High salt intake accelerates hypertension in humans and increases cardiovascular morbidity and mortality. The temporal relation between blood pressure (BP) deration and appearance of vascular lesions during salt-loading was studied in the spontaneously hypertensive rat (SHR). Starting at 5 weeks of age, SHRs and normotensive Wistar-Kyoto rats (WKYs) were given 1% NaCl in their drinking water; SHRs and WKYs on tap water served as controls. Animals from each group were sacrificed at 10 and 20 weeks of age, and the aorta and Intrarenal vessels were studied by light and electron microscopy. Neither BP nor vascular morphology of WKYs were affected by 1% NaCl. In SHRs, the course of BP was not affected by the addition of salt for at least 11 weeks, but vascular changes were significantly aggravated within 5 weeks. Thus, aortic intimal lesions progressed more rapidly so that, by 20 weeks of age, 50% of the animals had 3+ lesions while, in control SHRs, they did not exceed the 2+ grade. Salt-loading resulted in significant thickening of the aortic media between the 10th and 20th week of age while control SHRs showed no increment within the same time interval. Also, small intrarenal arterial vessels of salt-treated SHRs had significantly narrower lumina and greater wall thickness at both 10 and 20 weeks of age. In addition, they showed intimal proliferations and necrotizing lesions which were absent from control SHRs at these ages. These results show that, in this experimental model, the aggravation of vascular changes is not merely a sequela of further elevation of BP. Since the adverse effect of salt on the vessels was not teen In WKYs, it is likely that this effect is related to genetic factors or to higher susceptibility of hypertensive vessels.
- Endotneliumvascular smooth muscle
- Genetic hypertension vascular pathology