J. Oconpujadas et al., ROLE OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM IN THE HYPERTENSION OF THE PHEOCHROMOCYTOMA, Nefrologia, 15(4), 1995, pp. 328-334
Objective: To better define the role of the RAAS in the hypertension o
f 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 gr
oups at 8:00, resting BP was measured with an automatic non-invasive d
evice, 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 de
crease 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 bas
al 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 hype
rtension of pheochromocytoma, for the overflow of adrenergic drive, ei
ther at the intersynaptic space or in the general circulation, increas
ing release of renin and thereby increasing formation of Angiotensin I
I. It remains uncertain whether those tumors are capable of forming re
nin by themselves. Captopril by interfering with the production of Ang
iotensin II, helps to control one of the systems producing hypertensio
n in the chromaffin tumors.