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PubMed1980

Calcium dependence of prostaglandin release from the guinea pig Taenia coli.

We studied the calcium dependency of the stimulation of prostaglandin synthesis which occurs when perfusing strips of guinea pig Taenia coli with potassium-free media. Stimulation was rapidly reversed by removal of extracellular Ca from the bathing solution. The Ca ionophore A23187 markedly stimulated prostaglandin E2 synthesis, an effect that is dependent on the presence of extracellular Ca. Prostaglandin E2 production in strips in potassium-deficient media was also sensitive to increases in extracellular Ca, and was augmented at concentrations of 7-15 mM. In strips which had been incubated with [3H]arachidonic acid, exposure to potassium-free media caused an increased release of [3H]arachidonic acid and [3H]prostaglandin E2. Release of these labeled compounds with the strips in potassium-free media was further augmented by increasing extracellular [Ca2+] from 2.5 to 10 mM. Treatment with the Ca antagonist agent verapamil did not influence activation of prostaglandin synthesis by potassium-deficient media. The presence of Mn2+ of Ba2+ had similar effects on prostaglandin synthesis, although they had opposite effects on mechanical activity. We conclude that a plasma membrane associated Ca pool is involved in activation of phospholipid metabolism which results in release of esterified arachidonic acid and subsequent prostaglandin synthesis. This Ca pool is in rapid equilibrium with extracellular Ca, is not influenced by cytoplasmic Ca, and is not related to Ca involved in Ca gating in the surface membrane. These data also indicate dissociation between processes involved in muscle contraction and activation of prostaglandin synthesis.

Animals↗
PubMed1982

CNS control of active sodium transport in muscle during progressive hypokalemia in the rat.

The degree of plasma hypokalemia was graded with the duration of a potassium deficient diet. The intracellular Na+ and K+ contents ([Na]i and [K]i) of the innervated soleus muscle of hypokalemic rats were determined and plotted as a function of plasma K+ concentration following a potassium deficient diet during 1-8 weeks. The progression of plasma hypokalemia was highly correlated with both [Na]i accumulation and [K]i loss in the muscle. Denervation of muscles in the hypokalemic rat resulted in a rapid activation of the Na-pump in the denervated soleus muscle regardless of the degree of plasma hypokalemia. This pump activation in the denervated muscle was chronically maintained throughout the hypokalemia. Restoration of a normal, K+ containing, diet for 4 days in hypokalemic rats resulted in a complete recovery of normal Na+ and K+ contents in both the innervated muscle and plasma, while the [Na]i and [K]i in the denervated muscle was unaffected. The relationship between the CNS-induced inhibition of the muscle Na-pump and the plasma K+ levels in hypokalemic rats is discussed.

Animals↗
PubMed1979

Effects of prolonged infusions of potassium chloride, adrenocorticotrophin or angiotensin II upon serum aldosterone concentration and the conversion of corticosterone to aldosterone in rats.

The temporal relation between alterations in serum aldosterone and in the conversion of labelled corticosterone to aldosterone by incubated adrenal tissue was studied in conscious rats receiving long-term infusions of KCl, ACTH or angiotensin II. When potassium-deficient rats were given KCl, a marked increase in serum aldosterone was observed only after 12 h, i.e. at a time when the conversion of corticosterone to aldosterone had become normal. After 24 h of ACTH infusion into sodium- and potassium-replete rats the serum aldosterone was markedly elevated, whereas the conversion of corticosterone to aldosterone was significantly decreased. After 48 h of continued ACTH infusion the serum aldosterone returned to normal and there was a further decrease in the conversion rate. A 24-h angiotensin II infusion into sodium- and potassium-replete rats induced significant increases in both the serum aldosterone and the conversion. After 48 h of continued angiotensin infusion the serum aldosterone returned to normal while the conversion and the blood pressure remained elevated. These results indicate that the activity of the enzymes involved in the final steps of aldosterone biosynthesis may become rate-limiting for the secretion of aldosterone during potassium deficiency and during prolonged ACTH treatment. On the other hand, the observed transiency of aldosterone stimulation by exogenous angiotensin II was not due to a suppression of the final steps of aldosterone biosynthesis and remains unexplained.

Adrenocorticotropic Hormone↗
PubMed1991

Oxygen radicals in postischaemic damages in the kidney.

Oxygen radicals in postischaemic damages in the kidney: M. Wolgast, A. Bayati, O. Hellberg, O. Källskog, K. Nygren and G. Ojteg, Inst. of Physiology and Medical Biophysics, University of Uppsala, Sweden; Ischemic acute renal failure is characterized by a severe depression of the glomerular filtration rate (GFR), isosthenuria and deficient potassium secretion, whereas the total renal blood flow may remain largely intact. As to these symptoms, it would seem established that the depression of GFR results from an ischaemia-induced augmented aging and hence rejection of tubular cells, which thence blocks the tubular lumen. As expected this blockade can be prevented by osmotic diuretics. The isosthenuria and the deficient potassium excretion, on the other hand, results probably from a medullary ischaemia, the latter due to the action by oxygen-derived free radicals in the sense the subsequent damage to the capillary membrane leads to a massive extravasation of plasma and consequent intracapillary trapping of red cells. In line with this idea, superoxide-dismutase (SOD) or Allopurinol may ameliorate these changes. In the recovery phase of postischaemic renal failure, the most prominent feature is the blocking of the ascending loop of Henle with Tamm/Horsfall-protein which, if not washed-out during the first week, leads to a complete degeneration of the nephron. Unfortunately, the process would seem to be unaffected by treatment with e.g. osmotic diuretics and SOD or Allopurinol.

