The renin-angiotensin-aldosterone system in compensated and uncompensated cardiac insufficiency
Sánchez Torres, G.; Posadas Romero, C.; Olvera, S.; Boyer Martínez, J.L.; Guzmán Lara, J.; Serrano Mass, P.
Archivos del Instituto de Cardiologia de Mexico 51(2): 147-152
1981
ISSN/ISBN: 0020-3785 PMID: 7018436 Document Number: 180114
Renin Activity (PRA), Aldosterone (PA), Sodium (PNa) and Potassium (PK) in plasma and Aldosterone (UA), Sodium (UNa) and Potassium (UK) in 24 hrs urine were measured in 11 cases of heart failure compensated with treatment (HFCT) consisting in digoxin 0.25 mg daily, furosemide 40 to 80 mg daily, potassium chloride 1.5 g daily and low salt diet and in 12 cases of refractory heart failure (RHF). Mean and standard deviation of PRA, PA, PNa, PK, UA, UNa and UK were 9.7 +/- 8.2 mg/cc/hr. 24.2 +/- 14.0 mg/100 cc, 142.2 +/- 4.7 mEq/1, 4.9 +/- 0.3 mEq/1, 8.7 +/- 9.1 ug/24 hrs, 89.3 +/- 50.0 mEq/24 hrs and 50.0 +/- 26.7 mEq/24 hrs, respectively for cases with HFCT and 61.7 +/- 37.5, 120.3 +/- 125.8, 133.1 +/- 4.3, 4.9 +/- 0.4, 21.3 +/- 19.2, 9.9 +/- 19 and 33.3 +/- 12.0 respectively for subjects with RHF. The statistical analysis of PRA, PA, PNa and UNa, revealed differences between the two groups with p values of less than or equal to 0.05, less than or equal to 0.001, less than or equal to 0.001, less than or equal to 0.001, respectively. The other values were statistically non significant. These data suggest the existence of an stimulatory state of the renin-angiotensin-aldosterone system (RAAS) in the RHF and a normal state in HFCT. The lack of electrolytic changes suggestive of aldosteronism in RHF may be due to an alteration of aldosterone receptors or to hemodynamic renal factors. In heart failure hemodynamic changes rather than humoral factor seems to control RAAS.