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First, we will briefly describe how our study on the mechanisms of relaxant effects of nitroglycerin and related compounds (NG) on the vascular smooth muscle developed to a study on the sarcolemmal (SL) Ca(2+)-ATPase. These compounds were found to have no effects on the voltage-dependent Ca2+ channel and Ca(2+)-induced Ca2+ release from the sarcoplasmic reticulum (SR) and Na(+)-Ca2+ exchange mechanism has been shown not to play an important role in the vascular smooth muscle. Furthermore, when we initiated our study, the idea of receptor-operated Ca2+ channels and Ca2+ release from the SR by inositol triphosphates were not known. A major part of this review is devoted to a description of the characteristic features of SL Ca(2+)-ATPase and its regulation by various protein kinases. References to SR enzyme are made when necessary. Brief mention is made of the putative molecular structure and its possible variations as envisaged by genetic engineering techniques. However, particular attention is directed to the regulation by cyclic GMP-dependent protein kinase as this seems to be most important as regards the mechanisms of vascular smooth muscle relaxation by NG.

Studies on plasmalemmal Ca2+-pump ATPase. For a better understanding of the mechanisms of relaxation of smooth muscle.