Does high-salt intake alter the course of the development and magnitude of hypertension or influence renal function in two-kidney, one clip Goldblatt hypertensive rats?
In a 2K1C renovascular hypertension rat model, high-salt intake suppresses the renin-angiotensin system and delays the onset of hypertension without affecting its final magnitude, while improving function in the clipped kidney.
Arterial blood pressure and renal function of both clipped and non-clipped kidneys of benign two-kidney, one clip (2K1C) Goldblatt hypertension were evaluated in order to determine whether high-salt intake alters the course of the development and magnitude of hypertension or influences renal function. The administration of 0.9% sodium chloride as a drinking solution for 3 weeks suppressed plasma renin activity (PRA) and kidney renin content of the clipped kidney to normal values. Despite suppression of PRA and kidney renin content, the saline-drinking clipped rats still developed hypertension of the same magnitude as the water-drinking clipped rats. However, the onset of hypertension was delayed by 4 days. Urine flow, glomerular filtration rate (GFR) and sodium excretion rate from the clipped kidneys of the saline-drinking clipped rats were higher than the corresponding values in the water-drinking rats, and approached those observed in control animals. Thus, the high-salt intake which was associated with suppression of the activity of the renin-angiotensin system delayed the onset of, but not the final magnitude of, the hypertension. In addition, kidney function in the clipped kidneys of saline-drinking clipped rats was enhanced compared with that observed in the water-drinking clipped rats.
Jackson et al. (Tue,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: