P-244: Antihypertensive treatment, particularly ACE-inhibitors, restores the physiologic hemodynamic renal response to adrenergic activation in essential hypertension in humans

The nephroprotective action of different antihypertensive drugs has not yet been completely elucidated. This study was aimed at comparing the effects of antihypertensive drugs on renal hemodynamics during adrenergic activation induced by mental stress (MS), a stimulus that induces renal vasoconstriction. The renal hemodynamic profile was assessed in 15 patients (pts.) with essential hypertension (EH), aged 48-66 yrs. Each pt. was assessed twice: after two weeks of pharmacological wash-out and other two weeks of treatment with trandolapril (T, 4mg, n=5), verapamil (V, 280mg, n=5) or both (T 2mg + V 180mg, n=5). Each assessment consisted of four 30-minute experimental periods (baseline, MS, recovery I and II). All three antihypertensive regimens normalized the blood pressure (BP) similarly, and MS increased BP by a similar extent before and after each treatment. Conversely, the renal responses to MS were quite different. Before treatment, the rise in BP induced by MS was not associated with the physiological increase in renal vascular resistance, and no change occurred in effective renal plasma flow (ERPF, from PAI clearance) and in glomerular filtration rate (GFR, from inulin clearance). After antihypertensive treatment, the renal vascular response to MS was modified differently by the three drugs. In pts. treated with T (n=5) the renal vasoconstriction occurred only during the MS-related BP rise, while those receiving V (n=5) or the combination (n=5) had a more prolonged vasoconstriction. Therefore, only high doses of T restored the physiological renal hemodynamic response to adrenergic activation. In conclusion, the kidney of pts. with EH is unable to react to sympathetic activation. A short-term antihypertensive treatments can modify the pathological renal response of EH, but only high doses of T can revert renal reactivity back to normal.