RESUMO
BACKGROUND: In a previous study, we showed that a saponin mixture isolated from the roots of Ampelozizyphus amazonicus Ducke (SAPAaD) reduces urine excretion in rats that were given an oral loading of 0.9 % NaCl (4 ml/100 g body weight). In the present study, we investigated whether atrial natriuretic peptides (ANP) and renal ATPases play a role in the SAPAaD- induced antidiuresis in rats. METHODS: To evaluate the effect of SAPAaD on furosemide-induced diuresis, Wistar rats (250-300 g) were given an oral loading of physiological solution (0.9 % NaCl, 4 ml/100 g body weight) to impose a uniform water and salt state. The solution containing furosemide (Furo, 13 mg/kg) was given 30 min after rats were orally treated with 50 mg/kg SAPAaD (SAPAaD + Furo) or 0.5 ml of 0.9 % NaCl (NaCl + Furo). In the SAPAaD + NaCl group, rats were pretreated with SAPAaD and 30 min later they received the oral loading of physiological solution. Animals were individually housed in metabolic cages, and urine volume was measured every 30 min throughout the experiment (3 h). To investigate the role of ANP and renal Na(+) pumps on antidiuretic effects promoted by SAPAaD, rats were given the physiological solution (as above) containing SAPAaD (50 mg/kg). After 90 min, samples of urine and blood from the last 30 min were collected. Kidneys and atria were also removed after previous anesthesia. ANP was measured by radioimmunoassay (RIA) and renal cortical activities of Na(+)- and (Na(+),K(+))-ATPases were calculated from the difference between the [32P] Pi released in the absence and presence of 1 mM furosemide/2 mM ouabain and in the absence and presence of 1 mM ouabain, respectively. RESULTS: It was observed that SAPAaD inhibited furosemide-induced diuresis (at 90 min: from 10.0 ± 1.0 mL, NaCl + Furo group, n = 5, to 5.9 ± 1.0 mL, SAPAaD + Furo group n = 5, p < 0.05), increased both Na(+)-ATPase (from 25.0 ± 5.9 nmol Pi.mg(-1).min(-1), control, to 52.7 ± 8.9 nmol Pi.mg(-1).min(-1), p < 0.05) and (Na(+),K(+))-ATPase (from 47.8 ± 13.3 nmol Pi.mg(-1).min(-1), control, to 79.8 ± 6.9 nmol Pi .mg(-1).min(-1), p < 0.05) activities in the renal cortex. SAPAaD also lowered urine ANP (from 792 ± 132 pg/mL, control, to 299 ± 88 pg/mL, p < 0.01) and had no effect on plasma or atrial ANP. CONCLUSION: We concluded that the SAPAaD antidiuretic effect may be due to an increase in the renal activities of Na(+)- and (Na(+),K(+))-ATPases and/or a decrease in the renal ANP.
Assuntos
Fator Natriurético Atrial/urina , Rim/efeitos dos fármacos , Extratos Vegetais/farmacologia , Rhamnaceae/química , Saponinas/farmacologia , ATPase Trocadora de Sódio-Potássio/metabolismo , Micção/efeitos dos fármacos , Adenosina Trifosfatases/urina , Animais , Proteínas de Transporte de Cátions/urina , Diurese/efeitos dos fármacos , Inibidores Enzimáticos , Furosemida , Rim/metabolismo , Masculino , Ouabaína , Ratos , Ratos Wistar , Cloreto de Sódio/urinaRESUMO
OBJETIVO: Estudar as variações do peptídio natriurético atrial (PNA) introduzidas pela circulação extracorpórea (CEC) durante operação cardíaca e testar a hipótese de que existe correlação entre os níveis plasmáticos de PNA, pressão atrial direita (PAD) pressão atrial esquerda (PAE), diurese e natriurese. MÉTODO: Estudo de coorte de 15 pacientes submetidos a revascularização do miocárdio com CEC. Os intervalos de tempo de observação foram: t0 = 10 minutos antes da CEC (valor controle); t1 = 10 minutos depois de fluxo total em CEC; t2 30 minutos em fluxo total em CEC; t3 = fase final da CEC em temperatura nasofaringeana de 36º C; e t4 = 30 minutos após o término da CEC. RESULTADOS: Os valores do PNA, PAE e PAD variaram significativamente (p<0,001). O PNA diminuiu de t0 para t1 (NS) e após elevou-se progressivamente até t4 (p<0,001). A PAE e a PAD reduziram (p<0,001) entre t0 e t1, elevando-se progressivamente até t4 (p<0,001). O Na+ urinário aumentou entre t0 e t3 (p<0,001), com queda em t4. A diurese aumentou progressivamente em todos os tempos considerados (p<0,001). Foi encontrada correlação significativa entre PNA e o volume de diurese no t0, coeficiente de correlação de 0,535 (p=0,040), e no tempo igual a t2 entre PNA e PAD, coeficiente de correlação de 0,590 (p=0,021). CONCLUSÃO: As concentrações do PNA apresentam variações durante a operação de revascularização com CEC, o que favorece o conceito de estar relacionadas com as pressões atriais, e ao término da CEC, têm uma importante função na excreção de sódio e no volume da diurese
Assuntos
Humanos , Feminino , Masculino , Adulto , Pessoa de Meia-Idade , Diurese/fisiologia , Fator Natriurético Atrial/fisiologia , Fator Natriurético Atrial/sangue , Fator Natriurético Atrial/urina , Infarto do Miocárdio/cirurgia , Isquemia Miocárdica/cirurgia , Pressão Arterial , Angioplastia Coronária com Balão , Circulação Extracorpórea , Átrios do Coração , Revascularização Miocárdica , Cirurgia TorácicaRESUMO
We assessed sodium balance and extracellular volume regulation in very low birth weight infants by examining the effect of differences in sodium intake on postnatal sodium homeostasis and body water composition. Twenty infants (mean birth weight 1103 +/- 216 gm, mean gestation 28.5 +/- 1.7 weeks) were randomly assigned to receive sodium in doses of either 1 or 3 mmol.kg-1.day-1 for the first 10 postnatal days. Extracellular volume (estimated by the bromide dilution method), sodium excretion, creatinine clearance, fractional sodium excretion, plasma atrial natriuretic factor level, urine aldosterone concentration, and vasopressin excretion were measured on postnatal days 1, 5, 10, 20, and 30. The corrected bromide space was large at birth and decreased in both groups during the first 5 days of observation, concomitant with a negative sodium balance. After 5 days of age, sodium excretion decreased in both groups so that sodium balance became positive and the corrected bromide space increased in proportion to increasing body weight. Differences in sodium intake were associated with differences in tubular sodium reabsorption; corrected bromide space and net sodium balance were similar in the two groups. Serum sodium concentration was significantly lower in the low-sodium intake group. Creatinine clearance, plasma atrial natriuretic factor level, and excretion of aldosterone and vasopressin were not significantly different between the two groups. We conclude that very low birth weight infants are able to regulate sodium balance by altering renal sodium excretion. However, the renal response to sodium intake may be insufficient to prevent changes in serum sodium concentration. The roles of specific renal and hormonal mechanisms regulating sodium excretion in very low birth weight infants remain incompletely defined.