EXAGGERATED NATRIURESIS AFTER SELECTIVE AT1 RECEPTOR BLOCKADE IN DAHL SALT-SENSITIVE RATS

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 comp...

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Bibliographic Details
Published in:Clinical and experimental hypertension (1993) 2001, Vol.23 (8), p.623-631
Main Authors: Tallam, Lakshmi S., Jandhyala, Bhagavan S.
Format: Article
Language:English
Subjects:
Angiotensin Receptor Antagonists
Angiotensin-II (Ang-II)
Animals
Antihypertensive Agents - pharmacology
Arterial hypertension. Arterial hypotension
Benzimidazoles - pharmacology
Biological and medical sciences
Blood and lymphatic vessels
Candesartan
Cardiology. Vascular system
Experimental diseases
Hemodynamics
Humans
Hypertension - etiology
Hypertension - physiopathology
Kidney - drug effects
Kidney - physiopathology
Male
Medical sciences
Natriuresis - drug effects
Natriuresis - physiology
Radioligand Assay
Rats
Rats, Inbred Dahl
Receptor, Angiotensin, Type 1
Renal function
Renin - blood
Salt-sensitivity
Sodium, Dietary - administration & dosage
Sodium, Dietary - adverse effects
Tetrazoles - pharmacology
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Summary: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.
ISSN:1064-1963
1525-6006
DOI:10.1081/CEH-100107392