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
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.