We determined whether angiotensin II (ANG II) modulates the arterial baroreflex control of lumbar sympathetic nerve activity (LSNA) in chloralose-anesthetized rabbits. Intravenous infusion (iv) of ANG II caused significantly less reflex bradycardia and less inhibition of LSNA than iv phenylephrine (PE) for equivalent increments in arterial pressure. During a background iv infusion of ANG II, which caused a small sustained increase in arterial pressure, the reflex inhibition of heart rate (HR) and LSNA in response to further increases in pressure with graded doses of PE was attenuated, but the reflex increase in HR and LSNA in response to hypotension with graded doses of nitroprusside was unchanged. This modulation of the baroreflex by ANG II is specific since a similar background infusion of PE did not alter baroreflex responses to further increases or to decreases in arterial pressure. The frequency of aortic baroreceptors was comparable for equivalent increases in pressure caused by iv ANG II or PE. When ANG II was confined to the isolated carotid sinuses, the reflex inhibition of HR and LSNA during distension of carotid sinuses was unchanged. An excitatory effect of ANG II on the efferent limb of the baroreflex that would oppose the reflex bradycardia or inhibition of LSNA is unlikely because when the pressor effect of ANG II was prevented by nitroprusside, there were no changes in HR and LSNA. We conclude that through an effect on the central nervous system iv ANG II has a selective effect on the arterial baroreflex; it impairs reflex decreases in HR and LSNA during hypertension but not reflex increases in HR and LSNA during hypotension.

SUMMARY. We assessed the relative roles of aortic (ABR), carotid sinus (CBR), and vagal cardiopulmonary baroreceptors in the reflex control of heart rate and vascular resistance during changes in arterial blood pressure. Injections of phenylephrine (PE) and nitroglycerin (NG) were given intravenously to anesthetized rabbits (chloralose-urethane). Reflex heart rate responses were impaired significantly by denervation (X) of either CBR or ABR. In contrast, reflex vascular responses in the hindlimb (perfused at constant blood flow) were preserved except for a slight impairment of reflex vasoconstriction after ABRX. Vagotomy with intact CBR and ABR impaired only the reflex bradycardia. After vagotomy, neither CBRX nor ABRX altered significantly the reflex heart rate or vascular responses except, again, for an impairment of reflex vasoconstriction after ABRX. Combined CBRX and ABRX eliminated all reflex responses except for a small bradycardia and a biphasic change in perfusion pressure (constrictor-dilator) during PE. Vagotomy eliminated the bradycardia and the dilator phase; the constrictor phase persisted and was abolished by lumbar sympathectomy. The results indicate that (1) reflex control of heart rate may be impaired when reflex control of hindlimb resistance is preserved; thus reflex changes in heart rate may not be used as a reliable index of the integrity of arterial baroreceptor control of the total circulation; (2) one set of arterial baroreceptors does not compensate for the absence of the other with respect to activation of vagal neurons; in contrast, one set of baroreceptors compensates fully for the absence of the other with respect to inhibition of sympathetic neurons; (3) cardiopulmonary and other baroreceptors contribute minimally to reflex responses only during large PE-induced increases in arterial pressure. (Circ Res 50: 554-565, 1982)

After 6 wk of renal hypertension in rabbits, the arterial baroreflex control of heart rate (HR) is impaired but the baroreflex control of lumbar sympathetic nerve activity ( LSNA ) is preserved. This selective impairment may reflect a predominant abnormality in the baroreceptors. In this study, we tested the hypothesis that renal hypertension of longer duration may impair baroreflex control of LSNA through a defect in the central nervous system mediation of the reflex. Four months after induction of renal hypertension, baroreflex responses were determined during increases in arterial pressure with intravenous phenylephrine or decreases in pressure with vena caval occlusion under chloralose-urethan anesthesia. Reflex control of LSNA and HR was impaired markedly in hypertensive rabbits. Reflex inhibition of LSNA and HR in response to afferent electrical stimulation of the left aortic depressor nerve (all arterial baroreceptor afferents cut) was attenuated in hypertensive in contrast to normotensive rabbits. This attenuation was noted when the medullated fibers only were stimulated or when both medullated and nonmedullated fibers were stimulated. We conclude that baroreflex control of LSNA that is preserved after 6 wk of hypertension is impaired after 4 mo of hypertension. The impairment reflects an abnormality in the central nervous system mediation of the reflex.

