Aging Increases Physiological Function of TRPC3 Channels in Female Arterial Smooth Muscle

Abstract

Cardiovascular function declines with age, but patterns of vascular aging differ between the sexes across lifespan. In arterial smooth muscle, transient receptor potential canonical 3 (TRPC3) channels participate in the regulation of intracellular calcium and smooth muscle contractility. The effects of aging on TRPC3 function in female arterial smooth muscle is poorly understood. Here, we investigated physiological function of TRPC3 channels in pressurized, endothelium‐denuded middle cerebral arteries from young (~2 months) and old (~ 20 months) female CD (Sprague Dawley) IGS rats. Myogenic tone (60 mmHg) was similar between young and old cerebral resistance size arteries, however membrane depolarization‐induced vasoconstriction (60 mM K+) was reduced with age. Application of the selective TRPC3 channel inhibitor, Pyr3 (10 μM), elicited vasodilation in both young and old, however Pyr3‐mediated vasodilation was substantially larger in aged females. Application of 1‐oleoyl‐2‐acetyl‐sn‐glycerol (OAG, 50 μM), a diacylglycerol analog, enhanced myogenic tone to a greater degree in old females as compared to young, while administration of Pyr3+OAG resulted in a greater loss in developed tone in old females. In conclusion, physiological function of TRPC3 channels is elevated with age in female arterial smooth muscle, which could be an important compensatory mechanism to maintain myogenic tone in cerebral resistance size arteries.Support or Funding InformationFlorida State UniversityThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.