Effect of Reduced Nitric Oxide on Kidney Sodium Handling in Female Rats

Nearly 1 billion people suffer from hypertension, or high blood pressure. An estimated fifty percent of postmenopausal women experience moderate to severe hypertension and hypertension is one of the most common complicating medical conditions in pregnancy, which makes it of particular importance in women. Decreased sodium excretion, or pressure natriuresis, is observed in all instances of hypertension. Pressure natriuresis refers to the elimination of sodium by the kidneys in response to a rise in blood pressure. Failure to eliminate sodium promotes increased blood volume and blood pressure. Endothelial dysfunction, which refers to a diseased endothelium (the innermost lining of the blood vessels), has been found in many forms of hypertension, including both postmenopausal and pregnancy hypertension. Nitric oxide (NO), a vasodilator which lowers blood pressure, is released by a healthy endothelium, but impaired in dysfunction. This study seeks to investigate the relationship between endothelial dysfunction, pressure natriuresis, and hypertension, particularly in females. This will be accomplished through monitoring acute changes in urinary sodium excretion in response to a rise in blood pressure in 10 WKY strain female rats, produced by either artery ligations (tying off arteries), or by the administration of L-NAME a compound that inhibits the production of nitric oxide. This study should provide data that yields insight into the nature of hypertension in female subjects. Data collection and analysis will continue through the end of March. Thus far, mean arterial pressure in resting WKY rats has been found to be 100 mmHg, increasing to 125 mmHg with vessel ligation. A comparable rise in blood pressure will be produced by L-NAME infusion, and the resulting sodium excretion will be compared between the two groups