Glomerular and vascular atrial natriuretic factor receptors in cardiomyopathic hamsters: correlation with the peptide biological effects.
OBJECTIVE
The aim was to study glomerular and vascular atrial natriuretic factor (ANF) receptors and their relationship with the post-receptor effects of the peptide in experimental heart failure.


METHODS
Binding sites ANF were studied in renal glomerular and mesenteric artery membranes. The natriuretic and relaxing effects of ANF were evaluated in the intact animal and in noradrenaline precontracted aortic strips respectively. Plasma and tissue ANF levels were also assessed.


METHODS
The study was performed on cardiomyopathic (UM-X7.1) hamsters (n = 15) with a moderate degree of heart failure. Age matched Golden Syriam hamsters (n = 15) were used as controls.


RESULTS
Cardiomyopathic hamsters presented lower blood pressure, body weight, and plasma Na+, and higher heart weight than normal hamsters. Plasma ANF (1-98) and (99-126) levels and ventricular ANF content were higher in cardiomyopathic hamster than in controls. ANF and frusemide decreased blood pressure, and increased diuresis and natriuresis in normal hamsters. The blood pressure reduction by ANF in cardiomyopathic hamsters was approximately of the same magnitude as in normal hamsters but their renal response was blunted. The blood pressure lowering effect of frusemide was similar in both cardiomyopathic and normal hamsters, but the diuretic and natriuretic responses were greatly reduced in the former. Glomerular ANF receptor density was higher and receptor affinity was lower in cardiomyopathic hamsters than in controls. Noradrenaline precontracted vascular strips from cardiomyopathic hamster were more sensitive to the relaxant effect of ANF than those from controls. No differences in either density or affinity of vascular receptor were observed.


CONCLUSIONS
The results suggest that the renal hyporesponsiveness of cardiomyopathic hamsters to ANF is not due to a down regulation of glomerular ANF receptors. The fact that the natriuretic response to frusemide is also blunted suggest the involvement of other factors.
Cachofeiro
V
V
Laboratory of Experimental Hypertension and Vasoactive Peptides, Clinical Research Institute of Montreal, Quebec, Canada.
Schiffrin
E L
EL
Cantin
M
M
Garcia
R
R
D000818:Animals; D001011:Aorta / Q000502:physiology; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D006224:Cricetinae; D004231:Diuresis / Q000187:drug effects; D005665:Furosemide / Q000494:pharmacology; D006333:Heart Failure / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D066298:In Vitro Techniques; D007678:Kidney Glomerulus / Q000378:metabolism*; D008638:Mesenteric Arteries / Q000378:metabolism*; D008647:Mesocricetus; D009119:Muscle Contraction / Q000187:drug effects; D009318:Natriuresis / Q000187:drug effects; D010446:Peptide Fragments; D017461:Receptors, Atrial Natriuretic Factor; D011956:Receptors, Cell Surface / Q000378:metabolism*
D010446:Peptide Fragments; D011956:Receptors, Cell Surface; C055659:atrial natriuretic factor prohormone (1-98); D005665:Furosemide; D009320:Atrial Natriuretic Factor; D017461:Receptors, Atrial Natriuretic Factor