Nitric oxide generation significantly decreased angiotensin II receptor binding in rat vascular smooth muscle cells in vitro through a cGMP-independent mechanism (P < 0.05).
Nitric oxide downregulates angiotensin II receptors in vascular smooth muscle cells via a cGMP-independent mechanism.
p-value: p=< 0.05
The objective of this study was to determine whether an enhanced generation of nitric oxide (NO) causes regulation of angiotensin II receptors in vitro using rat vascular smooth muscle cells in culture. Chronic treatment of cells with a series of NO-generating drugs, sodium nitroprusside, S-nitroso-N-acetylpenicillamine and isosorbide dinitrate for 18h dose and time-dependently decreased 125I-angiotensin II binding to cells without any significant change in affinity. Induction of nitric oxide synthase following lipopolysaccharide (10 and 100 ng/ml) treatment of cells for 18 h increased basal nitric oxide synthase activity with a concomitant increase of nitrite and cyclic cGMP levels in the conditioned media. LPS treatment significantly (P < 0.05) decreased 125I-angiotensin II binding to these cells, an effect that was significantly (P < 0.05) attenuated in the presence of NG-nitro-L-arginine methyl ester. In contrast, treatment of cells with atrial natriuretic factor, dibutyryl cGMP, 8-bromo-cGMP, NaNO2 or NaNO3 failed to significantly alter the affinity or number of 125I-angiotensin II binding sites. These results suggest that NO regulates angiotensin II receptors in vitro through a cGMP-independent mechanism.
Cahill et al. (Sun,) reported a other. Nitric oxide-generating drugs and lipopolysaccharide was evaluated on [125I]-angiotensin II binding to cells (p=< 0.05). Nitric oxide generation significantly decreased angiotensin II receptor binding in rat vascular smooth muscle cells in vitro through a cGMP-independent mechanism (P < 0.05).