Subsarcolemmal Increase in Intracellular Ca²⁺ in Vascular Muscle Cells from Spontaneously Hypertensive Rats

Abstract

Ca²⁺ channel function appears to be altered in vascular muscle from the venous side of even newborn spontaneously hypertensive rats (SHR), suggesting that genetically determined alterations in vascular muscle cells occur which are likely to contribute to development of increased peripheral resistance [7]. Specifically, there is an increase in the probability for opening of the L-type Ca²⁺ channels (thought to be important for the filling of the Ca²⁺ stores necessary for contraction) compared to that seen in vascular muscle cells from normotensive rats [16]. Recent reports from our laboratory have indicated that this alteration in Ca²⁺ channel function does not result from inherent conductance properties of the channel, but can be identified with Ca²⁺ inactivation of the L-type Ca²⁺ channel [10]. As in other kinds of cells, the high-threshold, L-type Ca²⁺ channel normally inactivates as a function not only of depolarization, but also of the accumulation of Ca²⁺ in the region immediately inside the cell surface membrane, called the subsarcolemmal space [14,17]. These experiments were carried out to determine whether there was a change in the free Ca²⁺ ion concentration in the subsarcolemmal space that might explain the altered Ca²⁺ channel function.

This study was supported by NIH grants HL38537 and HL38645, by the Institute for Nutrition and Cardiovascular Research of the National Dairy Board, and by the Schweizerische Stiftung für Medizinische-Biologische Stipendien.