DIFFERENTIAL CONTRIBUTION OF ENDOTHELIAL FUNCTION TO VASCULAR REACTIVITY IN CONDUIT AND RESISTANCE ARTERIES FROM DEOXYCORTICOSTERONE-SALT HYPERTENSIVE RATS
Rm. White et al., DIFFERENTIAL CONTRIBUTION OF ENDOTHELIAL FUNCTION TO VASCULAR REACTIVITY IN CONDUIT AND RESISTANCE ARTERIES FROM DEOXYCORTICOSTERONE-SALT HYPERTENSIVE RATS, Hypertension, 27(6), 1996, pp. 1245-1253
The purpose of these studies was to compare changes in conduit and res
istance artery function in deoxycorticosterone-salt hypertensive rats.
We hypothesized that if there was a common mechanism producing change
s in vascular function in hypertension then there would be similar alt
erations in reactivity of conduit and resistance arteries. Helically c
ut strips of common carotid artery were prepared for measurement of is
ometric force generation, and segments of small mesenteric arteries we
re pressurized for video dimension analysis. Sensitivity of arteries t
o phenylephrine and acetylcholine was determined. Carotid arteries fro
m deoxycorticosterone-salt hypertensive rats were more sensitive to ph
enylephrine than arteries from control rats, whereas mesenteric resist
ance arteries from hypertensive rats were less sensitive to phenylephr
ine. In carotid arteries, endothelial denudation or incubation with N-
omega-nitro-L-arginine increased phenylephrine sensitivity in control
rats to the level seen in deoxycorticosterone-salt rats. These manipul
ations had no effect on phenylephrine sensitivity in arteries from deo
xycorticosterone-salt rats. In mesenteric resistance arteries, endothe
lium denudation normalized the depressed phenylephrine sensitivity in
arteries from hypertensive rats but had no effect on arteries from nor
motensive rats. This depressed phenylephrine sensitivity in deoxycorti
costerone-salt mesenteric arteries was not reversed by incubation with
N-omega-nitro-L-arginine. Acetylcholine-induced relaxation was depres
sed in carotid arteries from deoxycorticosterone-salt hypertensive rat
s, and N-omega-nitro-L-arginine blocked these relaxations. In contrast
, acetylcholine relaxation in the mesenteric arteries from normotensiv
e and hypertensive rats did not differ. N-omega-nitro-L-arginine sligh
tly but significantly attenuated acetylcholine dilation only in mesent
eric resistance arteries from the hypertensive rats. We conclude that
qualitatively different changes in vasoconstrictor sensitivity to phen
ylephrine occur in carotid arteries and mesenteric resistance arteries
of deoxycorticosterone-salt hypertensive rats. The increased phenylep
hrine sensitivity in carotid arteries in this model of hypertension is
due to the loss of endothelium-derived nitric oxide production. In co
ntrast, the decreased phenylephrine sensitivity in mesenteric resistan
ce arteries from deoxycorticosterone-salt rats is due to a non-nitric
oxide-mediated influence of the endothelium that is absent in arteries
from normotensive rats.