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tion with positive feedback and doublepulse instrumentation. Of course, the use of better amplifiers will improve the effectiveness of all the methods for interpretation of the data taken at short times.Even with advanced instrumentation, full advantage of the potentiostatic technique will be realized only by application of correction methods.

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Smooth muscle cells were cultured from rat thoracic aorta and labeled to a stable specific activity with 45Ca2+, myo-[2-3H]inositol, or 32p;. The efflux of 45Ca2+ was monitored over 10-sec intervals. Angiotensin II (All) increased the amount off5Ca21 lost by 5-fold in the first 10-sec interval after the addition of All and by 10-fold in the second 10-sec interval. AII-stimulated 45Ca2+ release was blocked by the angiotensin antagonist [1-sarcosine, 8-leucine]AII and byLa3+. The removal of external Ca2' had no effect on All-stimulated 45Ca2+ release. Depolarization with high external K+ only slightly increased 45Ca2' efflux and had no effect on Allinduced 45Ca2+ release. All had no effect on the initial rate of 45Ca2+ influx. These results indicate that the rapid 45Ca2+ efflux evoked by All is probably due to the release of 45Ca2+ sequestered intracellularly rather than to an increase in the Ca2+ permeability of the plasma membrane. All provoked rapid increases in the levels of phosphatidic acid and phosphoinositides in the cells. These increases in phospholipids were associated with increases in phospholipase C-generated inositol phosphates (tri-, di-, and mono-). It appears that All simultaneously increases phosphoinositide hydrolysis and synthesis in vascular smooth muscle, and both phospholipid effects may contribute to inositol triphosphate generation, which was sufficiently rapid to have a role in intracellular Ca2+ mobilization.Angiotensin II (All) is a potent vasoconstrictor that acts directly on vascular smooth muscle (1, 2). The binding of the hormone to a receptor on the surface of the smooth muscle cell (SMC) (3-6) somehow increases cytoplasmic calcium activity, which evokes a contractile response. The initial phase of the contractile response to AII (7) and other agonists (7-11) appears to be dependent on intra-rather than extracellular Ca2 . In contrast, the slow tonic component of agonist-induced contraction depends on extracellular Ca2+ (7-11). SMC cultured from rat aorta respond to AII by increasing the cycling of Na+ in and out of the cell (12-14). AII stimulates Na+ entry via an amiloride-inhibitable transporter, which results in an increased supply of Na+ to the Na+/K+ pump. Na+/K+ pump activity is thereby increased because cellular Na+ is the rate-limiting substrate for the pump in mammalian cells including vascular smooth muscle in vivo and in culture (15-17). AII depolarizes cultured aortic SMC by 10-15 mV as indicated by reciprocal changes in the steady-state distributions of [ H]tetraphenylphosphonium+ and 35SCN- (18).Recent evidence has suggested that inositol 1,4,5-(PO4)3 (Ins-P3), which is generated by agonist-induced hydrolysis of triphosphoinositide (19,20), releases calcium from a nonmitochondrial site, presumably the endoplasmic reticulum (21-23). All has been shown to provoke TPI breakdown in rat liver (24) and adrenal glomerulosa cells (25), and the effect of All in the latter tissue is apparently associated with an increase in de novo synthesis of phosphoinositides (26)....