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PHYS 1525 Cardiovascular 6 - CHAPTER 4 CARDlOVASCUtAR...

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Unformatted text preview: CHAPTER 4 . CARDlOVASCUtAR PHYSIOLOGY I4] Cardiac decelerator Sinoatrial node Nucleus tractus solitarius Contractility Cardiac Vaso ' accelerator constrictor Arterioles FIGURE 4—30. The baroreceptor reflex. The (-3 signs show increases in activity; 9 signs show decreases in activity; dashed lines show inhibitory pathways. carry the information to the brain stem; brain stem centers, which process the information and coordi- nate an appropriate response; and efferent neurons, which direct changes in the heart and blood vessels. Burorecepiors The baroreceptors are located in the walls of the carotid sinus, where the common carotid artery bifurcates into the internal and external carotid ar- teries, and in the aortic arch. The carotid sinus baroreceptors are responsive to increases or de- creases in arterial pressure, whereas the aortic arch baroreceptors are primarily responsive to increases in arterial pressure. The baroreceptors are mechanoreceptors, which are sensitive to pressure or stretch. Thus, changes in arterial pressure cause more or less stretch on the mechanoreceptors, resulting in a change in their membrane potential. Such a change in membrane potential is a receptor potential, which increases or decreases the likelihood that action potentials will be fired in the afferent nerves that travel to the brain stem. (If the receptor potential is depolarizing, then action potential frequency in— creases; if the receptor potential is hyperpolarizing, then action potential frequency decreases.) Increases in arterial pressure cause increased stretch on the baroreceptors and increased firing rate in afferent nerves. Decreases in arterial pres sure cause decreased stretch on the baroreceptors and decreased firing rate in the afferent nerves. Although the baroreceptors are sensitive to the absolute level of pressure, they are even more sensi~ tive to Changes in pressure and the rate of change of pressure. The strongest stimulus for the barorecep— tors is a rapid change in arterial pressure! The sensitivity of the baroreceptors can be al— tered by disease. For example, in chronic hyperten- sion (elevated blood pressure), the baroreceptors do not “see” the elevated blood pressure as abnor- mal. In such cases, the hypertension will be main— tained, rather than corrected, by the baroreceptor reflex. The mechanism of this defect is either de— creased sensitivity of the baroreceptors to increases in arterial pressure or an increase in the blood pres- sure set point of the brain stem centers. Information from the carotid sinus barorecep— tors is carried to the brain Stern on the carotid sinus nerve, which joins the glossopharyngeal nerve (cra- nial nerve iCN] IX). information from the aortic arch baroreceptors is carried to the brain stem on the vagus nerve (CN X). ‘to heart t T Heart rate FIGURE 4—31. Response of the baroreceptor reflex to acute hem- orrhage. The reflex is initiated by a decrease in mean arterial pres— sure (Pa). The compensatory re— sponses attempt to increase P. back to normal. TPR, total periph- ‘t Parasympathetic activity g 5 I t PaTOWARD NORMAL «rm-um} CHAPTER 4 CARMVASCULAR PHYSIOLOM i43 BAROHECEPTOR REFLEX ’ tPa it Stretch on Carotid sinus baroreceptors i , if Firing rate of carotid sinus nerve * ‘ J9 . ' ismp‘amam activity'to L ' heart and blood vessels T Heart rate _- ' T Contractility . ‘ ' Constriction starterioiestlTTFiR) ‘_ vyCohstriction of Veins ' , tUhstr‘essed volume ' 2T venous return . eral resistance. creases in Pa produce decreased stretch on the baro- receptors and decreased firing rate of the carotid sinus nerve. This information is received in the nu- cleus tractus solitarius of the medulla, which pro- duces a coordinated decrease in parasympathetic activity to the heart and an increase in sympathetic activity to the heart and blood vessels. Heart rate and contractility increase, which, together, produce an increase in cardiac output. There is increased constriction of arterioles, which produces an in- crease in TPR, and increased constriction of the veins, which decreases unstressed volume. The constriction of the veins increases venous return to contribute to the increase in cardiac output (Frank— Starling mechanism). Renin-Angioiensin Il—Aldasterone System The renin—angiotensin ll—aldosterone system reg» ulates Pa primarily by regulating blood volume. This system is much slower than the baroreceptor reflex because it is hormonally, rather than neurally, medi- ated. The renin—angiotensin ll—aldosterone system is activated in response to a decrease in the Pa. Activa— tion of this system, in turn, produces a series of responses that attempt to restore arterial pressure to normal. This mechanism, shown in Figure 4—32, has the following steps. 1. A decrease in Pa causes a decrease in renal perfusion pressure, which is sensed by mechanore ceptors in afferent arterioles of the kidney. The de— crease in Pa causes prorenin to be conVerted to renin in the juxtaglomerular cells (by mechanisms not entirely understood). Renin secretion. by the juxtaglomerular cells is also increased by stimula- tion of renal sympathetic nerves and by [32 agonists such as isoproterenol; renin secretion is decreased by 92 antagonists such as propranolol. 2. Renin is an enzyme. ln plasma, renin cata— lyzes the conversion of angiotensinogen (renin sub— strate) to angiotensin I, a decapeptide. Angiotensin I has little biologic activity, other than to serve as a precursor to angiotensin ll. 3. In the lungs and kidneys, angiotensin I is converted to angiotensin II. catalyzed by angioten- sin converting enzyme (ACE). 4. Angiotensin II is an octapeptide with sev— eral important biologic actions: on the adrenal cor— tex, on the arterioles, and on the kidney (as ex“, plained in Steps 5, 6, and 7). 