Na+,K+,2Cl(-)-cotransport and chloride permeability of the cell membrane in mezaton and histamine regulation of electrical and contractile activity in smooth muscle cells from the guinea pig ureter

Influence of Na+,K+,2Cl(-)-cotransport and chloride permeability of the cell membrane on electrically-induced action potential and contraction of smooth muscle cells from guinea pig ureter was examined with the methods of the double sucrose gap junction. Mesatone (10 microM) and histamine (10 microM) induced prolongation of the action potential and elevation of smooth muscle cell contraction, whereas hyperosmic medium (+150 mM sucrose), and recovery of solution osmolality in hyposmic condition (70 mM NaCl) after a single contraction. Inhibitor Na+,K+,2Cl(-)-cotransport bumetanide (10 microM) and chloride permeability blockers niflumic acid (10-100 microM) and SITS (10-500 microM) attenuated stimulating effects of mesatone, histamine and hyperosmic medium. In opposite to adenylate cyclase activation with forskolin (1 microM), guanylate cyclase activation with sodium nitroprusside (SN, 100 microM) decreased both inhibitory action of bumetanide, niflumic acid and activating effects of mesatone, histamine on action potential and elevation contraction of smooth muscle cells. Influence of forskolin rather and not SN on AP and SMC C was inhibited with tetraethylammonium (5 mM). These results suggest that influence of Na+,K+,2Cl(-)-cotransport on electrical and contractil properties of ureter smooth muscle cells is mediated by stimulation of Ca(2+)-activated chloride permeability of the cell membrane and modulated by intracellular cGMP, but not triggered by Ca2+ release from sarcoplasmic reticulum.