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Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha, Nebraska 68198
Both nitric
oxide (NO) and GABA are known to provide inhibitory inputs to the
paraventricular nucleus (PVN) of the hypothalamus and are involved in
the control of sympathetic outflow. The purpose of the present study
was to examine the interaction of NO and GABA in the regulation of
renal sympathetic nerve activity in rats. The responses of renal nerve
activity, blood pressure, and heart rate to microinjection of sodium
nitroprusside (SNP), an NO donor, into the PVN were measured in the
presence and absence of blockade of the GABA system (bicuculline; 2 nmol). Microinjection of SNP (50, 100, and 200 nmol) into the PVN
elicited significant decreases in renal nerve discharge, arterial blood
pressure, and heart rate, reaching
36.4 ± 9.7%,
11 ± 5 mmHg, and
34 ± 14 beats/min, respectively, at the
highest dose. These responses were eliminated by blockade of the GABA
system. Conversely, microinjection of
N
-nitro-L-arginine methyl ester
(L-NAME; 50, 100, and 200 nmol) elicited significant increases in the renal sympathetic nerve discharge, arterial blood pressure, and heart rate, reaching 88.9 ± 16.6%, 9 ± 1 mmHg, and 29 ± 9 beats/min, respectively, at the highest dose. These sympathoexcitatory responses were masked by prior
blockade of the GABA system with bicuculline. The sympathoexcitatory effect of L-NAME was also
eliminated by activation of the GABA system with muscimol. In
conclusion, our data indicate that the inhibitory effect of endogenous
NO within the PVN on the renal sympathetic nerve activity is mediated
by GABA.
blood pressure; heart rate; N
-nitro-L-arginine methyl ester; bicuculline
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