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 microns), small arterioles (< 25 microns), and the veins. Effects on hydrostatic capillary pressure (Pc,v) and transcapillary fluid exchange were simultaneously recorded. Close-arterially infused GTN (1-4096 micrograms kg tissue-1 min-1), SNP (0.5-32 micrograms 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 Pc,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 micrograms kg body wt-1 min-1) and SNP (4-64 micrograms 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 Pc,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.
Ekelund
U
U
Department of Physiology and Biophysics, University of Lund, Sweden.
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001158:Arteries / Q000187:drug effects* / Q000502:physiology; D002196:Capillaries / Q000187:drug effects* / Q000502:physiology; D002415:Cats; D007275:Injections, Intravenous; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000187:drug effects / Q000294:innervation / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000494:pharmacology*; D005996:Nitroglycerin / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology*; D013562:Sympathectomy; D014655:Vascular Resistance / Q000187:drug effects; D014680:Veins / Q000187:drug effects* / Q000502:physiology
D009599:Nitroprusside; D009569:Nitric Oxide; D001120:Arginine; D005996:Nitroglycerin; D019331:NG-Nitroarginine Methyl Ester