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Humans are intermittently exposed to large variations in potassium intake, which range from periods of fasting to ingestion of potassium-rich meals. These fluctuations would abruptly alter plasma potassium concentration if not for rapid mechanisms, primarily in skeletal muscle and the liver, that buffer the changes in plasma potassium concentration by means of transcellular potassium redistribution and feedback control of renal potassium excretion. However, buffers have capacity limits, and even robust feedback control mechanisms require that the perturbation occur before feedback can initiate corrective action. In contrast, feedforward control mechanisms sense the effect of disturbances on the system's homeostasis. This review highlights recent experimental insights into the participation of feedback and feedforward control mechanisms in potassium homeostasis. New data make clear that feedforward homeostatic responses activate when decreased potassium intake is sensed, even when plasma potassium concentration is still within the normal range and before frank hypokalemia ensues, in addition to the classic feedback activation of renal potassium conservation when plasma potassium concentration decreases. Given the clinical importance of dyskalemias in patients, these novel experimental paradigms invite renewed clinical inquiry into this important area.

* Objective: To determine the effect of trimethoprim-sulfamethoxazole (Tmp-Smx) on serum potassium concentration. * Design: Retrospective cohort study. * Setting: An urban teaching hospital. * Patients: Fifty-one persons hospitalized for symptomatic infection with human immunodeficiency virus (HIV). Twenty-five patients who were taking high-dose Tmp-Smx (trimethoprim 20 mg/kg per day; sulfamethoxazole, 100 mg/kg per day) for Pneumocystis carinii pneumonia were the study group. Twenty-six patients who had not received the drug were the control group. Patients who received potassium supplements, those taking medications known to alter potassium homeostasis or renal function, or those with a serum creatinine level more than 186 [Mu] mol/L were excluded. * Measurements and Main Results: Serum potassium concentration in the study group was 4.1 [+ or -] 0.1 mmol/L (mean [+ or -] SE) and increased by 1.1 mmol/L (Cl, 0.8 to 1.5 mmol/L) (P < 0.0001) 9.8 [+ or -] 0.5 days after starting Tmp-Smx therapy. Patients followed longitudinally showed a progressive increase in serum potassium levels during therapy and a progressive decline after discontinuing Tmp-Smx. Blood urea nitrogen and serum creatinine levels increased mildly from 4.3 [+ or -] 0.5 mmol/L and 85 [+ or -] 6 [m u] mol/L to 6.4 [+ or -] 0.7 mmol/L and 113 [+ or -] 8 [m u] mol/L, respectively. The serum potassium level in the control group was 4.3 [+ or -] 0.1 mmol/L and remained unchanged during hospitalization. * Conclusions: High-dose Tmp-Smx therapy used for the treatment of P. carinii pneumonia in HIV-infected patients leads to an increase in the serum potassium concentration and may result in life-threatening hyperkalemia. Patients receiving high doses of Tmp-Smx require close monitoring of their serum potassium concentration, particularly 7 to 10 days after the start of therapy., Treatment with high-dose trimethoprim-sulfamethoxazole (Tmp-Smx) for Pneumocystis carinii pneumonia may cause hyperkalemia in patients with HIV infection. Hyperkalemia is abnormally high blood levels of potassium. Among 51 patients hospitalized for HIV infection, 25 were treated with high-dose Tmp-Smx for P. carinii pneumonia and 26 were not been treated with Tmp-Smx (control group). Blood levels of potassium were similar in the two groups of patients before treatment with Tmp-Smx was begun. Potassium concentration increased progressively during treatment with Tmp-Smx among members of the treatment group, but declined after treatment was discontinued. Blood levels of potassium remained the same in patients from the control group. Patients treated with high-dose Tmp-Smx should be monitored closely for increases in their blood levels of potassium.

Essential hypertension is high blood pressure that has no obvious external cause. Left untreated, hypertension may result in kidney disease, arteriosclerosis, or other serious disorders. Epidemiological studies have shown that people with hypertension are more likely to have low intake of potassium. A diet low in potassium is also likely to be different from a high-potassium diet in many other ways. Therefore, it would invalid to assume that the low amounts of potassium contribute directly to the development of high blood pressure. To determine whether low potassium intake does, indeed, contribute directly to high blood pressure, 12 hypertensive, but otherwise healthy, subjects were given specially prepared meals in which only the potassium content was varied. The subjects ate standardized meals for five days, at which point they were switched to comparable meals low in potassium for the next 10 days. The sodium content of the meals was held constant throughout the experiment. At the end of 10 days, the blood pressure of the patients had increased. The average systolic (peak) blood pressure was 148 milliliters of mercury (mm Hg), in contrast with 141 mm Hg at the beginning of the low potassium diet. Similarly, the average diastolic blood pressure also rose to 96 mm Hg from 90 mm Hg. Blood and urine specimens taken during the course of the study indicated that the patients tended to retain sodium while on the low- potassium diet; at the same time, the excretion of calcium also rose. (A simultaneous increase in phosphorous excretion suggests that the calcium came from bone.) These changes may contribute to the elevation in blood pressure that occurs as body potassium is depleted. The details of the interactions between sodium, potassium, and calcium and their influence on blood pressure are not fully understood. (Consumer Summary produced by Reliance Medical Information, Inc.)