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Abstract
Salt-sensitive individuals are susceptible to develop hypertension when exposed to high salt-diet. Such a phenomenon is considered to be due to a genetic impairment in the renal excretion of sodium. In the present studies extent of endogenous angiotensin-II (Ang-II) mediated antinatriuresis was comparatively evaluated in Dahl salt-sensitive (SS) and salt-resistant (SR) rats, using a selective AT1 receptor antagonist, candesartan. In addition, differences in plasma renin activity and characteristics of Ang-II receptors in the renal cortical tubular membranes were also examined. Under INACTIN® anesthesia AT1 receptor blockade resulted in significant increases in renal sodium excretion, which was several-fold greater in SS rats than that observed in SR rats. These observations suggest that antinatriuretic function of endogenous angiotensin-II is exaggerated in SS rats. This functional overexpression appears to be related to an increase in the affinity of Ang-II receptors in renal cortical tubular membranes but not to receptor density or plasma renin activity. It is proposed that salt-dependent hypertension in Dahl salt-sensitive rats may be due to enhanced Ang-II mediated sodium retention.
| ABBREVIATIONS | ||
| Angiotensin-II | = | Ang-II |
| Dahl salt-sensitive | = | SS |
| Dahl salt-resistant | = | SR |
| Plasma renin activity | = | PRA |
| ABBREVIATIONS | ||
| Angiotensin-II | = | Ang-II |
| Dahl salt-sensitive | = | SS |
| Dahl salt-resistant | = | SR |
| Plasma renin activity | = | PRA |