ABSTRACT

The mammalian cardiovascular system comprises a muscular pump and a distribution network of arteries, veins, and capillaries. An increasing number of studies have detected expression of T-type Ca2+ channels in vascular smooth muscle isolated from cerebral, mesenteric, renal, coronary, pulmonary, ear and skeletal muscle arteries. In vascular smooth muscle, reactive oxygen species are generated through sources that include, but are not limited to, NADPH oxidase and mitochondria. Ca2+ influx through T-type channels has attracted considerable interest in regard to arterial function and the contractile state of vascular smooth muscle. Concerted research over the past decade has delineated T-type channels and started to define their regulation and functional impact in arterial smooth muscle. To limit arterial constriction, vascular smooth muscle is encoded with a range of K+ ion channels able to provide hyperpolarizing feedback in response to K+ efflux. Patch clamp electrophysiology along with carefully crafted pharmacology have successfully isolated the T-type current and separated it from the L-type current.