Acute Kidney Injury↗
PubMed1996

Reversal of potassium channel deficiency in cells from failing hearts by adenoviral gene transfer: a prototype for gene therapy for disorders of cardiac excitability and contractility.

Heart failure is a common, often lethal disorder in which conventional pharmacologic strategies have achieved limited success. Failing hearts exhibit a delay of electrical repolarization which predisposes to fatal arrhythmias. To explore the feasibility of gene therapy for this condition, we isolated myocytes from normal and failing dog hearts and quantified electrophysiologic and contractile parameters in primary culture. Action potentials were prolonged in failing cells as a result of diminished potassium currents. Exposure to AdShK, an adenovirus that overexpresses potassium channels, reversed the action potential prolongation of failing cells. The precise phenotype varied as a function of the density of expressed channels; modest increases in potassium current sufficed to mimic the non-diseased state most faithfully, while more robust expression of the transgene excessively abbreviated excitation and contraction. Our results demonstrate that viral gene transfer can modify the electrical properties of adult mammalian heart cells in a manner appropriate to reverse a fundamental disorder of excitability. Realistic application of this form of therapy will need to include a sensitive mechanism for control of the level and distribution of transgene expression.

Action Potentials↗
PubMed1979

Development of pump electrogenesis in hypokalaemic rat muscle.

In hypokalaemic rats maintained on a potassium deficient diets for 10-50 days, the isolated "Na-loaded" and "K-depleted" ("Na-rich") muscle fibers showed the membrane potential less than -115 mV in "fresh" muscles of normal rats in K+-free Krebs solution. Upon adding 5 mM K+ to the K+-free medium bathing the soleus muscles, the measured potentials of "Na-rich" muscles always exceeded the membrane potentials of "fresh" muscles in 5 mM K+. The hyperpolarization was dependent on the amount of intracellular Na+ concentration (["na]i) accumulated during the potassium deficiency. The electrogenic Na-pump was activated by an increase of [Na]i of less than 5 mM. Further increases in [Na]i resulted in increases in membrane potential which appeared to approach a limit at [Na]i levels higher than 65 mM.

Animals↗
PubMed2001

Chronic potassium depletion induces renal injury, salt sensitivity, and hypertension in young rats.

BACKGROUND: Chronic hypokalemia has been associated with renal hypertrophy, interstitial disease, and hypertension in both adult animals and humans. However, the effects of potassium (K(+)) depletion on the rapidly growing infant have not been well studied. The purpose of this study was to determine the effects of severe chronic dietary K(+) depletion on blood pressure (BP) and renal structural changes in young rats. METHODS: Sprague-Dawley rats (50 +/- 5 g) were fed either a control or a potassium-deficient diet (<0.05% K(+)) for 14 to 21 days. At the end of this period, the blood pressure (BP) was measured in all rats, and six rats in each group were sacrificed to determine changes in renal histology and renin-angiotensin system (RAS) activity. The remaining rats in each group were then switched to a high-salt (6% NaCl)--normal-K(+) (0.5%) diet or were continued on their respective control or K(+)-deficient diet for an additional six days. Blood pressure measurements were done every three days until the end of the study. RESULTS: K(+)-depleted animals had significant growth retardation and increased RAS activity, manifested by high plasma renin activity, recruitment of renin-producing cells along the afferent arterioles, and down-regulation of angiotensin II receptors in renal glomeruli and ascending vasa rectae. K(+)-depleted kidneys also showed tubulointerstitial injury with tubular cell proliferation, osteopontin expression, macrophage infiltration, and early fibrosis. At week 2, K(+)-depleted rats had higher systolic BP than control rats. Switching to a high-salt (6% NaCl)--normal-K(+) diet resulted in further elevation of systolic BP in K(+)-depleted rats, which persisted even after the serum K(+) was normalized. CONCLUSION: Dietary potassium deficiency per se increases the BP in young rats and induces salt sensitivity that may involve at least two different pathogenic pathways: increased RAS activity and induction of tubulointerstitial injury.

Animals↗
PubMed1989

Electrocardiographic findings and frequency of arrhythmias in Bartter's syndrome.

