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Abstract

Evidence for prostaglandin-independent mechanisms in renin release mediated by alpha adrenoceptors during renal nerve stimulation in anesthetized dogs.

H Hisa, K Takahashi and S Satoh
Journal of Pharmacology and Experimental Therapeutics May 1984, 229 (2) 547-550;
H Hisa
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K Takahashi
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S Satoh
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Abstract

We investigated alpha adrenoceptor-mediated renin release in relation to renal prostaglandin production in anesthetized dogs. The effects of intrarenally infused phentolamine (5 micrograms/kg/min) on renin and prostaglandin E2 release induced by renal nerve stimulation (RNS, 2.5-5 Hz) were studied in indomethacin (5 mg/kg i.v.)-treated and untreated dogs. In the control group, RNS reduced renal blood flow and increased both renin and prostaglandin E2 secretion rates. Phentolamine inhibited the blood flow response and attenuated the renin response; it did not affect the prostaglandin E2 response. In the indomethacin-treated group, the renal venous plasma prostaglandin E2 concentration was not changed, the renin secretion rate was increased during RNS. Phentolamine also attenuated the renin response in this prostaglandin-depleted state. These results suggest that alpha adrenoceptors participate in renin release induced by RNS and that some of the alpha adrenoceptor-mediated renin release is independent of renal prostaglandins. Prostaglandin release induced by RNS may be mediated by mechanisms other than alpha adrenoceptors.

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Journal of Pharmacology and Experimental Therapeutics
Vol. 229, Issue 2
1 May 1984
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Abstract

Evidence for prostaglandin-independent mechanisms in renin release mediated by alpha adrenoceptors during renal nerve stimulation in anesthetized dogs.

H Hisa, K Takahashi and S Satoh
Journal of Pharmacology and Experimental Therapeutics May 1, 1984, 229 (2) 547-550;

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Abstract

Evidence for prostaglandin-independent mechanisms in renin release mediated by alpha adrenoceptors during renal nerve stimulation in anesthetized dogs.

H Hisa, K Takahashi and S Satoh
Journal of Pharmacology and Experimental Therapeutics May 1, 1984, 229 (2) 547-550;
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