Abstract
Endogenous nitric oxide (NO), identified as one of the endothelium-derived relaxing factors, exists not only in the vascular endothelium, but also in other organs and tissues including the brain. Although the physiological roles of NO are not clearly defined yet, NO may be involved in the pressor mechanisms of salt loaded hypertension. To study the role of brain NO in the cardiovascular regulation of salt loaded hypertension, we measured semiquantitatively the constitutive NO synthase (cNOS) messenger RNA in salt-restricted or salt-loaded rats, and DOCA-salt hypertensive rats by using a reverse transcription-polymerase chain reaction. Relative expression levels of cNOS messenger RNA in the hypothalamus of the DOCA-salt hypertensive rats were significantly reduced as compared to those in the control rats, whereas urinary excretions of arginine vasopressin and norepinephrine were significantly increased in DOCA-salt hypertension. cNOS messenger RNA in the hypothalamus of salt-restricted rats showed a tendency to increase as compared to those in the high salt loaded rats. These results suggest that NO synthesized by cNOS in the hypothalamus may attenuate both the vasopressin releases and sympathetic nervous activities, which result in the inhibition of the pressor mechanisms of salt loaded hypertension.
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