Pathophysiology of intense physical conditioning in a hot climate. I. Mechanisms of potassium depletion. (73/127)

Serial estimations of exchangeable (42)K showed that six volunteer subjects undergoing intensive physical conditioning in a hot climate sustained a mean deficit of 517 mEq. This deficit occurred despite a daily potassium intake of 100 mEq. Simultaneous values for lean body mass rose suggesting that potassium deficiency was not the result of catabolism. Although sweating was the major avenue by which the deficit occurred, daily excretion of potassium into the urine when each subject was maximally deficient ranged from 46 to 75 mEq and thus was inappropriately high for potassium-depleted subjects. Despite high intakes of sodium and excretion of corresponding quantities into the urine, Na/K ratios in sweat were low thus indicating unsuppressed activity of aldosterone on sweat glands. Moreover, excretion and secretion of aldosterone and in many instances, plasma renin activity, appeared to be high with respect to sodium intake. These findings suggest that intense physical work in the heat stimulates higher production of aldosterone than would occur in nonexercising subjects on similar sodium intakes. Similar to the phenomenon of mineralocorticoid escape, such overproduction of aldosterone in the presence of conditions permitting excretion of sodium into the urine could facilitate continued excretion of potassium by the kidney despite serious potassium depletion. As a consequence, the kidney played a role in the genesis of potassium depletion in these subjects. In contrast to subjects undergoing conditioning in the summer months, potassium depletion did not occur in 16 subjects during identical training under cooler environmental conditions.  (+info)

Effects of potassium depletion and insulin on resting and stimulated skeletal rat muscle. (74/127)

The electrophysiological and metabolic responses to insulin of skeletal muscles from control and potassium-depleted rats were compared. Membrane potentials, action potentials, contraction parameters as well as oxygen uptake were measured in diaphragm strips or intact extremity muscles from the two groups, and similar measurements were made in vivo. The muscles were examined in solutions with normal potassium concentration [K]o , reduced [K]o, and in normal [K]o and in normal [K]o with ouabain, in each case before and after insulin, 400 mU/ml. In normal solution, the depleted muscle contractions were weaker and slower than control. The depleted muscles, already having low potassium conductance, are paralysed by the further reduction of potassium conductance after insulin. Hyperpolarising effects of insulin-induced Na/K pumping are offset in the depleted muscles with a high sodium conductance and low [K]o. Respiration is about normal at rest in depleted muscles, despite increased [Na]i, suggesting that the sodium is sequestered. After insulin, reduction of [K]o, or ouabain plus insulin, the depleted fibres take up more O2 than controls. In the presence of ouabain, this respiratory stimulation is believed to represent response to Ca++ influx. The K-depleted rat does not seem to be an entirely satisfactory model of the human disease hypokalaemic periodic paralysis.  (+info)

On the mechanism of rhabdomyolysis in potassium depletion. (75/127)

Rhabdomyolysis and myoglobinuria occur commonly in men who sustain environmental heat injury during intensive physical training in hot climates. These also occur in patients with potassium depletion. Since physical training in hot climates may be accompanied by serious losses of body potassium, the possibility was considered that performance of strenuous exercise when potassium deficient might enhance susceptibility to rhabdomyolysis. Potassium is released from contracting skeletal muscle fibers and its rising concentration in interstitial fluid is thought to dilate arterioles thereby mediating the normal rise of muscle blood flow during exercise. If potassium release from deficient muscle were subnormal, exercise would not be accompanied by sufficient muscle blood flow and rhabdomyolysis could occur by ischemia. This hypothesis was examined by comparing the effect of electrically stimulated exercise on muscle blood flow, potassium release, and histology of the intact gracilis muscle preparation in normal and potassium-depleted dogs. In normal dogs, muscle blood flow and potassium release rose sharply during exercise. In contrast, muscle blood flow and potassium release were markedly subnormal in depleted dogs despite brisk muscle contractions. Although minor histologic changes were sometimes observed in nonexercised potassium-depleted muscle, frank rhabdomyolysis occurred in each potassium-depleted animal after exercise. These findings support the hypothesis that ischemia may be the mechanism of rhabdomyolysis with exercise in potassium depletion.  (+info)

Potassium-sparing agents during diuretic therapy in hypertension. (76/127)

Three pharmacological agents in use as "potassium-sparing" drugs have been tested by serial measurements of total exchangeable potassium (K(E)) during 4 to 12 weeks of oral diuretic therapy in hypertensive subjects. Triamterene seemed ineffective in the dosage used (50 mg twice daily). Spironolactone (25 mg twice daily) reduced K loss to a considerable extent, while Slow-K (32 mEq daily) completely reversed previous K(E) deficits. Plasma K levels were a poor indication of degree of K(E) restoration.  (+info)

Effect of potassium supplements on the exchangeable potassium in chronic heart disease. (77/127)

