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

Authors
Citation
U. Ekelund, EFFECTS OF GLYCERYL TRINITRATE, NITROPRUSSIDE AND NITRIC-OXIDE ON ARTERIAL, VENOUS AND CAPILLARY FUNCTIONS IN CAT SKELETAL-MUSCLE IN-VIVO, Acta Physiologica Scandinavica, 152(1), 1994, pp. 93-105
Citations number
32
Categorie Soggetti
Physiology
ISSN journal
00016772
Volume
152
Issue
1
Year of publication
1994
Pages
93 - 105
Database
ISI
SICI code
0001-6772(1994)152:1<93:EOGTNA>2.0.ZU;2-5
Abstract
The aim of the present study was to analyse quantitatively, on a cat g astrocnemius preparation in vivo, the effects of i.a. or i.v. administ ered glyceryl trinitrate (GTN), sodium nitroprusside (SNP) or nitric o xide (NO dissolved in saline) on vascular resistance (tone) in the fol lowing consecutive vascular sections: Large-bore arterial resistance v essels (> 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 generalize d dose-dependent dilator response in all three sections, though with a preferential action on the arterial side. Further, these agents cause d an increase in P-c,P-v and transcapillary fluid filtration. The site s of action along the vascular bed of these exogenous vasodilators dif fered from that previously established for endogenous EDNO. Infusion o f 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 t ransmural pressure stimuli was clearly depressed by GTN and SNP. Intra venously infused GTN (4-512 pg kg body wt(-1) min(-1)) and SNP (4-64 m u g kg body wt(-1) min(-1)) decreased arterial pressure and elicited, via reflex sympathetic activation, a dose-dependent vasoconstriction i n skeletal muscle, a decrease in P-c,P-v, and net transcapillary fluid absorption. The constrictor response thus overruled the direct dilato r effect of the drugs. The plasma volume expansion known to result fro m long-term systematic administration of nitrovasodilators seems in pa rt to be caused by transcapillary fluid absorption in skeletal muscle.