A nonpeptide, piperidine renin inhibitor provides renal and cardiac protection in double-transgenic mice expressing human renin and angiotensinogen genes.
Subsequent treatment with cilazapril significantly improved LV morphology and function in those with residual LV hypertrophy or elevated plasma renin activity.
Both the activation of the renin angiotensin aldosterone system (RAAS) and elevations of circulating Fibroblast Growth Factor-23 (FGF-23) have been implicated in the pathogenesis of left ventricular hypertrophy (LVH) in chronic kidney disease.
Enalapril-induced regression of left ventricular hypertrophy and improvement in left ventricular impaired diastolic filling were significantly greater in the DD genotype group than they were in the ID and II genotype groups, suggesting that the circulating and tissue renin-angiotensin systems, particularly the former system, are most active in hypertensive patients with the DD genotype.