Increase in cytosolic calcium and phosphoinositide metabolism induced by angiotensin II and Argvasopressin in vascular smooth muscle cells.

Effects of angiotensin II and Argvasopressin on cytosolic free Ca2+ concentration (Ca2+i) and phosphoinositide metabolism were studied in cultured aortic smooth muscle cells obtained from Wistar-Kyoto rats and their spontaneously hypertensive substrain. Ca2+i was measured using the fluorescent Ca2+ indicator quin2. No clear differences in basal Ca2+i were detected between cells derived from the two strains. High concentrations of angiotensin II (greater than or equal to 10 nM) and Argvasopressin (greater than or equal to 100 nM) elicited large and rapid increases in Ca2+i, followed by a rapid return to control values. Low concentrations of these peptides (less than or equal to 1.0 nM) elicited small and slow increases in Ca2+i that persisted for minutes. These responses were blocked by specific antagonists for each of these peptides. Only high concentrations of angiotensin II caused Ca2+i increases in "Ca2+-free" medium, which suggested that high concentrations of angiotensin II could release Ca2+ from intracellular pools. A high concentration of angiotensin II and Argvasopressin elicited progressive accumulations of inositol phosphates. Only high concentrations of angiotensin II caused inositol phosphate accumulation in Ca2+-free medium. Maximal accumulation of inositol phosphate elicited by angiotensin II and Argvasopressin was found to be additive. A desensitization to the effects of both peptides on Ca2+ mobilization occurred despite the continued accumulation of inositol phosphates. These observations indicated that angiotensin II and Argvasopressin interacted with independent receptors, both of which are linked to phosphoinositide breakdown and Ca2+ mobilization.