Twenty four hour electrocardiograms in 20 patients with Bartter's syndrome, a disorder associated with chronic potassium deficiency, were analysed for atrial and ventricular extrasystoles, pauses (RR interval greater than 2 s), and heart rate. The 12 lead resting electrocardiogram was also evaluated. There were slight electrocardiographic changes with ST segment depression (greater than or equal to - 0.5 mm) in seven patients, flat or low amplitude T waves in seven, and U waves (greater than or equal to + 1.0 mm) in three patients. The QT interval was prolonged in 18 patients. Nine patients had one or more ventricular extrasystoles in 24 hours. Only two patients had more than 200 ventricular extrasystoles in 24 hours. No patient had ventricular tachycardia. A total of nine patients had one or more atrial extrasystoles in 24 hours, but only one patient had more than 200 in 24 hours. One patient had an attack of non-sustained supraventricular tachycardia. No patient had pauses. Dangerous tachycardia was rare in these patients with chronic potassium deficiency caused by Bartter's syndrome. The general pattern of slight electrocardiographic changes may reflect an adaptation of the myocardium to hypokalaemia. Further studies are, however, needed to determine whether these findings are relevant to long term prognosis.

Adult↗
PubMed1973

Vascular permeability of the renal medullary vessels in the mouse and rat.

The vascular permeability of the vessels of the renal medulla of normal rats and mice and potassium-deficient rats was studied by using ferritin, horseradish peroxidase and carbon particles as markers. Fenestrated endothelia are more permeable to ferritin and horseradish peroxidase than nonfenestrated endothelia. The ease with which the tracers are able to pass from the vascular lumina through the endothelia into the interstitium is directly related to the size of the tracers (horseradish peroxidase permeates most readily, followed by ferritin and carbon particles, in this order), suggesting the presence of a molecular sieving mechanism for the passage of substances through the capillary walls of the renal medulla. At the initial stage after injection of horseradish peroxidase and ferritin, these tracers pass from the medullary vascular lumina into the interstitium, not from the tubular lumina into the interstitium. It appears that the passage of ferritin and horseradish peroxidase through the vascular wall is enhanced in potassium-deficient rats.

Animals↗
PubMed1986

Disorders of the serum electrolytes, acid-base balance, and renal function in alcoholism.

This chapter reviews the disturbances of the serum sodium and potassium concentrations, acid-base imbalances, and acute renal dysfunction that are seen frequently in alcoholic patients. The hyponatremia common in decompensated cirrhotics is caused by an impairment of renal free water clearance and concomitant water ingestion. Excessive proximal renal tubular sodium reabsorption and nonosmotic vasopressin release underlie the defect in renal water excretion in cirrhosis. Restriction of water intake is the principal therapeutic measure for hyponatremia. Hypokalemia is common in alcoholics but when observed does not always represent true potassium depletion. Although most cirrhotics have a diminished total body potassium content, intracellular potassium concentration is usually normal. In some patients gastrointestinal and renal potassium losses and nutritional potassium deficiency may cause true potassium depletion. Respiratory and metabolic alkalosis are the acid-base disturbances seen most frequently in alcoholics. Acidosis is relatively uncommon and is usually due to renal insufficiency, lactic acid or keto-acid accumulation. Toxin ingestion (methanol, ethylene glycol, or isopropanol) may also cause severe acidosis. Rhabdomyolysis, common in severe alcoholism, may produce various electrolyte disturbances and acute renal failure. The prognosis for recovery is good although temporary dialysis may be necessary.

Acid-Base Equilibrium↗
PubMed2002

Effect of fertilisation on the potassium and radiocaesium distribution in tree stands (Pinus sylvestris L.) and peat on a pine mire.

This paper compares the effects of single and repeated fertilisation on the contents of potassium, 134Cs and 137Cs in different Scots pine compartments at different levels above ground and in the peat profile 9 years after the Chernobyl disaster. The material was collected from a ditch spacing and fertilisation experiment in Finland. Above a needle potassium concentration of 3.0 mg g(-1) in composed crown samples, 137Cs and 134Cs concentrations remained at about the same level but below that the values were higher on average. This potassium value corresponded to the potassium concentrations of 3.5-3.6 mg g(-1) in the current-year needles of two topmost whorls. The result indicates an enhanced radiocaesium uptake by pine trees under severe potassium deficiency. Fertilisation with potassium-containing fertilisers decreased the caesium uptake considerably. The inhibiting effect of fertilisation on caesium uptake by trees seemed to be fairly long lasting. Fertilisation had sped up the penetration of caesium downwards in the peat profile and its moving out of the active circulation of elements between soil and plants.

Cesium Radioisotopes↗
PubMed1975

[The effect of potassium chloride and organic potassium salts on the acid-base equilibrium in normo and hypokalemic rats].

The effects of intravenous infusions of potassium chloride, potassium acetate, potassium aspartate and potassium malate on plasma electrolytes and acid-base balance were investigated in normokalemic or hypokalemic alkalotic rats. Animals who obtained equal volumes of isotonic sodium chloride solution served as controls. All of these potassium solutions increased the plasma potassium concentrations to the same extent. Potassium chloride shifted the acid-base balance to acidotic values in normal rats or corrected metabolic alkalosis in hypokalemic rats. The potassium salts of organic acids, however, caused an increase in alkalosis, acetate acting stronger than aspartate and malate. In potassium deficiency combined with metabolic alkalosis the administration of potassium chloride is preferable to the organic potassium salts since it corrects both the electrolyte disturbances at the same time.

Acetates↗