Fall In Potassium Concentration Research Articles

Exercise-induced Rise in Arterial Potassium is Enhanced in Patients with Impaired Exercise Tolerance.

We assessed the changes in arterial potassium concentration during exercise and recovery in relation to exercise tolerance in patients with impaired exercise tolerance. Sixteen patients with cardiac disease were subjected to a cardiopulmonary exercise test on a cycle ergometer. Arterial potassium and lactate concentrations were measured every minute during and after exercise, and ventilatory threshold (VT) and lactate threshold (LT) were identified. Before exercise, arterial potassium concentration was 3.8 +/- 0.3 mEq/l. It increased to 4.1 +/- 0.3 mEq/l at LT (p < 0.002 versus at rest), to 4.2 +/- 0.3 mEq/l at VT, and to 4.8 +/- 0.5 mEq/l at peak exercise (p < 0.001 versus at LT, p < 0.001 versus at VT). At an exercise intensity equivalent to 30, 40, 50 or 60% of predicted maximum oxygen uptake, the increase in arterial potassium showed a negative and significant correlation with %LT (r = -0.62 approximately -0.72, p < 0.01 approximately 0.05) and %VT (r = -0.62 approximately -0.75, p < 0.001 approximately 0.05), where %LT and %VT represent the ratios of LT and VT to the predicted maximum oxygen uptake, respectively. There was a good correlation between the rate of fall in potassium concentration during recovery and its increase during exercise. It was concluded that in patients with impaired exercise tolerance, the greater the degree of exercise intolerance, the greater the increase in arterial potassium concentration during exercise, and the steeper the fall in potassium concentration during recovery. Because the rise in potassium concentration during exercise and its fall during recovery were greater when the exercise level exceeded the anaerobic threshold, exercise levels below the anaerobic threshold are recommended for patients with cardiac diseases.

Natriuretic action of angiotensin(1–7)

Evidence that angiotensin(1-7) (Ang(1-7)) is biologically active and can be synthesized by the kidney prompted us to examine its actions in the rat, isolated kidney. Ang(1-7) had three major effects producing, (1) a substantial natriuresis and diuresis, (2) an increase in urinary sodium concentration associated with a fall in potassium concentration and (3) an increase in glomerular filtration rate without affecting renal vascular resistance. Thus, Ang(1-7) may participate in the renal effects of the renin-angiotensin system.

The regulation of haemolymph potassium activity during initiation and maintenance of diuresis in fed Rhodnius prolixus.

The blood-sucking insect Rhodnius prolixus rapidly eliminates a Na(+)-rich K(+)-poor urine after its large meals. K(+)-rich fluid is first secreted by the upper Malpighian tubules and passes to the lower tubules where most of the potassium is reabsorbed. During the initial stimulation of the tubules, the lower tubules must be activated first to avoid loss of potassium. The major element in this is that they respond more rapidly than do the upper tubules to particular hormonal concentrations rather than that they react to lower hormonal concentrations than do the upper tubules. During subsequent diuresis, regulation of the haemolymph potassium concentration depends on three cooperative homoeostatic mechanisms in the tubules. A fall in potassium concentration of the medium bathing the tubules causes (i) a decrease in the rate of fluid secretion by the upper tubules, (ii) a decrease in potassium concentration in the fluid secreted by the upper tubules and (iii) an increase in the rate of potassium absorption by the lower tubules. The tubules respond in the opposite direction to an increase in potassium concentration of the medium. As a result, the potassium concentration of the urine can be adjusted to match the potassium concentration of the fluids absorbed from the gut, so that the potassium concentration of the insect's haemolymph remains unaltered.

Norepinephrine sensitivity of isolated rabbit aorta strips in solutions of varying pH and electrolyte content.

Using a preparation of isolated vessel wall, observations have been made upon the sensitivity of the smooth muscle to 10 µg/l. of norepinephrine in various extracellular media. Varying the pH from 7.14 to pH 7.56 did not alter the sensitivity. More gross alterations in pH in either direction (pH 6.80 or 7.70) diminished the response equally. Lowering the sodium concentration and raising the potassium concentration both singly or together increased the sensitivity of the arterial strip. A rise in sodium concentration and a fall in potassium concentration either individually or in combination caused a lessened response to norepinephrine. Increasing the norepinephrine concentration to 100 µg/l. caused a greater contraction of the vascular smooth muscle, the degree of this response then being unaltered by pH and electrolyte changes in its environment within the range investigated. This strip of vessel wall from the largest vascular compartment outside of the heart appears to show a remarkable stability and regularity of reaction, despite wide variation in its extracellular environment, well beyond the limits of acid-base and electrolyte alteration commonly encountered in clinical medicine and surgery.