Sodium nitroprusside-induced cGMP-independent vasodilator responses in the perfused rabbit ovarian vascular bed

Sodium nitroprusside (SNP) (10(-9)-10(-6) mol) and carbachol (10(-9)-10(-6) mol) induced dose-dependent vasodilatation in the perfused rabbit isolated ovarian vascular bed. Carbachol, but not SNP-induced vasodilatation was abolished by treatment with CHAPS (4. 7 mg ml-1, 30 s) to remove the endothelium. Carbachol-induced responses were also significantly attenuated by LY 83583 (10(-5) M) and methylene blue (3x10(-5) M). L-NOARG (10(-5) M) reduced carbachol-induced vasodilatation. None of these compounds affected SNP-induced vasodilator responses. Both SNP- and carbachol-induced vasodilatation were attenuated by raising the [K+] in the Krebs' solution to 40 mM. The responses were also reduced by TEA (20 mM) but not by glibenclamide. It was therefore concluded that SNP induced cGMP-independent vasodilator responses in the perfused rabbit ovarian vascular bed. This vasodilator response involved membrane hyperpolarisation since it was lost in high [K+] Krebs' solution. (c) 1998 The Italian Pharmacological Society.