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Vol. 280, Issue 2, 905-910, 1997
Department of Pharmacology, Osaka University of Pharmaceutical
Sciences, 4-20-1, Nasahara, Takatsuki, Osaka 569-11, Japan
We previously reported that endothelin (ET) may function as an
inhibitory modulator of renal noradrenergic neurotransmission (Suzuki
et al., J. Cardiovasc. Pharmacol. 19: 905-910, 1992). In our study, we examined the effect of sarafotoxin S6c (S6c), a
selective ETB receptor agonist, on changes in renal
function and norepinephrine overflow induced by renal nerve stimulation (RNS) in anesthetized dogs. RNS at a low frequency (0.5-2.0 Hz) caused
significant decreases in urine flow, urinary excretion of sodium and
fractional excretion of sodium and increased norepinephrine secretion
rate, without affecting systemic and renal hemodynamics. RNS at a high
frequency (2.5-5.0 Hz), which diminishes renal hemodynamics, produced
more potent decreases in urine formation and increase in norepinephrine
secretion rate than seen with low frequency RNS. When S6c (1 ng/kg/min)
was infused intrarenally, there was a slight and transient increase in
renal blood flow, and then this response was followed by a gradual
reduction. S6c administration produced increase in the basal level of
urine flow with no apparent effects on urinary excretion of sodium and
fractional excretion of sodium. During S6c infusion, low frequency
RNS-induced antidiuretic action and increase in norepinephrine
secretion rate were markedly attenuated. Qualitatively, similar results
were observed in the case of high frequency RNS. In addition, high
frequency RNS-induced decreases in glomerular filtration rate and
filtration fraction were significantly suppressed by S6c infusion.
Taken together with our previous findings, it seems likely that ET
plays an important role as an inhibitory modulator of renal
noradrenergic neurotransmission, through ETB receptor
mechanisms.
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