• The Korean Journal of Physiology
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• v.28 no.2
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• pp.197-202
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• 1994

The present study was aimed to determine if endogenous L-arginine-nitric oxide (NO) pathway has central, rather than peripheral, mechanisms in blood pressure regulation. Arterial blood pressure and heart rate responses to acute inhibition of the t-arginine-NO pathway were examined in rats anesthetized with thiopental (50 mg/kg, IP). An intracerebroventricular (ICV) cannula was placed in the left lateral ventricle. The right femoral artery was cannulated to measure arterial blood pressure and the vein to serve as an infusion route. $N^G-nitro-L-arginine$ methyl ester (L-NAME) was infused either intracerebroventricularly or intravenously. ICV infusion $(1.25\;{\mu}L/min)$ of L-NAME $(20\;or\;100\;{\mu}g/kg)$ per minute for 60 min) increased the mean arterial pressure and heart rate. Plasma renin concentrations(PRC) were significantly lower in L-NAME-infused group than in the control. L-Arginine $(60\;{\mu}g/min,\;ICV)$ prevented the pressor response to ICV L-NAME. The pressor response was not affected by simultaneous intravenous infusion of saralasin, but was abolished by hexamethonium treatment. Intravenous infusion $(40\;{\mu}L/min,\;10{\sim}100\;{\mu}g/kg\;per\;minute\;for\;60\;min)$ also increased blood pressure, while it decreased heart rate. These results indicate that endogenous L-arginine-NO pathway has separate central and peripheral mechanisms in regulating the cardiovascular function. The central effect may not be mediated via activation of renin-angiotensin system, but via, at least in part, activation of the sympathetic outflow.

• Childhood Kidney Diseases
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• v.14 no.2
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• pp.132-142
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• 2010

Hypokalemia usually reflects total body potassium deficiency, but less commonly results from transcellular potassium redistribution with normal body potassium stores. The differential diagnosis of hypokalemia includes pseudohypokalemia, cellular potassium redistribution, inadequate potassium intake, excessive cutaneous or gastrointestinal potassium loss, and renal potassium wasting. To discriminate excessive renal from extrarenal potassium losses as a cause for hypokalemia, urine potassium concentration or TTKG should be measured. Decreased values are indicative of extrarenal losses or inadequate intake. In contrast, excessive renal potassium losses are expected with increased values. Renal potassium wasting with normal or low blood pressure suggests hypokalemia associated with acidosis, vomiting, tubular disorders or increased renal potassium secretion. In hypokalemia associated with hypertension, plasam renin and aldosterone should be measured to differentiated among hyperreninemic hyperaldosteronism, primary hyperaldosteronism, and mineralocorticoid excess other than aldosterone or target organ activation. Hypokalemia may manifest as weakness, seizure, myalgia, rhabdomyolysis, constipation, ileus, arrhythmia, paresthesias, etc. Therapy for hypokalemia consists of treatment of underlying disease and potassium supplementation. The evaluation of hyperkalemia is also a multistep process. The differential diagnosis of hyperkalemia includes pseudohypokalemia, redistribution, and true hyperkalemia. True hyperkalemia associated with decreased glomerular filtration rate is associated with renal failure or increased body potassium contents. When glomerular filtration rate is above 15 mL/min/$1.73m^2$, plasma renin and aldosterone must be measured to differentiate hyporeninemic hypoaldosteronism, primary aldosteronism, disturbance of aldosterone action or target organ dysfunction. Hyperkalemia can cause arrhythmia, paresthesias, fatigue, etc. Therapy for hyperkalemia consists of administration of calcium gluconate, insulin, beta2 agonist, bicarbonate, furosemide, resin and dialysis. Potassium intake must be restricted and associated drugs should be withdrawn.