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Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha, Nebraska 68198-4575
One characteristic of heart failure
(HF) is increased sympathetic activation. The paraventricular
nucleus (PVN) of the hypothalamus (involved in control of sympathetic
outflow) has been shown to have increased neuronal activation during
HF. This study examined the influence of endogenous GABA input
(inhibitory in nature) into the PVN on renal sympathetic nerve
discharge (RSND), arterial blood pressure (BP), and heart rate (HR) in
rats with HF induced by coronary artery ligation. In 
-chloralose-
and urethane-anesthetized rats, microinjection of bicuculline (a GABA
antagonist) into the PVN produced a dose-dependent increase in RSND,
BP, and HR in both sham-operated control and HF rats. Bicuculline
attenuated the increase in RSND and BP in HF rats compared with control
rats. Alternatively, microinjection of the GABA agonist muscimol
produced a dose-dependent decrease in RSND, BP, and HR in both control and HF rats. Muscimol was also less effective in decreasing RSND, BP,
and HR in HF rats than in control rats. These results suggest that
endogenous GABA-mediated input into the PVN of rats with HF is less
effective in suppressing RSND and BP compared with control rats. This
is partly due to the post-release actions of GABA, possibly caused by
altered function of post-synaptic GABA receptors in the PVN of rats
with HF. Reduced GABA-mediated inhibition in the PVN may contribute to
increased sympathetic outflow, which is commonly observed during HF.
paraventricular nucleus; renal sympathetic nerve activity; muscimol; bicuculline
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