SummaryDuring animal evolution the circulatory system has shown a progressive modification in structure, function and short‐term control.Short‐term circulatory control has evolved from the limitation of a rising blood pressure via a reflex bradycardia to bidirectional control of blood pressure by appropriate reflex changes in heart rate, vascular resistance and impedance.Relevant experimental data ranges from extensive in mammals to nugatory in invertebrates. Baroreceptor research in intervening animal groups is varied, being particularly sparse in birds. This research is reviewed. There are few interspecies comparisons of baroreceptor physiology. Available data is complicated by variation in the techniques employed for assessing baroreceptor function. In non‐mammalian research the correlation of heart rate changes to pharmacologically induced changes in blood pressure predominate. In mammalian baroreceptor research methods based upon the ability of discrete baroreceptor sites to effect changes in the peripheral vasculature are more prevalent. All methods are susceptible to modification by other experimental variables, particularly the anaesthetic state of the animal.Available evidence shows a consistent response of a decreasing heart rate to baroreceptor loading throughout the vertebrates, with a progressive increase in the ability of the baroreceptors to change peripheral vascular resistance. These findings are consistent with the known, progressive trend from cholinergic to adrenergic control of the vascular system during evolution.Known baroreceptor sites appear to be located so as to protect the end‐organ or‐organs primarily at risk from inappropriate blood pressure changes; namely the gill vasculature in the fish, pulmonary circulation in the Amphibia and Reptilia, and the brain and heart in higher animal groups.It is postulated that the carotid sinus baroreceptors have developed in the Mammalia as a second functional baroreceptor site to provide extra protection against hypoperfusion of vital organs, particularly the heart and brain. In humans the dynamic aspects of cardiovascular carotid sinus control, particularly of skeletal muscle flow and integration with cardiopulmonary baroreceptors, may represent a specific response to the adoption of an upright stance. Extremes of environmental stress encountered in contemporary life may exceed the limitation of baroreceptor function in humans, as, for example, during gravitational loading particularly following periods of weightlessness and modification by endurance training.

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The regional differentiation of carotid sinus control of arterial pressure-flow relationships was studied in chloralose-anesthetized dogs. Simulatneous pressure-flow measurements were made in the ascending aorta, the celiac artery, the cranial mesenteric artery, the renal artery, and the femoral artery. The carotid sinuses were bilaterally isolated and perfused with pulsatile pressure. The open-loop reflex gain was not symmetrical about and was maximum at pressures below the closed loop operating point pressure. Changes in both peripheral resistance and cardiac output contributed significantly to the open-loop gain with the former predominating. Aortic impedance for frequencies above 3 Hz was at a minimum at the closed-loop operating point and increased for both higher and lower values of carotid sinus pressure. For the frequency range from 3 to 9 Hz, regional impedance in all of the beds varied inversely with carotid sinus pressure. The sensitivity of the various beds to changes in carotid sinus pressure around the operating point increased in the order celiac less than mesenteric less than renal less than femoral. Following vagotomy, operating point values of regional resistance and sensitivity were significantly increased. This fact suggests that the aortic arch receptors exert a significant influence on regional vascular impedance at operating point pressures. The fraction of cardiac output in the celiac, mesenteric, and renal beds was nearly independent of carotid sinus pressure before and after vagotomy, but that in the femoral bed increased with carotid sinus pressure. These results demonstrate the nonuniform nature of carotid sinus and aortic arch baroreceptor control of regional blood flow.

SUMMARY Segments of carotid, femoral, saphenous, and left circumflex coronary arteries were obtained from control, renal hypertensive, and nephrectomized hypertensive dogs for in vitro study of mechanical properties. Hypertension was produced in two-kidney dogs by unilateral renal artery constriction. After 3 months, the compromised kidney was removed in half of the dogs. Mean arterial pressure was significantly elevated in the hypertensive dogs after 3 months (127 ± 2 vs 94 ± 1 mm Hg for controls) and partially returned toward normal 3 months after nephrectomy (105 ± 2 mm Hg). Pressure-diameter relations were determined under conditions of rmnrimnm active and passive smooth muscle activation. Contiguous segments were used for the determination of water and connective tissue content. Hypertension was associated with increased passive arterial wall stiffness at most sites, with a partial return toward normal after nephrectomy. Maximum responses to smooth muscle activation (active stress and constriction response) were augmented in arteries from hypertensive dogs and partially returned toward normal in the nephrectomized hypertensive group. The elastin content of these arteries was unchanged, while collagen content was nonuniformly decreased in renal hypertensive dogs. Small decreases were found in the radius-wall thickness ratio of some arteries. No significant mechanical changes occurred in the saphenous artery. The largest hypertension-related changes were found in the coronary arteries, which also exhibited the smallest recovery toward normal properties after nephrectomy. 1 -2 These include changes in arterial smooth muscle mechanics, wall composition, responsiveness to vasoactive agents, and functional properties of smooth muscle cell membranes.3 -6 Some of these changes in arterial wall properties are thought to be responsible for the pathogenesis of hypertension, 3 -6 while some have been shown to be the direct result of the elevated blood pressure per se.7 -9 Elevated blood pressure is presumed to exert some influence on the synthetic machinery in vascular smooth muscle cells, causing them to alter the balance between synthesis and degradation of wall components. The exact nature of these signals has not been clearly defined, but they are thought to be due at least in part to increased arterial wall stress or strain. 10 These altered arterial wall properties have profound effects on circulatory function in the hypertensive subject, including changes in peripheral resistance, neural control of the circulation, and the mechanical work of the heart. Elevated arterial pressure also produces increased wear and tear on blood vessels, ultimately leading to pathological changes in the coronary, cerebral, and renal circulations and hence to the increased morbidity and mortality 1 '-14 associated with hypertension.The goal of antihypertensive therapy is to lower or normalize arterial blood pressure, thereby removing at least those components of the signal(s) producing arterial wall degenerative changes in hypertensi...

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