Release of nitric oxide in response to acetylcholine is unaltered in spontaneously hypertensive rats

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ObjectiveAlthough a decreased responsiveness to acetylcholine, an endothelium-dependent vasodilator, has been reported in arteries isolated from spontaneously hypertensive rats (SHR), the precise role of nitric oxide (NO) in the in vivo regulation of blood pressure is not clear. We investigated the effects of acetylcholine and of NG-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor, on mean arterial pressure and the production of NO metabolites (nitrate and nitrite) in SHR and in Wistar-Kyoto (WKY) rats, their normotensive control strain.DesignWe determined serum levels of nitrate and nitrite before and after the intravenous injection of 40 μg/kg acetylcholine following the administration of L-NAME (30mg/kg) or its vehicle in adult SHR and WKY rats.ResultsAcetylcholine administration significantly reduced mean arterial pressure in both SHR and WKY rats, accompanied by a significant rise in serum nitrate and nitrite. Administration of L-NAME significantly increased the mean arterial pressure in SHR and in WKY rats. L-NAME inhibited the hypotension induced by acetylcholine and the rise in serum nitrate and nitrite both in SHR and in WKY rats.ConclusionThe release of NO stimulated by acetylcholine was unaltered in SHR, supporting previous in vitro results.

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