ROLE OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM IN THE HYPERTENSION OF THE PHEOCHROMOCYTOMA

Objective: To better define the role of the RAAS in the hypertension of the pheochromoytoma, we have compared the effects of captopril upon 6 subjects harbouring a pheochromocytoma and 6 essential hypertensive hyporeninemic patients. Methods: Captopril, 50 mg was given to both groups at 8:00, resting BP was measured with an automatic non-invasive device, Dinamap (ri, and blood samples were taken for PRA, aldosterone, and plasma catecholamines at 7:50, 11:00, 11:15, 11:30 and 12:00 A.M. Results: We observed a higher basal MAP, PRA, aldosterone and NE, in the pheochromocytoma group compared with the essential hypertensives. (MAP: 137.66 +/- 14.41 vs 122.83 +/- 19.90 mmHg; PRA: 7 +/- 2.20 vs 1.02 +/- 0.56 ng/ml/h: NE: 2.635 +/- 1.413 vs 348 +/- 136 ng/ml). The decrease in MAP at 12:00 h, was greater in the pheochromocytomas, (-137 %), than in the essential hypertensives, in whom it rose slightly (9.8 %). NE did not change in either group. The regresion line between basal PRA and NE, basal and post-captopril was, r = 0.80 and 0.97, p < 0.05, and with basal MAP, r = 0.89 p < 0.01. Conclusions: We think there is enough evidence that the RAAS plays an additional role in the hypertension of pheochromocytoma, for the overflow of adrenergic drive, either at the intersynaptic space or in the general circulation, increasing release of renin and thereby increasing formation of Angiotensin II. It remains uncertain whether those tumors are capable of forming renin by themselves. Captopril by interfering with the production of Angiotensin II, helps to control one of the systems producing hypertension in the chromaffin tumors.