Endothelial NOS‐independent Release of Nitric Oxide in The Aorta of The Spontaneously Hypertensive Rat

In the aorta of spontaneously hypertensive (SHR), but not in that of Wistar‐Kyoto (WKY) rats the endothelium inhibits contractions to phenylephrine despite the presence of indomethacin (inhibitor of cyclooxygenase) and L‐NAME [inhibitor of nitric oxide synthase (NOS)]. The present studies were designed to examine the mechanism underlying this endothelium‐dependent inhibition. Contractions to phenylephrine were smaller in SHR aortae with than in those without endothelium. The inhibitory effect if the endothelium was larger in preparations from 38 – 48weeks than those from 12 – 22weeks old SHR. The endothelium‐dependent difference in contraction to the phenylephrine was prevented by carboxy‐PTIO, oxyhemoglogin or ODQ. The contraction of aortic rings with and without endothelium of 38 – 48weeks old WKY was not affected by carboxy‐PTIO, oxyhemoglobin or ODQ. Sodium nitrite relaxed SHR aortae with or without endothelium to the same extent and this relaxation was eliminated by ODQ. In the SHR aorta, there is an endothelium‐dependent release of nitric oxide which is not produced by NOS. This NOS‐independent nitric oxide release is only seen in preparations from hypertensive animals and augments with aging when endothelial dysfunction develops. Nitrite may not be the source of the NOS‐independent nitric oxide. Supported by a small Project grant of the University of Hong Kong.