Arterial baroreceptors have minimal physiological effects on adrenal medullary secretion

Abstract

The influence of arterial baroreceptors on secretion of catecholamines from the adrenal medulla was evaluated by several methods. Conscious mongrel dogs with surgically denervated hearts were hemorrhaged until an estimated 16% of their blood volume had been removed. On a separate day they were anesthetized and their blood pressure was lowered with intravenous nitroglycerin. Neither of these maneuvers produced appreciable increases in heart rate in these dogs. In contrast, in a group of sham-operated control dogs, hemorrhage induced a mean increase in heart rate of 20 beats/min (P less than 0.05), and nitroglycerin-induced hypotension induced an increase of 50 beats/min (P less than 0.05). In a separate group of conscious dogs with aortic arch denervation but intact cardiac nerves, occlusion of the common carotid arteries for 5 min increased blood pressure and heart rate significantly but elicited only small, insignificant increases in plasma epinephrine and norepinephrine; the peak concentration of epinephrine achieved was considerably less than the amount necessary to cause appreciable effects on blood pressure and heart rate as determined in another experiment by infusing varying amounts of epinephrine into conscious, cardiac-denervated dogs. We conclude that the arterial baroreceptor reflex, within the range of activity likely to occur during most physiological and pathophysiological adjustments in the conscious dog, exerts only minimal effects on the secretion of catecholamines from the adrenal medulla.

Blood Pressure of Sinoaortic-Denervated Dogs Is Not Increased by Cardiac Denervation

“…There were no significant differences in mean arterial pressure or heart rate in the values obtained before and after cardiac denervation. These values are comparable to values obtained from normal instrumented, conscious dogs which have averaged 96.5 mm Hg and 101.3 beats/ min in recent studies from our laboratory (16,(18)(19)(20) and slightly higher than control data estimated to be 9 1 mm Hg and 88 beats/ min from studies in other laboratories (2, 6, 7). Thus chronic sinoaortic denervation caused, at most, only small increases in mean arterial pressure in these conscious, resting dogs.…”

“…Over 90% of our cardiac denervation operations during the past 6 years have yielded animals with complete cardiac denervation as judged by a broad set of criteria (see Materials and Methods). Moreover, animals denervated by this method in an earlier study have been shown to lack the ability to elicit cardiac reflexes; left atrial distension in those animals did not produce reflex tachycardia, natriuresis, diuresis, or inhibition of the secretion of vasopressin or renin ( 18). All of these responses occur normally in dogs with innervated hearts.…”

Renal responses to intra-arterial administration of adrenomedullin in dogs

“…Previous studies have indicated that the secretion of catecholamines (epinephrine and norepinephrine) from the adrenal medulla was relatively unaffected by bilateral carotid occlusion in conscious dogs. 27 . It also seems unlikely that there were direct interactions between catecholamine release and NO in modulating renal responses to NO donor infusion.…”

“…Hypotension produced by either hemorrhage or infusion of nitroglycerin (a nitrovasodilator) induced similar effects on heart rate and arterial pressure in conscious dogs. 27 Although the neural modulation of NO activity is a subject of recent interest, at present there is no evidence to suggest that the effects of NO will be different in innervated kidneys.…”

Sinoaortic Denervation Does Not Increase Cardiovascular/ Endocrine Responses to Stress

“…The location of this interac tion is not known but could be in central integrative areas which could affect centrally driven responses in addition to reflex responses. Fater et al [27] demonstrated that in sulin-induced tachycardia central hypoglycemia is not exaggerated in aortic-arch-denervated dogs. Since heart rate responses to stress are partially dependent upon adrenal catecholamine secretion [28], and adrenal epi nephrine secretion to stress is equivalent in SAD and controls [4], this would explain why we have observed equivalent tachycardia responses in SAD and control animals.…”