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Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha, Nebraska 68198-4575
We have demonstrated a
decreased neuronal nitric oxide (NO) synthase (nNOS) message in the
hypothalamus of rats with heart failure (HF). Subsequently, we have
demonstrated that NADPH diaphorase (a commonly used marker for nNOS
activity) positive neurons are decreased in paraventricular nucleus
(PVN) of rats with coronary artery ligation model of HF. The goal of
the present study was to examine the influence of endogenous NO within
the PVN on renal sympathetic nerve discharge (RSND) during HF. In
-chloralose- and urethane-anesthetized rats, an inhibitor of NO
synthase, NG-monomethyl-L-arginine
(L-NMMA) microinjected into the PVN (50, 100, and 200 pmol
in 50-200 nl) produced a dose-dependent increase in RSND, blood
pressure, and heart rate in control and HF rats. These responses were
attenuated in rats with HF compared with control rats. On the other
hand, the NO agonist, sodium nitroprusside, microinjected in PVN
produced a dose-dependent decrease in RSND and blood pressure in
control and HF rats. These responses were less in rats with HF compared
with control rats. These data suggest that the endogenous NO-mediated
effect within the PVN of HF rats is less potent in suppressing RSND
compared with control rats. These data support the conclusion that the
NO system within the PVN involved in controlling autonomic outflow is
altered during HF and may contribute to the elevated levels of renal
sympathoexcitation commonly observed in HF.
hypothalamus; sympathetic outflow; cardiovascular regulation
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