5. Angiotensin ll acts on the zona glomerulosa cells of the adrenal cortex to stimulate the produc— tion of aldosterone. Aldosterone then acts on the principal cells of the renal distal tubule and collect— lM PHYSIOLOGY l , Yanglmensmdg ' ,, ,(renin ubstrate t Pa TOWARD NORMAL FIGURE 4—32. The renin-angio— tensin II-aldosterone system. The system is described in terms of the response to a decrease in Pa. ing duct to increase Na+ reabsorption and, thereby, to increase ECF volume and blood volume. The ac— tions of aldosterone require gene transcription and synthesis of new proteins in the kidney, which re- quires hours to days to occur and accounts for the slow response time of the renin—angiotensin ll- aldosterone system. 6. Angiotensin II also acts directly on the arte- rioles to cause vasoconstriction, thereby producing an increase in TPR and increase in Pa. 7. Angiotensin II also acts directly on the kid- ney, independent of its actions through aldosterone. Angiotensin II stimulates Na+—H+ exchange in the renal proximal tubule, which not only increases Nat rcabsorption but aids in the reabsorption of HCOg. In summary, a decrease in Pa activates the renin- TPR, total peripheral resistance. angiotensin lI—aldosterone system, producing a set of responses that attempt to increase Pa back to normal. The most important of these responses is the effect of aldosterone to increase renal Na‘ reab— sorption. When Na‘i’ reabsorption is increased, total body Nat content increases, which increases ECF volume and blood volume. Increases in blood vol- ume produce an increase in mean systemic pres- sure, which increases cardiac output (see Figure 4—28A) and Pa. There also is a direct effect of angio— tensin H to constrict arterioles, increasing TPR, and contributing to the increase in Pa (Box 4—2). Other ’ Regulatory Mechanisms In addition to the baroreceptor reflex and the renin-angiotensin II-aldosterone system, other mech- anisms that may aid in regulating mean arterial pres— CHAPTER 4 CARDIOVASCULAR PHYSIOLOGY 151 TABLE 4~7. Control of Special Circulations Circulation Local Metabolic Control Vasoactive Metabolites Sympathetic Control Mechanical Effects Coronary Most important Hypoxia l Least important Mechanical compression mechanism Adenosine l mechanism .L during systole Cerebral Most important C02 Least important Increases in intracranial mechanism l-l* mechanism pressure decrease cerebral blood flow Skeletal muscle Most important Lactate Most important Muscular activity mechanism during Kt mechanism at rest compresses blood vessels exercise Adenosine (on receptors, l vasoconstriction: [32, % receptors, vasodilation) ‘ Skin Least important —— Most important —— mechanism mechanism for temperature regulation ‘ (or; receptors, vasoconstriction) ._..L_ . Pulmonary Most importnat Hypoxia vasoconstricts Least important Lung inflation mechanism mechanism r“ Renal Most important ~- Least important ‘ —- mechanism (myogenic; mechanism tubuloglomerular feedback) WNW—m compression causes a brief period of occlusion and reduction of blood flow. When the period of occlu— sion is over (i.e., systole is over), reactive hyperemia occurs to increase blood flow and 02 delivery and to repay the Oz debt that was incurred during the compression. Cerebral Circulation The cerebral circulation is controlled almost en- tirely by local metabolites and exhibits autoregula— tion and active and reactive hyperemia. The most important local vasodilator in the cerebral circula— tion is CO; (or 141+) An increase in cerebral PC02 (producing an increase in Hi concentration and a decrease in pH) causes vasodilation of the cerebral arterioles, which results in an increase in blood flow to assist in removal of the excess C02. It is interesting that many circulating vasoactive substances do not affect the cerebral circulation be— cause their large molecular size prevents them from crossing the blood-brain barrier. Pulmonary Circulation The regulation of pulmonary circulation is dis~ cussed fully in Chapter 5. Briefly, the pulmonary circulation is controlled by local metabolites, pri— marily by 02. The effect of 02 on pulmonary arterio— lar resistance is the exact opposite of its effect in other vascular beds: in the pulmonary circulation, hypoxia causes vasoconstriction. This seemingly counterintuitive effect of Oz also is explained in Chapter 5. Briefly, regions of hypoxia in the lung cause local vasoconstriction. which effectively shunts blood away from poorly ventilated areas where the blood flow would be “wasted” and toward well—ventilated areas where gas exchange can occur. Renal Circulation The regulation of renal blood flow is discussed in detail in Chapter 6. Briefly, renal blood flow is tightly autoregulated so that flow remains constant even when renal perfusion pressure changes. Renal autoregulation is independent of sympathetic in— nervation, and it is retained even when the kidney is denervated (eg, in a transplanted kidney). Auto- regulation is presumed to result from a combination of the myogenic properties of the renal arterioles and tubuloglomerular feedback (see Chapter 6). Skeletal Muscle Circulation Blood flow to skeletal muscle is controlled both by local metabolites and by sympathetic innerva- tion of its vascular smooth muscle. Incidentally, the degree of vasoconstriction of skeletal muscle arteri— oles is a major determinant of TPR because the mass of skeletal muscle is so large, compared with that of other organs. 0 At rest, blood flow to skeletal muscle is regu— lated primarily by its sympathetic innervation Vascular smooth muscle in the arterioles of skeletal muscle is densely innervated by sympa— thetic nerve fibers. Some fibers are vasocon- stricting (0:1 receptors), and others are vasodi— lating ([32 receptors and muscarinic receptors). Thus, activation of a, receptors causes vasocon— ...
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