Approach to hypokalemia.

Hypokalemia is frequently encountered in clinical practice. It can be due to either potassium deficiency (inadequate potassium intake or excessive potassium loss) or to net potassium shifts from the extracellular to the intracellular compartment. Inadequate dietary intake of potassium alone rarely causes hypokalemia since kidney is able to lower potassium excretion below 15 mmol per day. Hypokalemia due to excessive potassium loss can be due to renal or extrarenal losses. It is not necessary to wait for a timed urine collection for potassium to determine the etiology of hypokalemia. Measurement of spot urine for potassium and creatinine as well as evaluation of acid-base status can be used as an initial step in the diagnosis of hypokalemia. Subsequent evaluations such as measurement of spot urinary chloride, blood pressure, serum aldosterone, renin and cortisol levels may be needed in certain circumstances.

Manejo del potasio por el riñón: trasplantado / Managing of the potassium for the kidney: transplanted

Se estudiaron 40 trasplantados renales con función renal estable y 30 individuos sanos como control. Se excluyeron los pacientes que presentaban creatinina sérica superior a 2 mg/dl, concentración de sodio en orina menor de 25 mEq/L y una fracción excretada de sodio menor de 0.4 por ciento. De esta manera fueron analizados 31 trasplantados renales y 25 controles. Los tasplantados recibían: ciclosporina, prednisona, azatioprina, micofenolato y bloqueantes cálcicos. Se aplicó la técnica de clearences de 2 horas. Se calculó gradiente transtubular de K mas (GTTK). Posteriormente, 16 trasplantados y 9 controles recibieron 2 dosis de 75 mg de diclofenato sódico y se repitieron las pruebas. Se utilizó el test de la T de Student para datos apareados y no apareados. ANOVA para cambios secuenciales en el tiempo. Como soporte informático Microsoft Word, Power Point y Stat View 4.5 de Abacus. Los resultados mostraron diferencias en el GTTK entre trasplantados y controles tras recibir el diclofenato sódico (5,6  3,6 vs 11,9  3,5 respectivamente, p mayor 0.0003). Esto indicaría una mayor excreción de K más por los controles. Al ajustar los resultados.por unidad de tiempo y volumen urinario, se detectó una disminución en la excreción renal de K más por los trasplantados, (0,018  0,012 vs 0,069  0,028 mEq/ml/min; p mayor 0.001). Esto hace suponer que se sobrestimó al GTTK producto de un flujo urinario reducido. En conclusión, la administración de diclofenato sódico induce en el riñón trasplantado alteraciones en la secreción de potasio a nivel de la nefrona distal. El mecanismo por el cual los riñones trasplantados presentan esta dificultad, podría obedecer al tratamiento con ciclosporina, que además inhibir la síntesis de prostaglandinas, bloquearía la Na más/K más/ATPasa basolateral, comprometiendo la secreción de K más, evidenciada al recibir diclofenato sódico.

Fluoxetine inhibits L-type Ca2+ and transient outward K+ currents in rat ventricular myocytes

The most common cardiovascular side effects of antidepressants are cardiac arrhythmias and orthostatic hypotension. Little is known, however, about the mechanisms by which these adverse reactions may occur, especially with regard to newer drugs such as fluoxetine. We hypothesized that these side effects may have an electrophysiological basis at the level of the cardiac myocyte. Thus, we investigated the effects of fluoxetine and other antidepressants on action potentials and ionic currents of rat ventricular myocytes using the amphotericin B perforated patch clamp technique. Fluoxetine (10 microM) prolonged the action potential duration (APD50) to 146.7 +/- 12.9% of control value without altering resting membrane potential. Fluoxetine and sertraline potently inhibited the L-type Ca2+ current (IC50 = 2.82 and 2.31 microM, respectively), but did not significantly modify the steady-state inactivation. Amitriptyline and imipramine had similar, but slightly weaker, effects (IC50 = 3.75 and 4.05 microM, respectively). Fluoxetine attenuated the peak transient outward K+ current and also altered current kinetics, as shown by accelerated decay. Fluoxetine did not change the voltage-dependence of the steady-state inactivation. Sertraline, amitriptyline and imipramine inhibited the transient outward K+ current with potencies very similar to fluoxetine. In contrast to the other antidepressants tested, trazodone weakly inhibited the Ca2+ and K+ currents and moclobemide had no detectable effect. Our comparative pharmacology data suggest that selective serotonin reuptake inhibitors, such as fluoxetine, are as potent as tricyclic antidepressants in inhibiting L-type Ca2+ and transient outward K+ currents. These inhibitory effects may contribute to cardiovascular complications such as arrhythmias and orthostatic hypotension.

Outward potassium current oscillations in macrophage polykaryons: extracellular calcium entry and calcium-induced calcium release

Outward current oscillations associated with transient membrane hyperpolarizations were induced in murine macrophage polykaryons by membrane depolarization in the absence of external Na+. Oscillations corresponded to a cyclic activation of Ca2+ -dependent K+ currents (IKCa) probably correlated with variations in intracellular Ca2+ concentration. Addition of external Na+ (8mM) immediately abolished the outward current oscillations, suggesting that the absence of the cation is necessary not only for their induction but also for their maintenance. Oscillations were completely blocked by nisoldipine. Ruthenium red and ryanodine reduced the number of outward current cycles in each episode, whereas quercetin prolonged the hyperpolarization 2- to 15-fold. Neither low molecular weight heparin nor the absence of a Na+ gradient across the membrane had any influence on oscillations. The evidence suggests that Ca+ entry through a pathway sensitive to Ca2+ channel blockers is elicited by membrane depolarization in Na+ -free medium and is essential to initiate oscillations, which are also dependent on the cyclic release of Ca2+ from intracellular Ca2+ -sensitive stores; Ca2+ ATPase acts by reducing intracellular Ca2+, thus allowing slow deactivation of IKCa. Evidence is presented that neither a Na+/Ca2+ antiporter nor Ca2+ release from IP3 -sensitive Ca2+ stores participate directly in the mechanism of oscillation.

Secretory effect of serotonin on jejunal response to cholera toxin, in dog

A substância mediadora liberada pela toxina da cólera e que estimula a secreçäo intestinal é ainda desconhecida. Sabe-se que a serotonina está envolvida no estímulo secretor intestinal de água e eletrólitos. Tendo em vista a avaliaçäo de um provável papel da serotonina na induçäo secretora jejunal pela toxina da cólera, calcularam-se os volumes de água, sódio, potássio e cloreto, bem como os níveis imunorreativos de serotonina, em alça de Thiry-Vella canina. A administraçäo de toxina provocou um aumento na secreçäo de todos os eletrólitos e do fluxo de serotonina. Esses resultados sugerem que a toxina da cólera induz à liberaçäo de serotonina na luz intestinal, talvez como um mediador da secreçäo hidroeletrolítica entérica

Efeitos antagônicos de plantas medicinais na diurese do rato / Antagonistic effects of medicine plants in the rat diuresis

Os autores estudaram os efeitos da sobrecarga aquosa de folhas secas de jamboläo e de casca seca de barbatimäo, por via gástrica, na excreçäo renal de água, de sódio e de potássio do rato. Em relaçäo ao volume urinário observou-se uma diurese com o emprego do jamboläo e uma antidiurese com o emprego do barbatimäo, entretanto näo se observou alteraçäo na excreçäo de sódio e de potássio, após o emprego dos extratos das duas plantas