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At least 19 recordsLinked to original sources
PubMed1976

Improvement of growth hormone response to stimulation in primary aldosteronism with correction of potassium deficiency.

Potassium depletion frequently occurs in primary aldosteronism and has been implicated as the cause of the impaired carbohydrate tolerance frequently associated with this syndrome. Glucose, insulin, and growth hormone regulation were studied in a 42-yr-old, male patient with an aldosterone-secreting adenoma when the patient was potassium-depleted and again after potassium repletion. Potassium repletion was documented by serial body potassium measurements, with an increase in body potassium from 2400 mEq to 2850 mEq after 400 mg spironolactone and 80 mEq supplemental potassium chloride were administered daily for 7 days. Potassium repletion resulted in improvement of the patient's glucose tolerance test, with a decrease in the peak glucose level from 184 mg/100ml to 130 mg/100ml and an increase in the peak insulin level from 46 muU/ml to 85 muU/ml. Intravenous administration of arginine resulted in a subnormal insulin response of 28 muU/ml in the base-line test and an increase to 59 muU/ml after potassium stores were repleted. Growth hormone response to arginine infusion was also initially minimal at 12.5 ng/ml, increasing markedly to 26 ng/ml after potassium replenishment. Insulin-induced hypoglycemia resulted in a depressed growth hormone response of 8 ng/ml when the patient was potassium-deficient, but a normal response of 30 ng/ml after potassium repletion. These observations demonstrate that impairment of both insulin and growth hormone responses to stimulation occur in primary aldosteronism with potassium depletion. These abnormalities may be reversed by potassium repletion.

Adenoma↗
PubMed2003

Effects of potassium deficiency on potassium, polyamines and amino acids in mouse tissues.

Sexual dimorphism in potassium content was found in plasma, kidney, heart and skeletal muscle of CD1 mice. We observed that feeding mice with a K(+)-deficient diet had an uneven and gender-dependent effect on organ weight and tissue potassium concentrations. Treatment produced a marked decrease in plasma, pancreas and skeletal muscle K(+) levels in both sexes, and a reduction in kidney, liver and heart potassium concentrations in females. Moreover, K(+) deficiency produced a 2-3-fold increase in the concentrations of cationic amino acids, such as arginine and lysine in both heart and skeletal muscle of the two sexes, a slight increase ( approximately 37%) in renal arginine in the male mice. The concentrations of these amino acids in plasma and other tissues in both sexes remained unaltered. Polyamine levels in heart, liver, skeletal muscle and pancreas from male and female mice were not affected by K(+) deficiency. However, in the male kidney potassium deficiency was accompanied by an increase of putrescine and spermidine concentration, and a reduction of putrescine excretion into the urine, even though renal K(+) concentration was not significantly affected and ornithine decarboxylase activity was dramatically decreased. The general lack of correlation between tissue potassium decrease and the increase in organic cations suggests that it is unlikely that the changes observed could be related with an attempt of the tissues to compensate for the reduction in cellular positive charge produced by the fall in K(+) content. The mechanisms by which these changes are produced are discussed, but their physiological implications remain to be determined.

Amino Acids↗
PubMed1985

Reduced hepatic fatty-acid synthesis and lowered plasma triacylglycerol (TG) in potassium deficient rats.

Potassium deficiency was induced in rats by feeding a potassium- free synthetic diet containing 5% Resonium A. Feeding this diet for 1 week resulted in a decrease of plasma potassium by about 50% vs. pair fed controls. In hypokalemic rats hepatic fatty-acid synthesis and TG secretion by the liver were significantly reduced. In contrast the removal of an intravenous lipid load occurred optimally under this condition. As a consequence plasma TG levels were reduced in potassium-deficient rats.

Animals↗
PubMed1984

Mechanism of decreased vascular reactivity to angiotensin II in conscious, potassium-deficient rats.

Chronic potassium deficiency in the rat results in a decrease in the pressor sensitivity to exogenous angiotensin II (AII). To define the mechanism of this resistance to AII, studies were performed in conscious rats after 14-21 d of dietary potassium deficiency. The pressor response to graded doses of AII was 50% less in potassium-deficient than control animals. In contrast, the pressor response to graded doses of norepinephrine was preserved in potassium-deficient rats; therefore, the decreased response to AII was not due to a generalized defect in vascular reactivity. Pretreatment with either the converting enzyme inhibitor, teprotide, or the prostaglandin synthesis inhibitor, indomethacin, failed to normalize the response to AII. Thus, neither prior receptor occupancy with endogenous AII nor the presence of vasodilatory prostaglandins caused the decreased AII response in potassium deficiency. Since the pressor response to AII involves angiotensin interaction with its vascular receptor, binding studies of mesenteric artery and uterine smooth muscle AII receptors were performed. Scatchard analysis showed that potassium deficiency resulted in a decrease in binding affinity (50% increase in Kd) in both uterine (6.00 vs. 3.82 nM; P less than 0.05) and vascular (1.39 vs. 0.973 nM; P less than 0.005) smooth muscle. Furthermore, despite increased circulating AII, there was an increase in AII receptor number in potassium-deficient uterine (308 vs. 147 fmol/mg protein; P less than 0.005) and vascular (470 vs. 316 fmol/mg protein; 0.05 less than P less than 0.1) smooth muscle. Although potassium deficiency resulted in alterations in receptor-binding parameters, the changes in binding affinity and number were directionally opposite, so that in potassium deficiency there was either no change or an increase in total AII binding. We conclude that the decrease in angiotensin pressor sensitivity in potassium-deficient rats is mediated by a postreceptor defect since it occurs subsequent to the binding of AII to its vascular smooth muscle receptor.

