The subtype 2 of angiotensin II receptors and pressure-natriuresis in adult rat kidneys

Détails

ID Serval
serval:BIB_0705A8E43320
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
The subtype 2 of angiotensin II receptors and pressure-natriuresis in adult rat kidneys
Périodique
British Journal of Pharmacology
Auteur⸱e⸱s
Liu  K. L., Lo  M., Grouzmann  E., Mutter  M., Sassard  J.
ISSN
0007-1188 (Print)
Statut éditorial
Publié
Date de publication
02/1999
Volume
126
Numéro
3
Pages
826-32
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Feb
Résumé
The present work examined the effects of the subtype 2 of angiotensin II (AT2) receptors on the pressure-natriuresis using a new peptide agonist, and the possible involvement of cyclic guanosine 3', 5' monophosphate (cyclic GMP) in these effects. In adult anaesthetized rats (Inactin, 100 mg kg(-1), i.p.) deprived of endogenous angiotensin II by angiotensin converting enzyme inhibition (quinapril, 10 mg kg(-1), i.v.), T2-(Ang II 4-8)2 (TA), a highly specific AT2 receptor agonist (5, 10 and 30 microg kg(-1) min(-1), i.v.) or its solvent was infused in four groups. Renal functions were studied at renal perfusion pressures (RPP) of 90, 110 and 130 mmHg and urinary cyclic GMP excretion when RPP was at 130 mmHg. The effects of TA (10 microg kg(-1) min(-1)) were reassessed in animals pretreated with PD 123319 (PD, 50 microg kg(-1) min(-1), i.v.), an AT2 receptor antagonist and the action of the same dose of PD alone was also determined. Increases in RPP from 90 to 130 mmHg did not change renal blood flow (RBF) but induced 8 and 15 fold increases in urinary flow and sodium excretion respectively. The 5 microg kg(-1) min(-1) dose of TA was devoid of action. The 10 and 30 microg kg(-1) min(-1) doses did not alter total RBF and glomerular filtration rate, but blunted pressure-diuresis and natriuresis relationships. These effects were abolished by PD. TA decreased urinary cyclic GMP excretion. After pretreatment with PD, this decrease was reversed to an increase which was also observed in animals receiving PD alone. In conclusion, renal AT2 receptors oppose the sodium and water excretion induced by acute increases in blood pressure and this action cannot be directly explained by changes in cyclic GMP.
Mots-clé
Angiotensin I/pharmacology Angiotensin-Converting Enzyme Inhibitors/pharmacology Angiotensins/pharmacology Animals Blood Pressure/drug effects Cyclic GMP/urine Diuresis/drug effects/physiology Glomerular Filtration Rate/drug effects Imidazoles/pharmacology Isoquinolines/pharmacology Kidney/blood supply/drug effects/*physiology Kidney Function Tests Male Natriuresis/drug effects/*physiology Peptide Fragments/pharmacology Perfusion Pressure Pyridines/pharmacology Rats Rats, Sprague-Dawley Receptor, Angiotensin, Type 2 Receptors, Angiotensin/agonists/*physiology Renal Circulation/drug effects *Tetrahydroisoquinolines Urination/drug effects
Pubmed
Web of science
Création de la notice
25/01/2008 11:55
Dernière modification de la notice
20/08/2019 13:29
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