title: Angiotensin II and atrial natriuretic factor-binding sites in various tissues in hypertension: comparative receptor localization and changes in different hypertension models in the rat.
abstract: The peptides angiotensin II (ANGII) and atrial natriuretic factor (ANF) regulate blood pressure and salt and water balance by producing antagonistic physiological effects in a variety of tissues. We used in vitro autoradiography with [125I] ANGII and [125I]ANF to compare receptor regulation for both peptides in various tissues in three experimental models of hypertension [two-kidney, one-clip (2K-1C); one-kidney, one-clip (1K-1C); desoxycorticosterone-salt (DOCA-SALT)] and three nonhypertensive control groups [two-kidney (2K-CON); one-kidney (1K-CON); salt-loaded (SALT-CON)]. Blood pressures at death were significantly higher in all three hypertensive groups compared to those in normotensive controls, but there were no significant differences among the hypertensive or normotensive groups, respectively. PRA was highest in the 2K-1C group and lowest in the DOCA-SALT and SALT-CON groups, but plasma ANF levels did not differ significantly among the hypertensive or normotensive groups. In the aorta, ANGII receptor binding was decreased in 2K-1C rats and increased in DOCA-SALT and SALT-CON rats; ANF receptor binding was moderately increased in all three hypertensive groups. Adrenal zona glomerulosa binding for ANGII was highest in the 2K-1C group and lowest in DOCA-SALT rats, while ANF binding was decreased in DOCA-SALT and SALT-CON animals. ANGII renal glomerular binding was increased in DOCA-SALT and SALT-CON groups, and ANF glomerular binding was decreased in the same two groups. In the brain, the subfornical organ showed increased binding for both ANGII and ANF in DOCA-SALT rats. Our results show that tissue receptor binding of ANGII and ANF is regulated in distinct patterns in different models of hypertension, and that these patterns are tissue specific and more complex than simple reciprocal regulation.
authors.affiliation: Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
authors.forename: S K
authors.initials: SK
authors.lastname: Wilson
authors.forename: D R
authors.initials: DR
authors.lastname: Lynch
authors.forename: P W
authors.initials: PW
authors.lastname: Ladenson
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism*; D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D001011:Aorta / Q000378:metabolism*; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000378:metabolism*; D001921:Brain / Q000378:metabolism*; D001933:Brain Stem / Q000378:metabolism; D004195:Disease Models, Animal; D006973:Hypertension / Q000378:metabolism*; D006978:Hypertension, Renovascular / Q000378:metabolism*; D007678:Kidney Glomerulus / Q000378:metabolism*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D011945:Receptors, Angiotensin / Q000378:metabolism*; D017461:Receptors, Atrial Natriuretic Factor; D011956:Receptors, Cell Surface / Q000378:metabolism*; D012016:Reference Values; D012083:Renin / Q000097:blood
chemical_list: D011945:Receptors, Angiotensin; D011956:Receptors, Cell Surface; C472610:atrial natriuretic peptide, rat; D000804:Angiotensin II; D009320:Atrial Natriuretic Factor; D012083:Renin; D017461:Receptors, Atrial Natriuretic Factor