Hypertension, Vol 21, 476-484, Copyright © 1993 by American Heart Association
H Kumagai, DB Averill, MC Khosla and CM Ferrario
This study evaluated the actions of nitric oxide on the blood pressure and
renal sympathetic nerve activity responses produced by angiotensin II (Ang
II) blockade in conscious spontaneously hypertensive rats. Two days after
implantation of electrodes, we measured mean arterial pressure, heart rate,
and renal sympathetic nerve activity. Baroreceptor reflex function was
assessed with a logistic function curve; the maximum slope of the curve
estimated the baroreceptor reflex gain. Data were obtained in rats given
acute intravenous administration of either vehicle, the Ang II type 1
receptor antagonist losartan, the type 2 antagonist CGP 42112A, or the
converting enzyme inhibitor lisinopril. In comparison with vehicle (-1.1
+/- 0.2%/mm Hg), both losartan (-1.8 +/- 0.3%/mm Hg) and lisinopril (-2.4
+/- 0.2%/mm Hg) significantly increased the maximum gain of the
baroreceptor reflex control of nerve activity (p < 0.05). In contrast,
the type 2 receptor antagonist did not alter baroreceptor reflex function.
Similar studies were performed in rats that received an intravenous
injection of NG- monomethyl L-arginine (10 mg/kg). The nitric oxide
synthase inhibitor increased baseline blood pressure and decreased renal
sympathetic nerve activity. Subsequent administration of losartan or
lisinopril returned blood pressure to initial hypertensive level, whereas
sympathetic nerve activity was increased to a level above the initial
control value. The maximum gain of the baroreceptor reflex control of renal
nerve activity was increased after the nitric oxide inhibition. The present
study demonstrates that blunted baroreceptor reflex function in conscious
spontaneously hypertensive rats is mediated by an Ang II type 1
receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Role of nitric oxide and angiotensin II in the regulation of sympathetic nerve activity in spontaneously hypertensive rats
Department of Brain and Vascular Research, Cleveland Clinic Foundation, Ohio.
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