RGD Reference Report - Exaggerated natriuresis after selective AT1 receptor blockade in Dahl salt-sensitive rats. - Rat Genome Database

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Exaggerated natriuresis after selective AT1 receptor blockade in Dahl salt-sensitive rats.

Authors: Tallam, LS  Jandhyala, BS 
Citation: Tallam LS and Jandhyala BS, Clin Exp Hypertens 2001 Nov;23(8):623-31.
RGD ID: 1299144
Pubmed: PMID:11728007   (View Abstract at PubMed)

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.

Objects referenced in this article
Gene Agtr1b angiotensin II receptor, type 1b Rattus norvegicus

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