The Effects of High Salt Intake on Endothelial‐Mediated Dilation and Constriction in the Vasculature

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Hypertension is a major health problem in the United States, where more than 50 million people have the condition. High dietary salt intake has been shown to contribute to the development of hypertension in the DOCA‐salt model. However, elevations in salt intake alone may cause significant changes in microvascular response to vasoactive drugs. Therefore, this study is focused on the determination that increased dietary salt intake alone will have a major effect on the sensitivity of microvessels/macrovessels exposed to various vasoactive agents. Male Sprague‐Dawley rats were fed a high salt diet (1.2% Na+) or a normal salt diet (0.4% Na+) for 2 and 4 weeks. Intravital microscopy was used to observe the response of arterioles in the rat cremaster. In vitro aortic rings were used to observe the responses of large conduit vessels. Blood pressures were similar for all groups studied. In vivo and in vitro studies involved dose responses to acetylcholine (ACH, endothelium‐dependent vasodilator), sodium nitroprusside (NP, endothelium‐independent vasodilator) and endothelin‐1 (endothelium‐derived vasoconstrictor). Aortic tissue levels of eNOS, iNOS and SOD were also observed by Western Blot Analysis. Our data suggests that the dilator and constrictor responses in the microvasculature are decreased. However, there appears to only be an increase in constrictor response and similar decrease in dilator response in the macrovasculature. Thus, impairment of the arteriolar and aortic responses due to increased dietary conditions could predispose rats to the development of hypertension. Our data also demonstrate that these alterations could be due to an increase in oxidative stress.