Insulin increases vascular smooth muscle recovery from intracellular calcium loads.

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Abstract
Insulin has previously been shown to attenuate vasoconstrictor responses to pressor agonists and accelerate vascular smooth muscle relaxation and vascular smooth muscle Ca2+ efflux. To further determine the role of insulin in regulating vascular smooth muscle Ca2+, quiescent A7r5 cultured vascular smooth muscle cells and human vascular smooth muscle cells were incubated with or without 10(-7) or 10(-8) M insulin for 1 hour and then loaded with fura 2-AM; intracellular Ca2+ responses to and rates of recovery from angiotensin II (200 nM) and arginine vasopressin (AVP) (10 microM) were studied fluorometrically in stirred suspension. Insulin (10(-7) M) caused an increase in the peak intracellular Ca2+ response to angiotensin II (peak/baseline x 100 = 469 +/- 96 versus 288 +/- 74, P < .05) and a decrease in the peak Ca2+ response to vasopressin (288 +/- 50 versus 389 +/- 33, P < .025). However, insulin also caused a marked increase in the rate of intracellular Ca2+ recovery to baseline after stimulation with both angiotensin II (77.3 +/- 13.8 versus 30.6 +/- 6 nM/min, P < .03) and vasopressin (P < .05), such that the cumulative exposure to elevated intracellular Ca2+ after stimulation with either agonist (ie, area under the intracellular Ca2+ curve) was reduced with insulin treatment. Insulin (10(-8)) caused small but still significant effects on all parameters in the A7r5 cells. Insulin also caused comparable effects on Ca2+ recovery in the human cells but was without significant effect on peak Ca2+ responses to AVP.(ABSTRACT TRUNCATED AT 250 WORDS)