Renal hemodynamic response to stress is influenced by ACE-inhibitors

Cardiovascular responses to new antihypertensive agents have been studied extensively under resting and stress conditions. However, the effects of antihypertensive agents on renal hemodynamics have only been investigated at rest. To test whether antihypertensive therapy leads to disparate renal hemodynamic effects during exposure to mental stress as opposed to resting conditions, we performed a double-blind, placebo-controlled crossover study. In 17 normotensive healthy men, glomerular filtration rate (GFR; inulin clearance) and renal plasma flow (RPF; para-aminohippuric acid clearance) were measured at rest and after a standardized mental stress test, with or without one week's treatment with a new, long-acting ACE-inhibitor cilazapril 2.5 mg/day. ACE-inhibition did not change resting blood pressure, RPF, GFR, or derived parameters, such as filtration fraction, renal vascular resistance and renal fraction of cardiac output. Mental stress caused an acute increase in GFR (p < 0.001) and filtration fraction with both treatments (0.001). However, the increase in GFR and filtration with mental stress was greater (p < 0.05) with cilazapril treatment than with placebo. Thus, renal hemodynamic responses to mental stress were influenced by ACE inhibitors. We conclude that the impact of antihypertensive agents on renal hemodynamics during stress cannot a priori be delineated from measurements at rest.