Renal endothelial effects of anti hypertensive therapy

Purpose of review To review the influence of anti hypertensive therapy on the contribution of nitric oxide (NO) to renal perfusion in essential hypertension. Recent findings The contribution of endothelium-derived NO to renal perfusion can be examined in detail by studying isolated glomerular arterioles and by immunohistochemical techniques. Only few functional studies in human arterial hypertension exist analysing the role of NO for renal perfusion and the change in renal NO bioavailability due to arterial hypertension and its modification by antihypertensive therapy. Summary NO critically contributes to renal perfusion. There is evidence of reduced but also of unchanged NO bioavailability in the renal vasculature of patients with arterial hypertension both from protein expression and functional studies. In particular, drugs interacting with the renin-angiotensin-aldosterone system (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and aldosterone antagonists) and third-generation beta blockers are promising candidates to improve renal endothelial function. It is not yet clear whether these specific effects translate into prevention of nephrosclerosis.