title: Renal response to blood pressure elevation in normal and glomerulonephritic rats.
abstract: Concurrent renal disease appears to augment greatly the adverse effects of systemic hypertension on renal function and the development of glomerulosclerosis. This study examined the effects of systemic hypertension and treatment of hypertension in groups of normal non-nephritic rats and rats submitted to 16 wk of glomerulonephritis induced by the administration of anti-glomerular basement membrane antibody. Hypertension was produced by application of a clip to the right renal artery and blood pressure was treated with an angiotensin-converting enzyme (ACE) inhibitor, quinapril. Glomerulosclerosis of two types developed: a diffuse type that is characteristic of anti-glomerular basement membrane glomerulonephritis, and a focal segmental glomerulosclerosis that is characteristic of systemic hypertension. Glomerulonephritis significantly reduced the capacity of ACE inhibitors to decrease systolic blood pressure in awake animals. In addition, glomerulonephritis produced significant effects on plasma angiotensin II concentrations, whereby ACE inhibition no longer lowered plasma angiotensin II levels and in fact produced an increase. Glomerular capillary hydrostatic pressure and hydrostatic pressure gradient correlated with systolic blood pressure and with the incidence of focal glomerulosclerosis in non-nephritic rats. However, in glomerulonephritis, systolic blood pressure no longer correlated with glomerular capillary pressure, and glomerular capillary pressure no longer correlated with the development of glomerulosclerosis, although systolic blood pressure did correlate with the degree of focal segmental glomerulosclerosis. Concurrent glomerulonephritis strongly conditions the effects of superimposed hypertension by altering the relationship between systemic blood pressure and glomerular capillary hydrostatic pressure and by decreasing the response of hypertension to therapy.
authors.affiliation: Division of Nephrology-Hypertension, University of California, San Diego School of Medicine, USA.
authors.forename: F B
authors.initials: FB
authors.lastname: Gabbai
authors.forename: L
authors.initials: L
authors.lastname: De Nicola
authors.forename: O W
authors.initials: OW
authors.lastname: Peterson
authors.forename: S
authors.initials: S
authors.lastname: Obagi
authors.forename: S C
authors.initials: SC
authors.lastname: Thomson
authors.forename: B J
authors.initials: BJ
authors.lastname: Tucker
authors.forename: J A
authors.initials: JA
authors.lastname: Keiser
authors.forename: C B
authors.initials: CB
authors.lastname: Wilson
authors.forename: R C
authors.initials: RC
authors.lastname: Blantz
mesh_terms: D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D004195:Disease Models, Animal; D005921:Glomerulonephritis / Q000150:complications / Q000209:etiology / Q000503:physiopathology*; D006978:Hypertension, Renovascular / Q000150:complications / Q000209:etiology / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D012044:Regression Analysis
chemical_list: D000804:Angiotensin II