreturn arterial pressure to the normal level when pressure fallsor rises. With chronic hypertension, a new set-point is established, whereby baroreceptor activity is aimed at maintainingthe higher resting blood pressure. Although this change appears,on the surface, to be maladaptive, it allows adequate short-termregulation of blood pressure despite higher basal bloodpressure.results in release of the enzyme renin by the kidney.
Reninenzymatically cleaves the plasma protein angiotensinogen(a liver product) to form angiotensin I, which is convertedto angiotensin II by endothelial angiotensin-convertingenzyme. This mechanism is important in short-term regulation of blood pressure only during pathophysiologic statessuch as hemorrhage.Role of Low-Pressure Baroreceptors andAtrial StretchLow-pressure baroreceptors are found in low-pressure sitesof the circulation, specifically the atria and large vessels of thepulmonary circulation, and respond to changes in bloodvolume.
The Bainbridge reflex was discussed earlier; increasedatrial stretch initiates a reflexive increase in heart rate. Reduction of blood volume, for example during hemorrhage, isdetected by low-pressure baroreceptors in the left atrium, aswell as arterial baroreceptors. Neural afferent signals throughthe vagus nerve to the hypothalamus result in vasopressinrelease by the posterior pituitary. Like angiotensin II, vasopressin participates in short-term responses to hemorrhage,but not in acute regulation of blood pressure under normalcircumstances.Increased blood volume and stretch of atria stimulates atrialmyocytes to secrete stored atrial natriuretic peptide (ANP).ANP dilates some vessels (although it has little role in acuteblood pressure regulation) and has important effects onsodium and water balance (see Section 5) and long-term regulation of blood pressure (see following section).Long-Term Regulation of Blood PressureIn contrast to moment-to-moment regulation of blood pressure, which relies heavily on baroreceptor reflexes and adjustments to cardiac and vascular function, long-term regulationof blood pressure is accomplished mainly by mechanisms thatcontrol blood volume through neural and humoral pathways(Fig.
12.7). These mechanisms are covered in further detail inSections 5 and 7. Briefly, when blood volume is depleted andblood pressure is consequently reduced, direct effects ofreduced renal perfusion, as well as increased sympatheticnerve activity, stimulate renin production by the kidneys132Cardiovascular PhysiologyVasopressin releasedin response to reducedblood volumeBrainCN IXCN XCN XHigh-pressure baroreceptorsCarotidsinusHigh-pressure baroreceptorresponseAortic archBaroreceptor afferent nervedischarge (% baseline)PulmonaryvesselsANP releasedin response toincreased bloodvolumeCardiacatriaLow-pressure baroreceptors20010000Juxtaglomerularapparatus ofthe kidney100MAP (mm Hg)200BloodpressureReninBloodpressureReninFigure 12.6 Monitoring of Blood Pressure To maintain adequate blood flow to tissues, the bodyhas a complicated system for monitoring and regulating blood pressure.
High-pressure baroreceptors in theaortic arch and carotid sinus are extremely important in acute regulation of blood pressure, through theireffects on the autonomic nervous system. Afferent arterioles in the renal juxtaglomerular apparatus alsocontain high-pressure baroreceptors; these are involved in regulation of renin release, and consequently,regulation of sodium and water balance, important in long-term regulation of blood pressure. Low-pressurebaroreceptors in the heart and pulmonary circulation respond to changes in blood volume and modulatesympathetic activity and vasopressin release.
The cardiac atria also release atrial natriuretic peptide (ANP)in response to elevated blood volume.The Peripheral CirculationResponse to Decreased Blood Volume and PressureThirstSympatheticnerve activityADHBrain133Response to Increased Blood Volume and PressureSympatheticnerve activityADHBrainCN IX, XCN IX, XAngiotensin IIHeartandlungsHeartandlungsANPAdrenalsLiverAdrenalsAngiotensinogenAngiotensin I(decreases NaClexcretion)ReninReninandangiotensin IIAldosteroneAldosterone(stimulates reninsecretion anddecreases NaClexcretion)(decreases water excretion)KidneysKidneysNaCl and H2OexcretionNaCl and H2OexcretionBlood volumeand pressure(increased H2O intake)Blood volumeand pressureFigure 12.7 Long-Term Response to Changes in Blood Volume and Pressure In additionto evoking mechanisms for acute adjustment of blood pressure, changes in blood volume and pressure willalso activate renal mechanisms for adjusting blood volume.
Reduced blood volume (and therefore arterialpressure) will stimulate the renin-angiotensin-aldosterone system, with the end result of sodium and waterretention. Reduced blood pressure will also activate the sympathetic nervous system, which will stimulaterenin secretion as well as have direct effects on the kidneys. On the other hand, increased volume willstimulate atrial natriuretic peptide (ANP) release by the heart.
ANP has direct renal effects(natriuresis and diuresis) and also inhibits aldosterone release by the adrenal medulla.(sympathetic activation occurs in part due to baroreceptorresponses). Renin action produces elevation of angiotensin I,which is subsequently cleaved to angiotensin II by endothelialcell angiotensin-converting enzyme (much of this enzymaticcleavage occurs in the pulmonary circulation). Angiotensin IIhas direct effects on sodium retention by the kidney and hasthe important effect of stimulating aldosterone release by thezona glomerulosa of the adrenal cortex.
Aldosterone alsopromotes renal sodium (and hence fluid) retention. Lowblood volume, through reflexes discussed earlier, stimulatesposterior pituitary antidiuretic hormone (ADH; also knownas vasopressin). ADH release, as well as thirst, is also stimulated by elevated plasma osmolality associated with volumedepletion. ADH promotes water retention by the kidney.134Cardiovascular PhysiologyThus, the effects of multiple hormones (ADH, angiotensin II,aldosterone) on sodium and fluid retention and water intakeresult in an increase in blood volume, which helps to maintainblood pressure. These mechanisms are important in the physiological responses to hemorrhage or dehydration; variousaspects are also implicated in elevation of blood pressure insome forms of hypertension.The diving reflex is a specialized mechanism for regulation of blood pressure and heart rate.
This reflex is anadaptation for conservation of oxygen in diving mammals,allowing protracted stays underwater without breathing. Duringdiving, the heart rate is slowed by increased vagal activity, whilepressure is maintained by arterial vasoconstriction. Thus, bloodflow to vital organs is maintained, while blood flow to much ofthe body besides the coronary and cerebral circulations isreduced; the work of the heart is also reduced. Although thediving reflex is weaker in humans, its effects can still be observedwhen the face is submerged in cold water and breath is held.Receptors in the face and nasal cavities are stimulated, andreflexive bradycardia and peripheral vasoconstriction occur.The diving reflex is thought to be responsible for the survivalof some children after long periods of accidental submersion incold water.The circle of Willis provides a high degree of collateralization between the large arteries that supply oxygenatedblood to the brain.
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