Insulin increases vascular smooth muscle recovery from intracellular calcium loads.
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)
- Copyright © 1993 by American Heart Association