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Differences of calcium channels in vascular muscle in hypertension.

Recent investigations on the role calcium channels in the activation of vascular muscle suggest that calcium channels act in the capacity of voltage sensors in the excitation-contraction (EC) coupling sequence, rather than acting merely as gateways for calcium influx. In this study, recordings were made of calcium currents under various conditions using voltage-clamp techniques and isolated vascular muscle cells of spontaneously hypertensive rats (SHR) and genetically matched, normotensive Wistar-Kyoto (WKY) rats. Vascular muscle cells from azygos veins showed both transient (T), and long-lasting (L) currents in all of the spontaneously active cells studied. The ratio of L-type to T-type currents was greater in SHR than in WKY controls, even though the cells studied were from the venous side in newborn animals, in which there are no differences in either arterial or venous blood pressure. Data suggest that there are enhanced L-type calcium currents in SHR compared to WKY controls even in the prehypertensive state and that, in this form of gentic hypertension, there are fundamental changes in the membrane signal that triggers contraction. Diltiazem showed a preferential effect on blocking the L-type calcium channels, beginning at 100 pmol/L. At levels of 1 nmol/L to 1 mumol/L, diltiazem blocked L-type calcium current without a detectable effect on gating currents or on T-type calcium current. These findings may indicate fundamental differences between vascular muscle and cardiac muscle channel gating processes.