A study of the effect of additional oral potassium on the low body potassium of seven patients with severe valvular heart disease showed that the potassium supplements were retained. After one month's treatment the exchangeable potassium was significantly increased, but the predicted value was not reached in any of the patients. There was no significant change in plasma potassium. These results suggest that it is of benefit to increase the dose of oral potassium for at least one month preoperatively in patients undergoing cardiac surgery.  (+info)

The effect of uncomplicated potassium depletion on urine acidification. (78/127)

Studies were performed on normal human subjects to determine the effects of potassium depletion on urine acidification. Depletion was induced by ingestion of a low potassium diet either alone or in combination with a potassium-binding resin, and the response of each subject to an acute ammonium chloride load in the potassium-depleted state was compared to his normal response. Urine pH was significantly higher during potassium deficiency if sufficient potassium depletion had been induced. No differences in blood acid-base parameters, urinary flow rate, or urinary fixed buffer excretion rate were found to account for this change; however, the increase in urine pH was accompanied by a concomitant increase in net acid and ammonium excretion. It is proposed that these changes during potassium depletion reflect an increase in ammonia diffusion into the urine, presumably as a result of increased renal ammonia production. In addition, it is speculated that changes in ammonia metabolism may be a physiologic control mechanism for potassium conservation.  (+info)

Urine concentration during solute diuresis in potassium-depleted rabbits. Evidence for a defect in tubular sodium transport. (79/127)

1. The relationship between osmolal clearance (C(osm)) and the reabsorption of solute-free water by the kidney (T(H2O) (c)) was examined during 10% mannitol and 2.3% saline diuresis in normal and potassium-depleted rabbits.2. In normal rabbits at osmolal clearances close to 3.0 ml./min, T(H2O) (c) during mannitol diuresis was 0.87 +/- 0.06 ml./min and during saline diuresis 1.19 +/- 0.07 ml./min. The mean difference in T(H2O) (c) of 0.32 +/- 0.05 ml./min was highly significant (P < 0.001).3. In one group of potassium-depleted rabbits with a reduction in maximal urinary concentration, T(H2O) (c) during both mannitol and saline diureses was reduced significantly below normal and the increment in T(H2O) (c) normally seen during saline diuresis was abolished.4. In a second group of potassium-depleted rabbits maximal urinary concentration (1253 +/- 88 m-osmole/kg H(2)O) was not significantly different from that in normal rabbits (1272 +/- 116 m-osmole/kg H(2)O). In these animals, T(H2O) (c) at osmolal clearances close to 3.0 ml./min was not significantly different during mannitol diuresis (0.83 +/- 0.07 ml./min) from that in normal animals, whereas it was reduced significantly during saline diuresis (0.89 +/- 0.07 ml./min, P < 0.001) and the difference in T(H2O) (c) normally seen between mannitol and saline diuresis was abolished.5. The inability to increase T(H2O) (c) during saline diuresis above that achieved during mannitol appears to be the earliest manifestation of the concentrating defect associated with potassium depletion. It probably results from an impairment of sodium transport by the ascending limb of the loop of Henle. This is supported by the fact that potassium-depleted rabbits excreted a greater percentage of the filtered load of sodium than did normal controls.  (+info)

The influence of previous salt ingestion on the renal function of sheep subjected to intravenous hypertonic saline. (80/127)

1. Sheep, which had access to a solution containing 1.3% sodium chloride as their sole source of drinking water for 6 months or more, were infused with a hypertonic solution (10%) of sodium chloride, and their ability to tolerate this salt load was compared with that of a similar group of sheep which drank only rain water.2. The sheep which drank the rain water were often affected by the infusion and exhibited signs resembling potassium deficit. No such signs were apparent in the animals which consumed saline water.3. Glomerular filtration rates were increased in all sheep by the hypertonic saline infusion, the increases being greater in the sheep which were maintained on the saline water. Effective renal plasma flow rates, though extremely variable, behaved in a similar manner.4. Plasma values for sodium and chloride were increased in all sheep, but remained at a higher level for a longer period in the sheep which consumed rain water. The diuresis produced by hypertonic saline appeared to persist for a longer period in the sheep which drank rain water, while the excretion of sodium and chloride tended to be greater in the sheep maintained on saline water.5. Plasma potassium was reduced in all sheep and urinary excretion of potassium increased. The latter response was more pronounced in the sheep which drank the rain water.6. Filtered loads of sodium, chloride and potassium were greater in the sheep which were accustomed to drinking saline water. However, the amounts of potassium excreted were greater than those filtered in the rain water sheep and less than those filtered in the sheep which drank saline water. It therefore seems that secretion of potassium into the kidney tubules predominated in the former group and reabsorption prevailed in the latter.7. Reabsorption of free water in excess of solute was greater in the kidney tubules of the sheep which drank saline water.8. Increased blood volume and greater dilution of plasma proteins occurred in the sheep which drank rain water.  (+info)