SUMMARY. The first purpose of this study was to determine if the baroreflex control of hindlimb resistance is preserved in hypertension even though reflex control of heart rate is impaired. The second purpose was to compare the capacity of one remaining set of arterial baroreceptors to compensate for the loss of the other in normotensive and hypertensive states. Baroreflex responses of heart rate, perfusion pressure in the hindlimb (perfused at constant flow), and lumbar sympathetic nerve activity were examined in rabbits anesthetized with chloralose and urethane 6 weeks after induction of renal hypertension (1-K-l-W). Intravenous injections of phenylephrine caused increases in arterial pressure and reflex bradycardia, vasodilarion, and inhibition of lumbar sympathetic nerve activity. The converse occurred with nirroglycerin. With all baroreceptors intact, baroreflex control of heart rate was impaired in hypertensive rabbits, whereas control of vascular resistance and lumbar sympathetic nerve activity was preserved in hypertensive as compared with normotensive sham-operated rabbits. Denervation of either the carotid sinus or aortic baroreceptors in normotensive rabbits resulted in the following: (a) reflex control of heart rate with phenylephrine and nitroglycerin was impaired; (b) reflex inhibition of lumbar sympathetic nerve activity was preserved and reflex vasodilation was augmented; and (c) reflex excitation of lumbar sympathetic nerve activity was reduced but reflex vasoconstriction was preserved after section of carotid sinus baroreceptors and reduced slightly after section of aortic baroreceptors. In hypertensive rabbits, section of carotid sinus or aortic baroreceptors resulted in the following: (a) reflex control of heart rate was markedly impaired; (b) reflex inhibition of lumbar sympathetic nerve activity and vasodilation were suppressed; and (c) reflex excitation and vasoconstriction were impaired to a much greater extent than in normotensives. Our conclusions are as follows.(1) Baroreflex control of hindlimb vascular resistance and lumbar sympathetic nerve activity is preserved in hypertension, even though control of heart rate is impaired. Therefore, impaired baroreflex control of heart rate cannot be taken as evidence of a generalized impairment of baroreflex control of vascular resistance, (2) In normotensives, one remaining set of arterial baroreceptors compensates for the loss of the other in the reflex regulation of hindlimb vascular resistance and in reflex inhibition of lumbar sympathetic nerve activity but not in the regulation of heart rate. Thus, there is a 'redundancy" in the arterial baroreflex control of hindlimb resistance and lumbar sympathetic nerve activity but not in the control of heart rate, (3) This compensatory capacity or 'redundancy' of baroreflex control is significantly impaired in renal hypertensive rabbits, and the impairment may be related to impaired baroreceptors or abnormal central mediation of the reflex. (Circ Res 53: 223-234, 1983) IT has been show that, in hy...

At low concentrations and in physiologic states vasopressin is a potent antidiuretic hormone. Its cardiovascular effects have been more complex and their role in circulatory adjustments to hypovolemia and hypotension difficult to define with precision. Although recognized as a powerful vasoconstrictor, its pressor effect in intact animals, even at high concentrations, is minimal. The reasons for this blunted pressor response have been explored. This report is a review of previously published work from our laboratories which highlights the direct and indirect vasodilator actions of this hormone in animals and humans. The indirect vasodilator effect is caused by inhibition of sympathetic efferents, and facilitation of the baroreflex through a central action of the hormone and its sensitization of arterial baroreceptors as well as cardiac afferents.