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Vol. 287, Issue 1, 223-231, October 1998
Center for Clinical Pharmacology, Departments of Pharmacology
(R.M., G.G.R., A.K.S., E.K.J.) and
Medicine (S.J.V., E.K.J., T.I.),
University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania
The objectives of the present study were to determine whether
angiotensin II (Ang II) modifies
beta-adrenoceptor-induced cAMP production in
preglomerular microvascular smooth muscle cells (PMVSMCs), to determine
whether the Ang II/beta-adrenoceptor interaction on cAMP
production differs in PMVSMCs from normotensive Wistar-Kyoto (WKY) rats
vs. PMVSMCs from spontaneously hypertensive rats (SHR), and to elucidate the mechanism of Ang
II/beta-adrenoceptor interactions on cAMP production in
PMVSMCs. In cultured PMVSMCs, isoproterenol increased cAMP levels and
this effect was markedly enhanced by Ang II. The Ang II enhancement of
isoproterenol-induced cAMP was significantly greater in SHR PMVSMCs
compared with WKY PMVSMCs. Neither inhibition of calcineurin with
FK506, inhibition of calcium-calmodulin with W-7 and calmidazolium, nor
inhibition of Gi proteins with pertussis toxin attenuated
Ang II enhancement of isoproterenol-induced cAMP in PMVSMCs from either
SHR or WKY rats. Moreover, the effect of Ang II on
isoproterenol-induced cAMP was not mimicked by alpha-2 adrenoceptor stimulation. In contrast, chelation of intracellular calcium with BAPTA-AM attenuated, increasing intracellular calcium with
A23187 augmented, and inhibition of protein kinase C with either
calphostin C or chelerythrine chloride abolished Ang II enhancement of
isoproterenol-induced cAMP. We conclude that in cultured PMVSMCs Ang II
enhances the cAMP response to beta-adrenoceptor agonists
via a mechanism that involves coincident activation of adenylyl cyclase by stimulatory G proteins and protein kinase C. Thus,
protein kinase C-mediated activation of adenylyl cyclase may attenuate
Ang II-induced vasoconstriction in the renal microcirculation by
raising the intracellular levels of cAMP, and this mechanism may be
augmented in genetic hypertension.
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