Early blood pressure normalization independent of the class of antihypertensive agent prevents augmented renal fibronectin and albuminuria in experimental diabetic nephropathy.

Background/aims: This study tested the hypothesis that prevention of the development of hypertension, and not the class of antihypertensive agent, inhibits the increase in renal fibronectin and albuminuria in experimental diabetes.

Methods: Four-week-old spontaneously hypertensive rats (SHR), with diabetes induced by streptozotocin, were randomized for no treatment, or treatment with captopril, amlodipine, an association of captopril and amlodipine (Cap+A) or an association of captopril and verapamil (Cap+V) for 12 weeks.

Results: Systolic blood pressure increased similarly in control (187 +/- 5 mm Hg, mean +/- SE) and diabetic (186 +/- 4) SHR and was kept within the normal range by amlodipine (131 +/- 3), captopril (127 +/- 3), Cap+A (134 +/- 4) and Cap+V (134 +/- 9, p < 0.

The genetics of hypertension modifies the renal cell replication response induced by experimental diabetes.

To investigate whether the genetics of hypertension modifies renal cell responses in experimental diabetes, we studied the renal cell replication and its regulation by two cyclin-dependent kinase (Cdk) inhibitors, p27(Kip1) and p21(Cip1), in prehypertensive spontaneously hypertensive rats (SHR) and their genetically normotensive counterparts, Wistar Kyoto (WKY) rats, with and without streptozotocin-induced diabetes. In diabetic SHR, the number of proliferating glomerular (0.6 +/- 0.