Angiotensin II and acetylcholine differentially activate mobilization of inositol phosphates in Xenopus laevis ovarian follicles.

Angiotensin II (AII) evokes a Ca(2+)-dependent Cl- current in Xenopus laevis ovarian follicles that appears to involve a pertussis-toxin-sensitive G protein mediating phosphoinositide hydrolysis and Ca2+ mobilization from intracellular stores. Follicle responses to AII closely resemble the two-component response stimulated by acetylcholine (ACh) in this tissue. Intraoocyte injections of phytic acid, heparin, and inositol 1,4,5-trisphosphate [Ins(1,4,5)P3], acting as inhibitors of Ins(1,4,5)P3-induced Ca(2+)-release, resulted in loss of responsiveness to AII and ACh. As previously reported for ACh [Moriarty et al. (1988) Proc Natl Acad Sci USA 85: 8865-8869], pertussis toxin and microinjected GTP[gammaS] were found to inhibit follicle responses to AII, implying the involvement of a G protein. However, ACh and AII responses differ strikingly in the way they mobilize inositol phosphates and in densitization characteristics. We have previously been unable to find significant increases in inositol phosphates after 60 min stimulation (with Li+) by AII, although ACh potently activated increases in these [McIntosh and McIntosh (1990) Arch Biochem Biophys 283: 135-140]. In the present paper, AII was found to activate rapid increases in inositol bis- and trisphosphates after 1 min stimulation without Li+. ACh and AII also exerted different actions on follicle adenylate-cyclase-dependent responses. We conclude that at least two separate inositol-phosphate-linked receptor mechanisms may exist in ovarian follicles, resulting from involvement of one or more pertussis-toxin-sensitive G protein(s).