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Adenylate cyclase of rat renal cortex was inhibited by angiotensin II (AII). Inhibition required Na+ (100-200 mM) and GTP (10(-8)-10(-4) M) and was opposed by the receptor antagonist [1-sarcosine, 8-isoleucine]AII. The EC50 value (+/- SE)for inhibition by AII was 3.7 +/- 1.2 nM, and the maximum inhibition (+/- SE) was 23 +/- 3%. Inhibition was specific for AII, since both AI and AIII, at concentrations up to 1 microM, were ineffective in producing inhibition. The maximum decrease (+/- SE) in adenylate cyclase activity was from 2.45 +/- 0.08 to 1.78 +/- 0.1 pmol.min/mg protein. A similar absolute decrease was observed when adenylate cyclase was stimulated by calcitonin, vasopressin, or isoproterenol. The inhibition of PTH-stimulated activity [16.7 +/- 0.5 (+/- SE) to 12.2 +/- 0.7 pmol.min/mg protein) was significantly greater than the inhibition of basal activity. Therefore, at least some of the inhibitory angiotensin receptors are coupled to adenylate cyclase molecules which also coupled to receptors for PTH.
E A Woodcock, and
C I Johnston
August 1983,
FEBS letters,
E A Woodcock, and
C I Johnston
January 1989,
Pharmacology,
E A Woodcock, and
C I Johnston
December 1983,
Biochemical and biophysical research communications,
E A Woodcock, and
C I Johnston
March 1981,
The Journal of biological chemistry,
E A Woodcock, and
C I Johnston
July 1976,
Biomedicine / [publiee pour l'A.A.I.C.I.G.],
E A Woodcock, and
C I Johnston
October 1986,
Endocrinology,
E A Woodcock, and
C I Johnston
January 1982,
Journal of endocrinological investigation,
E A Woodcock, and
C I Johnston
January 1984,
Journal of cardiovascular pharmacology,
E A Woodcock, and
C I Johnston
January 1998,
Life sciences,
E A Woodcock, and
C I Johnston
June 1991,
Anti-cancer drugs,
