Insulin attenuates vasopressin-induced calcium transients and a voltagedependent calcium response in rat vascular smooth muscle cells

P. R. Standley, F. Zhang, J. L. Ram, M. B. Zemel, J. R. Sowers

Research output: Contribution to journalArticlepeer-review

132 Scopus citations

Abstract

Insulin attenuates the contractile responses of vascular smooth muscle (VSM) to various agonists. Insulinopenic and insulinresistant rats lack this normal attenuation of vascular contractile responses. To study this attenuating mechanism, the effects of insulin on calcium (Ca2+) responses of cultured VSM cells (a7r5) to arginine vasopressin (AVP) and membrane potential were investigated. Insulin (I and 100 mU/ml) shifted AVP dose-response curves to the right, reducing relative potency of AVP by 16-fold and 220-fold, respectively. Responses to AVP were significantly attenuated within 30 min of insulin application. The AVP-elicited rise in [Ca2+]i was partially dependent upon extracellular Ca2+. AVP-elicited inward current was reduced by 90 min of insulin treatment (100 mU/ml), from a peak current of -103 ± 27 pA (normal) to -37 ± 15 pA (insulin treated). Peak voltage-dependent Ca2+-dependent inward current was unaffected by insulin; however, the current-voltage curve was shifted 16 ± 3 mV to the right by insulin. Thus, insulin may reduce VSM contractile responses by attenuating agonistmediated rises in [Ca2+], mediated, in part, by reductions in Ca2+ influx through both receptor- and voltage-operated channels.

Original languageEnglish (US)
Pages (from-to)1230-1236
Number of pages7
JournalJournal of Clinical Investigation
Volume88
Issue number4
StatePublished - 1991

Keywords

  • Diabetes
  • Fura-2
  • Hypertension
  • Whole cell recording

ASJC Scopus subject areas

  • General Medicine

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