Nephritis blunts urinary kallikrein excretion and aggravates DOCA/NaCl hypertension in rats

RESUMO

1. Normal rats and passive Heymann membranous glomerulonephritic rats were chronically treated with DOCA/NaCl for 9 weeks. Normal and untreated nephritic rats were used as controls. Urinary kallikrein excretion (UKE), proteinuria and tail blood pressure (BP) were determined in awake rats. Glomuerular filtration rate (GFR), plasma renin activity (PRA), and plasma potassium (PK) concentration were measured at the end of the experiment. 2. Comparasion between basal and 9th-week measurements indicated that DOCA/NaCl administration significantly increased (P < 0.05) UKE (3.96 ñ 0.30 vs 7.60 ñ 1.51 U/24 h) and 118 ñ 2 vs 135 ñ 6 mmHg) in normal rats, whereas in nephritic DOCA/NaCl-treated rats, UKE was unaltered (3.80 ñ 0.50 vs 3.40 ñ 0.30 U/24 h) and BP increased to higher levels (117 ñ 2 vs 152 ñ 3 mmHg) than in the normal DOCA/NaCl group (P < 0.05). Passive Heymann nephritis alone did not affect UKE (3.56 ñ 0.40 vs 3.60 ñ 0.80 /24 h) or BP (124 ñ 2 vs 125 ñ 2 mmØg). At the end of the study, PK was decrease and PRA totally suppressed in both normal and nephritic DOCA/NaCl - treated rats. Proteinuria was more pronounced in nephritic DOCA/NaCl - treated rats (44.8 ñ 5.2 mg/day) than in control nephritic animals (15.1 ñ 2.4 mg/day) and GFR was increased equally in both DOCA/NaCl-treated groups. 4. The failure of nephritic rats respond to DOCA/NaCl by increasing UKE was not associated with any significant derangement of renal function or structure and may have been related to the aggravation of arterial hypertension in this group