TY - JOUR
T1 - Enalaprilat augments arterial and cardiopulmonary baroreflex control of sympathetic nerve activity in patients with heart failure
AU - Dibner-Dunlap, Mark E.
AU - Smith, Michael L.
AU - Kinugawa, Toru
AU - Thames, Marc D.
N1 - Funding Information:
Fmm the Depanment of kdicine (cardidogy), Uoiwtity Haspitak of cteveld case Weatem Rewve university and Department of veteran.5 Ahha h4ediml Center, CTkdad, Ohio. Thir work was supported by hinds from the Medical Rexarc Se&e of the Dpartmeot of Veterans Main, Washing-ton, D.C; by Grant HL MSM Finn the National Heart, Lung, and Blood laahte, Natkmaf iilstitutes of Health. Fietks%, Mmyfaad; and by a bkdii School Grant from Merck Hyan Eealth Div+!oq West Point, t’etmsyfvania. L$.~-~ismeteEipiwt.~ta~Iove~a~Awvdfromtbe DepamneadVetermoA5irs.Dr.KinogawaisthereeipientdaResearch Fek+&@AwdtmmtheAwicanHeart,kociaticm,NortheastObio
PY - 1996/2
Y1 - 1996/2
N2 - Objectives. This study sought to determine the effects of enalaprilat on reflex control of sympathetic nerve activity. Background. Angiotensin-converting enzyme inhibitors decrease mortality in patients with congestive heart failure. Their efficacy appears to be related importantly to antiadrenergic effects, the mechanism for which has not been determined. Because baroreflexes tonically inhibit sympathetic outflow, and baroreflexes are blunted in heart failure, we hypothesized that these agents reduce sympathetic activity by augmenting baroreflexes. Methods. We assessed baroreflex control of sympathetic nerve activity and heart rate in patients with congestive heart failure and in control subjects before and after enalaprilat (0.02 mg/kg body weight intravenously). Arterial baroreflexes were perturbed by bolus administration of sodium nitroprusside and phenylephrine. Cardiopulmonary baroreflexes were perturbed by lower body negative pressure and head-down tilt. Muscle sympathetic nerve activity was recorded by microneurography. Results. Enalaprilat decreased systolic blood pressure in patients with heart failure and control subjects. Sympathetic nerve activity increased in control subjects but decreased in patients with heart failure after enalaprilat despite reductions in central venous pressure in this group. Baroreflex control of sympathetic nerve activity was unchanged by enalaprilat in control subjects. In patients with heart failure, both arterial and cardiopulmonary baroreflex control of sympathetic nerve activity was enhanced by enalaprilat. Baroreflex control of heart rate was unchanged by enalaprilat in either group. Conclusions. Enalaprilat augments both arterial and cardio pulmonary baroreflex control of sympathetic activity in heart failure. These augmented inhibitory influences are associated with a reduction in sympathetic outflow and may contribute to the beneficial effects of angiotensin-converting enzyme inhibitors in heart failure.
AB - Objectives. This study sought to determine the effects of enalaprilat on reflex control of sympathetic nerve activity. Background. Angiotensin-converting enzyme inhibitors decrease mortality in patients with congestive heart failure. Their efficacy appears to be related importantly to antiadrenergic effects, the mechanism for which has not been determined. Because baroreflexes tonically inhibit sympathetic outflow, and baroreflexes are blunted in heart failure, we hypothesized that these agents reduce sympathetic activity by augmenting baroreflexes. Methods. We assessed baroreflex control of sympathetic nerve activity and heart rate in patients with congestive heart failure and in control subjects before and after enalaprilat (0.02 mg/kg body weight intravenously). Arterial baroreflexes were perturbed by bolus administration of sodium nitroprusside and phenylephrine. Cardiopulmonary baroreflexes were perturbed by lower body negative pressure and head-down tilt. Muscle sympathetic nerve activity was recorded by microneurography. Results. Enalaprilat decreased systolic blood pressure in patients with heart failure and control subjects. Sympathetic nerve activity increased in control subjects but decreased in patients with heart failure after enalaprilat despite reductions in central venous pressure in this group. Baroreflex control of sympathetic nerve activity was unchanged by enalaprilat in control subjects. In patients with heart failure, both arterial and cardiopulmonary baroreflex control of sympathetic nerve activity was enhanced by enalaprilat. Baroreflex control of heart rate was unchanged by enalaprilat in either group. Conclusions. Enalaprilat augments both arterial and cardio pulmonary baroreflex control of sympathetic activity in heart failure. These augmented inhibitory influences are associated with a reduction in sympathetic outflow and may contribute to the beneficial effects of angiotensin-converting enzyme inhibitors in heart failure.
UR - http://www.scopus.com/inward/record.url?scp=0030042369&partnerID=8YFLogxK
U2 - 10.1016/0735-1097(95)00484-X
DO - 10.1016/0735-1097(95)00484-X
M3 - Article
C2 - 8557906
AN - SCOPUS:0030042369
SN - 0735-1097
VL - 27
SP - 358
EP - 364
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 2
ER -