Activity and responsiveness of the renin-angiotensin system in the aging rat.

The systemic renin-angiotensin system (RAS) is suppressed in normal aging, but the activity of the tissue RAS is not well defined. We examined the systemic and intrarenal RAS status of aging normal rats and responses to suppression and stimulation of the production of endogenous ANG II. Studies were performed in young (3 mo) and early aging (15 mo) male Sprague-Dawley rats.

Impaired adaptation to renal mass reduction in the polycystic rat.

Autosomal dominant polycystic kidney disease (ADPKD) is a serious cause of renal failure. In many renal-disease models, surgical renal mass reduction accelerates disease progression. We explored whether surgical renal mass reduction and the method of renal mass reduction accelerate the course of ADPKD.

Hypertension and renal injury in experimental polycystic kidney disease.

Unlabelled: Hypertension and renal injury in experimental polycystic kidney disease.

Background: Hypertension accelerates renal failure in autosomal dominant polycystic kidney disease (ADPKD), and evidence suggests a role for the renin-angiotensin system (RAS) in the functional and structural changes. To explore the hypothesis that RAS adaptations contribute to disease progression, we examined RAS activity and the long-term consequences of antihypertensive drugs, which suppress (enalapril) or stimulate (hydralazine) the RAS, in experimental polycystic kidney disease.

Acute and chronic renal effects of recombinant human TGF-beta2 in the rat.

The expression of transforming growth factor-beta (TGF-beta) correlates with the incidence of renal glomerular and interstitial injury, however, nothing is known of the effect of these proteins on renal hemodynamics. This study examines the renal hemodynamic and morphologic effects of recombinant human TGF-beta2 in normal male Sprague Dawley rats. Acute infusion of TGF-beta (1.

Role of angiotensin II in diabetic nephropathy.

Classically, the renin-angiotensin system (RAS) in diabetes was thought to be suppressed, and relatively unimportant in the regulation of hemodynamics and the development of complications. However, recent developments have caused reconsideration of this notion. Studies of pharmacological interruption of the RAS with angiotensin converting enzyme (ACE) inhibition have implicated this hormonal system in the progression of diabetic nephropathy, both experimentally and clinically.