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1 Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha, Nebraska 68198-4575; and 2 Department of Cardiovascular Medicine, University of Oxford, Oxford, United Kingdom OX3 9DU
The paraventricular
nucleus (PVN) of the hypothalamus is known to be involved in the
control of sympathetic outflow. Nitric oxide (NO) has been shown to
have a sympathoinhibitory effect in the PVN. The goal of the present
study was to examine the influence of overexpression of neuronal NO
synthase (nNOS) within the PVN on renal sympathetic nerve discharge
(RSND). Adenovirus vectors encoding either nNOS (Ad.nNOS) or
-galactosidase (Ad.-Gal) were transfected into the PVN in vivo.
Initially, the dose of adenovirus needed for infection was determined
from in vitro infection of cultured fibroblasts. In Ad.nNOS-treated
rats, the local expression of nNOS within the PVN was confirmed by
histochemistry for NADPH-diaphorase-positive neurons. There was a
robust increase in staining of NADPH-diaphorase-positive cells in the
PVN on the side injected with Ad.nNOS. The staining peaked at 3 days
after injection of the virus. In 
-chloralose- and
urethane-anesthetized rats, microinjection of
NG-monomethyl-L-arginine
(L-NMMA), a NO antagonist, into the PVN produced a
dose-dependent increase in RSND, blood pressure, and heart rate. There
was a potentiation of the increase in RSND, blood pressure, and heart
rate due to L-NMMA in Ad.nNOS-injected rats compared with
Ad.-Gal-injected rats. These results suggest that the endogenous
NO-mediated effect in the PVN of Ad.nNOS-treated rats is more effective
in suppressing RSND compared with Ad.-Gal-treated rats. These
observations support the contention that an overexpression of nNOS
within the PVN may be responsible for increased suppression of
sympathetic outflow. This technique may be useful in pathological conditions know to have increased sympathetic outflow, such as hypertension or heart failure.
paraventricular nucleus; renal sympathetic nerve activity; neuronal nitric oxide synthase gene transfer
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