J. Varagic et al., Regional hemodynamics after chronic nitric oxide inhibition in spontaneously hypertensive rats, AM J MED SC, 320(3), 2000, pp. 171-176
Citations number
31
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Background: Inhibition of nitric oxide (NO) synthase by L-arginine analogs
is associated with elevation of blood pressure in rats. Because endothelium
-dependent vasomotion in different vascular beds is not homogenous, the aim
of this study was to characterize and compare regional hemodynamic respons
es in carotid, femoral, and renal vascular beds after chronic NO inhibition
in spontaneously hypertensive rats. The possible role of circulating endot
helin and renin angiotensin systems in mediating the effects of chronic NO
inhibition was also studied. Methods: Systemic and regional hemodynamics, l
eft ventricular mass, plasma renin activity, and plasma endothelin-l were d
etermined in control and N-omega-nitro-L-arginine methyl ester (L-NAME)-tre
ated (10 mg/kg/day, 4 weeks) spontaneously hypertensive rats. Results: L-NA
ME treatment increased arterial pressure and total peripheral and regional
vascular resistance and decreased cardiac output, stroke volume, and region
al blood flow. An in-crease in blood flow ratio and a decrease in vascular
resistance ratio between carotid and renal as well as femoral and renal vas
cular beds in rats treated with L-NAME was found. Blood flow and vascular r
esistance ratios between femoral and carotid vascular beds remained unchang
ed. L-NAME increased plasma renin activity and left ventricular weight/body
weight ratio, whereas plasma endothelin-l was not modified. Conclusions: T
he results of this study showed that the renal circulation seemed to be mor
e sensitive to the effects of chronic NO inhibition than carotid and femora
l vascular beds. Simultaneous activation of the renin angiotensin system ma
y further potentiate cardiovascular effects of chronic NO inhibition. No ev
idence that circulating endothelin-l plays a role in this model of hyperten
sion was found. KEY INDEXING TERMS: Nitric oxide; Regional hemodynamics; Pl
asma renin activity; Endothelin; Spontaneously hypertensive rats.