Mode of inhibition of renin release by angiotensin II.
Inhibition of renin release by angiotensin II (ANG II) is a calcium-dependent process and is thought to reflect the calcium-mobilizing action of ANG II observed in several tissues. However, in some tissues, such as liver and vascular smooth muscle, ANG II induces cellular responses through inhibition of adenylate cyclase. We examined the possibility that ANG II-induced inhibition of renin release from the kidney is also partly mediated through adenylate cyclase inhibition, by using pertussis toxin (PT), which selectively inactivates the coupling protein Ni, which couples inhibitory hormone receptors to adenylate cyclase. Rats were injected intravenously (i.v.) with 2 micrograms/100 g PT. In isolated kidneys, perfused in an open system with a synthetic medium 3, 5 and 10 days after PT treatment, the inhibition of renin release by ANG II as well as its vasoconstrictor response were significantly attenuated. This effect, which was most pronounced at lower concentrations of ANG II, indicates that ANG II may inhibit renin release partly through inhibition of adenylate cyclase activity.
Hackenthal
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Department of Pharmacology, University of Heidelberg, Federal Republic of Germany.
Aktories
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Jakobs
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D037361:Adenylate Cyclase Toxin; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D066298:In Vitro Techniques; D008297:Male; D037342:Pertussis Toxin; D051381:Rats; D017207:Rats, Sprague-Dawley; D012083:Renin / Q000097:blood*; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
D037361:Adenylate Cyclase Toxin; D010566:Virulence Factors, Bordetella; D000804:Angiotensin II; D037342:Pertussis Toxin; D012083:Renin