Cellular calcium control in hypertension

Membrane mechanisms that are rudimentary to excitation that causes contraction were found to be altered in isolated, single vascular muscle cells of spontaneously hypertensive rats (SHR) compared to normotensive Wistar-Kyoto (WKY) controls. Even in veins of newborn rats, Ca2+ channel proportions are altered to increase the fractional sustained Ca2+ current, providing more Ca2+ that ultimately signals contractile activation. The increase in Ca2+ in SHR could be visualized as a local buildup just inside the cell membrane, suggesting that the process of uptake and removal of Ca2+ at the periphery of the cell may be insufficient to regulate the increased Ca2+ entry. Ca2+ control alterations by subcellular membranes are of sufficient importance to merit consideration as a primary cause of increased peripheral resistance in SHR.