CHARACTERISTICS AND POSSIBLE MECHANISMS OF LOW-NA+ INDUCED CONTRACTIONS IN RAT AORTA

The influence of reducing external Na+ concentration ([Na+](ex)) upon vascular smooth muscle contractility was investigated using the rat is olated aorta. NaCl from the physiological saline solution (PSS) was re placed with either choline-Cl, sucrose, or LiCl to give the following [Na+](ex) (mM): 115, 85, 55, and 25 (115NaPSS to 25NaPSS). Small reduc tions in [Na+](ex) (115NaPSS) induced a biphasic contraction, comparab le in amplitude with the control one induced by phenylephrine 10(-6) M . Elimination of the endogenous catecholamine participation using eith er phentolamine 10(-5) M or guanethidine 3.10(-6) M similarly reduces these contractions to 25% (sucrose replacement). A similar relaxing ef fect was obtained with D600 10(-5) M, an antagonist of the voltage ope rated Ca2+ channels (25-30% residual tension for all the substitutes). Large reductions in [Na+](ex) (25NaPSS) induced contractions comparab le in amplitude and shape, but less sensitive to phentolamine and guan ethidine (residual tension 65-75%, sucrose replacement) and insensitiv e to D600 (all the substitutes). The Na+/K+ ATP-ase inhibitor ouabain (10(-4) M) elicited slowly developing contractions, the amplitude bein g 115% of the phenylephrine 10(-6) M control. Phenylephrine further co ntracted the 115NaPSS precontracted preparations, but was significantl y less effective in 25NaPSS, although the precontraction levels were s imilar for the same substitute used. The amplitude of the superimposed phenylephrine contractions exhibited [Na+](ex) dependence. Phenylephr ine 10(-6) M failed to further contract the ouabain 10(-4) M precontra cted rings. We conclude that relatively small reductions in [Na+](ex) are able to induce contractions of rat aorta primarily through release of endogenous catecholamines, probably through neural Na+/Ca2+ exchan ge. Larger reductions in [Na+](ex) appear to cause contraction through muscular Na+/Ca2+ exchange.