ROLE OF NA-CA2+ EXCHANGE IN THE REGULATION OF VASCULAR SMOOTH-MUSCLE TENSION()

To determine the role of the Na+-Ca2+ exchange systems of nerve termin al and sarcolemmal membrane on development of tension in rabbit aortic rings, internal or external Na+ concentration was changed with either ouabain or Na+-free solution, respectively. Ouabain produced a verapa mil-insensitive but external Na+- and Ca2+-dependent biphasic tension with distinct lag periods both of which were shortened by depolarizati on with KCl. The first phase of tension was inhibited by prazosin, phe ntolamine, in vitro neurolysis with 6-hydroxydopamine and in vivo trea tment with reserpine to deplete catecholamines in nerve terminals. The refore, first phase of tension was attributed to catecholamines releas ed from nerve terminals induced by increased axoplasmic Ca2+ concentra tion mediated by the neural Na+-Ca2+ exchanger due to the increased ax oplasmic Na+ concentration resulting from inhibition of the Na+-Ka+ pu mp with ouabain. In the absence of the first phase of tension, the sec ond phase of tension was enhanced by caffeine, presumably by preventin g sequestration of the sarcolemmal Na+-Ca2+ exchanger-mediated increas e in cytosolic Ca2+ concentration in vascular smooth muscle cells. The prazosin-insensitive tension was dependent on the external Na+ concen tration and was also attributed to the sarcolemmal Na+-Ca2+ exchanger of vascular smooth muscle. The magnitude of the increase in tension wi th ouabain or Na+-free solution attributed to the sarcolemmal Na+-Ca2 exchanger of vascular smooth muscle was larger than that mediated by the exchanger of the nerve terminal. It was concluded that the Na+-Ca2 + exchange systems of both the nerve terminal and the vascular smooth muscle sarcolemma contribute to the development of tension by differen t mechanisms and to different extents when internal or external Na+ co ncentration was changed.