EFFECTS OF GLYCERYL TRINITRATE, NITROPRUSSIDE AND NITRIC-OXIDE ON ARTERIAL, VENOUS AND CAPILLARY FUNCTIONS IN CAT SKELETAL-MUSCLE IN-VIVO

The aim of the present study was to analyse quantitatively, on a cat gastrocnemius preparation in vivo, the effects of i.a. or i.v. administered glyceryl trinitrate (GTN), sodium nitroprusside (SNP) or nitric oxide (NO dissolved in saline) on vascular resistance (tone) in the following consecutive vascular sections: Large-bore arterial resistance vessels (> 25 mu m), small arterioles (< 25 pm), and the veins. Effects on hydrostatic capillary pressure (P-c,P-v) and transcapillary fluid exchange were simultaneously recorded. Close-arterially infused GTN (1-4096 mu g kg tissue(-1) min(-1)), SNP (0.5-32 mu g kg tissue(-1) min(-1)) and NO (0.14-0.82 mg kg tissue(-1) min(-1)) elicited a generalized dose-dependent dilator response in all three sections, though with a preferential action on the arterial side. Further, these agents caused an increase in P-c,P-v and transcapillary fluid filtration. The sites of action along the vascular bed of these exogenous vasodilators differed from that previously established for endogenous EDNO. Infusion of GTN, SNP and NO during EDNO blockade (L-NAME) could, therefore, not restore the vascular resistance distribution to that prevailing in the initial control state. Myogenic vascular reactivity to standardized transmural pressure stimuli was clearly depressed by GTN and SNP. Intravenously infused GTN (4-512 pg kg body wt(-1) min(-1)) and SNP (4-64 mu g kg body wt(-1) min(-1)) decreased arterial pressure and elicited, via reflex sympathetic activation, a dose-dependent vasoconstriction in skeletal muscle, a decrease in P-c,P-v, and net transcapillary fluid absorption. The constrictor response thus overruled the direct dilator effect of the drugs. The plasma volume expansion known to result from long-term systematic administration of nitrovasodilators seems in part to be caused by transcapillary fluid absorption in skeletal muscle.