title: Glomerular and vascular atrial natriuretic factor receptors in saralasin-sensitive and -resistant two-kidney, one-clip hypertensive rats.
abstract: We have investigated whether there is a relation between renin dependency of two-kidney, one-clip (2K1C) hypertensive rats and the density of renal glomerular and vascular atrial natriuretic factor (ANF) receptors. Conscious 2K1C rats with blood pressure of 150 mm Hg or higher were classified according to their sensitivity to the blood pressure-lowering effect of the angiotensin II antagonist saralasin. Both hypertension groups had lower body weights and greater relative heart weights than normotensive controls. Hematocrit was lower and plasma volume higher in saralasin-resistant animals than in either saralasin-sensitive or control rats. Plasma renin activity was higher in the saralasin-sensitive group than in the resistant rats. Plasma ANF concentration was greater in saralasin-resistant than in either normotensive or saralasin-sensitive animals. ANF was reduced in both atria of saralasin-resistant 2K1C animals but only in the left atrium of the sensitive group. Both hypertensive groups showed an increased ventricular ANF concentration. The number of glomerular ANF binding sites was significantly lower in the clipped kidney of both hypertensive groups. This lower density of binding sites was accompanied by an increased affinity. In saralasin-sensitive rats, the density of glomerular ANF receptors in the nonclipped kidney was significantly higher than in the controls. Saralasin-resistant rats exhibited a decreased number of vascular ANF binding sites in both mesenteric arteries and aorta. We conclude that through modulation of its glomerular and vascular receptors, ANF may contribute to the differential sodium handling of saralasin-sensitive and -resistant 2K1C hypertensive rats and to the reduced vascular responsiveness to ANF observed in the saralasin-resistant hypertensive rats.
authors.affiliation: Laboratory of Experimental Hypertension and Vasoactive Peptides, Clinical Research Institute of Montreal, Quebec, Canada.
authors.forename: R
authors.initials: R
authors.lastname: Garcia
authors.forename: G
authors.initials: G
authors.lastname: Gauquelin
authors.forename: M
authors.initials: M
authors.lastname: Cantin
authors.forename: E L
authors.initials: EL
authors.lastname: Schiffrin
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism*; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000378:metabolism; D001665:Binding Sites; D004351:Drug Resistance; D006978:Hypertension, Renovascular / Q000097:blood / Q000378:metabolism*; D007678:Kidney Glomerulus / Q000378:metabolism*; D008297:Male; D008638:Mesenteric Arteries / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D017461:Receptors, Atrial Natriuretic Factor; D011956:Receptors, Cell Surface / Q000378:metabolism*; D012504:Saralasin / Q000494:pharmacology*
chemical_list: D011956:Receptors, Cell Surface; D009320:Atrial Natriuretic Factor; D017461:Receptors, Atrial Natriuretic Factor; D012504:Saralasin