Assuntos
Captopril/uso terapêutico , Insuficiência Cardíaca/tratamento farmacológico , Doença Crônica , Terapia Combinada , Dieta Hipossódica , Avaliação de Medicamentos , Quimioterapia Combinada , Insuficiência Cardíaca/fisiopatologia , Hemodinâmica/efeitos dos fármacos , Humanos , Rim/efeitos dos fármacos , Rim/fisiopatologia , Cardiopatia Reumática/tratamento farmacológico , Cardiopatia Reumática/fisiopatologiaRESUMO
Sublingual administration of nifedipine (N) at a dose of 20 mg to 8 persons without cardiovascular and renal pathology and to 19 patients with congestive heart failure (CHF) increased renal excretion of sodium (by an average of 51.1-132.8%), water (by an average of 31.7-101.9%), potassium (by an average of 43.2-63.2%) and calcium (by an average of 118%). The natriuretic effect of N appeared in 20 min reaching its maximum in 45-60 min, being more noticeable in CHF. An increment of natriuresis resulted from a decrease in sodium tubular reabsorption (correlation factor--0.92) rather than from an increase in glomerular filtration (correlation factor +0.50). N suppressed sodium reabsorption in the proximal tubule (by an average of 34.1%) as well as in the segment, more distal of Henle's loop (by an average of 6.8%). N might suppress directly calcium-dependent mechanisms of sodium transtubular transport but it could also produce a mediated effect as a result of shifts of renal hemodynamics.
Assuntos
Insuficiência Cardíaca/tratamento farmacológico , Rim/efeitos dos fármacos , Nifedipino/uso terapêutico , Diurese/efeitos dos fármacos , Taxa de Filtração Glomerular/efeitos dos fármacos , Insuficiência Cardíaca/fisiopatologia , Humanos , Rim/fisiopatologia , Equilíbrio Hidroeletrolítico/efeitos dos fármacosRESUMO
The effect of captopril on renal function, central hemodynamics and the hormonal status was studied in 14 patients with chronic congestive heart failure in single administration of the drug at a dose of 25 mg and during short-term course therapy at a daily dose of 75 mg for 7 days. Captopril single administration was shown to cause an increase in natriuresis by 121% and diuresis by 120%. Correlation analysis showed that the natriuretic effect of captopril resulted from a decrease in tubular sodium reabsorption which, in its turn, was determined by a decrease in the production of angiotensin II and changes of pritubular circulation. Seven-day course therapy was accompanied by the patients' improved general status, improved indices of hemodynamics, and better tolerance to physical exercise. At the same time diuresis and renal excretion of sodium were above the basal level by 113 and 86%, respectively. It can be assumed that this natriuretic effect was determined by the suppression of angiotensin II, aldosterone and probably norepinephrine and vasopressin production. The analysis has shown that a favorable captopril renal effect is not mediated through improved central hemodynamics but results from changes of the hormonal and neurohumoral status.
