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The role of endothelium-derived nitric oxide in the regulation of blood pressure in the anesthetized rabbit was studied with N omega-monomethyl-L-arginine (L-NMMA), a specific inhibitor of its formation from L-arginine. L-NMMA (3-100 mg.kg-1), but not its D-enantiomer, induced a dose-dependent long-lasting (15-90 min) increase in mean systemic arterial blood pressure. L-NMMA (100 mg.kg-1) also inhibited significantly the hypotensive action of acetylcholine, without affecting that of glyceryl trinitrate. Both these actions of L-NMMA were reversed by L-arginine (300 mg.kg-1), but not by D-arginine (300 mg.kg-1), indomethacin (1 mg.kg-1), prazosin (0.3 mg.kg-1), or by vagotomy. The effects of L-NMMA in vivo were associated with a significant inhibition of the release of nitric oxide from perfused aortic segments ex vivo. This inhibition was reversed by infusing L-arginine through the aortic segments. These results indicate that nitric oxide formation from L-arginine by the vascular endothelium plays a role in the regulation of blood pressure and in the hypotensive actions of acetylcholine.
D D Rees, and
R M Palmer, and
S Moncada
May 2006,
Life sciences,
D D Rees, and
R M Palmer, and
S Moncada
January 2003,
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D D Rees, and
R M Palmer, and
S Moncada
July 1992,
The American journal of physiology,
D D Rees, and
R M Palmer, and
S Moncada
May 1990,
Hypertension (Dallas, Tex. : 1979),
D D Rees, and
R M Palmer, and
S Moncada
November 1990,
The Journal of clinical investigation,
D D Rees, and
R M Palmer, and
S Moncada
May 2009,
Endocrinology,
D D Rees, and
R M Palmer, and
S Moncada
June 1999,
Nature,
D D Rees, and
R M Palmer, and
S Moncada
March 1998,
Current opinion in nephrology and hypertension,
D D Rees, and
R M Palmer, and
S Moncada
October 1991,
Cardiovascular research,
D D Rees, and
R M Palmer, and
S Moncada
January 2000,
Circulation,
