Korean J Intern Med.
1997 Jan;12(1):58-61.
Attenuated central pressor response to nitric oxide synthesis inhibition in
chronic renal failure rats
- Affiliations
-
- 1Department of Physiology, Chonnam University Medical School, Kwangju.
Abstract
OBJECTIVES
Central and peripheral roles of nitric oxide (NO) in blood pressure
regulation have been suggested. The present study was aimed at examining if the
role of NO in blood pressure regulation is altered in chronic renal failure.
METHODS: Blood pressure responses to acute inhibition of NO were examined in 5/6
nephrectomized rats. Three weeks after the renal ablation, under thiopental (50
mg/kg, i.p.) anesthesia, an intracerebroventricular cannula was placed in the
left lateral ventricle and the femoral vein was cannulated to serve as an
infusion route. The arterial blood pressure was measured in the right femoral
artery. NG-nito-L-arginine methyl ester (L-NAME) was infused (100 microgram/kg
per min for 60 min either intracerebroventricularly or intravenously. RESULTS:
Chronic renal failure rats showed a significantly higher arterial pressure than
the control rats (147 +/- 14 mmHg vs. 122 +/- 13 mmHg). Intracerebroventricular
L-NAME did not affect the arterial pressure in chronic renal failure rats (0.5
+/- 4 mmHg increase from the basal), while it significantly increased the
arterial pressure in normal rats (22 +/- 3 mmHg increases from the basal).
Intravenous L-NAME increased the arterial pressure, the magnitude of which did
not differ between the normal and chronic renal failure rats (24 +/- 3 vs. 16
+/- 3 mmHg increases from the basal). CONCLUSION: These results indicate that
the central role of NO in the regulation of blood pressure is altered in chronic
renal failure.