Angiotensin II↗
PubMed1997

The IGF-I axis in kidney and skeletal muscle of potassium deficient rats.

Potassium deficiency in the rat results in growth retardation, muscle wasting and renal hypertrophy. This study tests the thesis that K deficiency leads to tissue distinct changes in the local IGF-I system and cell sensitivity to IGF-I that favors renal enlargement on the one hand and impaired muscle growth on the other. In rats after eight days of K deficiency, compared to pair-fed control rats, food utilization and muscle and body wt gain were attenuated while the kidneys enlarged. In muscle GH receptor and IGF-I gene expression, IGF-I peptide and IGF binding protein-5 (IGFBP) levels were decreased. Together with reduced food utilization, these changes may contribute to the attenuated muscle growth. In the enlarged kidneys despite a fall in IGF-I mRNA level, IGF-I peptide concentration was increased more than twofold. This increase in IGF-I could be caused by the increase in kidney IGFBP-1 gene and protein expression and the decrease in kidney IGF-I degrading activity noted in K deficiency. Treatment with IGF-I failed to induce body or muscle growth, but induced a further increase in kidney size and enlargement of the spleen. Thus, in K deficiency the spontaneous increase in IGF-I levels in the kidney that is IGF-I sensitive may well be a cause of the renal hypertrophy.

Animals↗
PubMed2004

Growth hormone-mediated janus associated kinase-signal transducers and activators of transcription signaling in the growth hormone-resistant potassium-deficient rat.

Potassium deficiency (KD) is associated with severe growth failure, in part caused by growth hormone (GH) resistance. This study set out to determine whether the resistance could be caused by a defect in GH-mediated janus associated kinase-signal transducers and activators of transcription (STAT) signaling as occurs in uremia. To this end, rats were fed a K-deficient diet for 8 d and pair-fed controls received a K-replete diet. Animals from each group received GH or vehicle, and during this period, KD rats were GH resistant; GH induced body and liver weight gain and linear body growth were severely attenuated in these rats. In addition, signal transduction was studied in the liver of rats that were killed 10 or 15 min after an intravenous GH bolus or vehicle. When the rats were killed, GH receptor mRNA and protein levels were similar in the two groups. The abundance of STAT5, STAT3, and STAT1, proteins that mediate GH signaling, was significantly increased by 40 to 130% in KD. Furthermore, GH induced a far greater increase in STAT5 and STAT3 phosphorylation in this group. STAT5 phosphorylation was enhanced fourfold even when normalized for total STAT5 content. Phosphorylated STAT5 and STAT3 proteins were also increased in nuclear extracts, suggesting normal nuclear translocation of the activated signaling proteins. DNA binding of nuclear STAT5 was unaltered. Thus, in KD, there is resistance to the growth-promoting action of GH despite hyperactivation of the janus associated kinase-STAT signaling pathway. This suggests the presence of a defect distal to the nuclear binding of STAT or, alternatively, a defect in a STAT-independent GH-activated signaling pathway.

Animals↗
PubMed1978

Morphologic abnormalities in potassium-deficient dogs.

Potassium deficiency was produced in 16 dogs by means of a diet containing less than 0.03% potassium. Decreases in serum potassium were first observed after 3 weeks. Morphologic changes occurred only in heart, skeletal muscle, and kidney. Focal myocardial necrosis was observed in 6 of 16 deficient dogs, and skeletal muscle degeneration and necrosis were observed in 14 of 16 deficient dogs. A complex nephropathy consisting primarily of epithelial hypertrophy and hyperplasia in the collecting tubules of the inner stripe of the outer medulla occurred in all the deficient dogs.

Animals↗
PubMed1969

Effect of potassium deficiency upon translocation of C in attached blades and entire plants of sugarcane.

A deficiency in potassium decreased the translocation of labeled photosynthate from the leaf to the rest of the plant. Translocation was inhibited in blades which exhibited no visible symptoms of potassium deficiency and in which no decrease in photosynthesis was detected. In more severe deficiency both the rate of photosynthesis and the conversion of intermediates to end products decreased. The rate of respiration in deficient blades increased. The decrease in translocation caused by potassium deficiency is considered to be a primary effect and not secondary to the development of the well-known symptoms of potassium deficiency.

Journal Article↗
PubMed1978

Urinary excretion of prostaglandin E2 and prostaglandin F2alpha in potassium-deficient rats.

Potassium-deficiency was induced in rats by dietary deprivation of potassium. The animals became polyuric and urine osmolality decreased more then three-fold compared to controls. Urinary excretion of prostaglandin E2 (PGE2) and prostaglandin F2alpha (PGF2alpha) did not increase during 2 weeks of potassium depletion. Partial inhibition of renal prostaglandin synthesis by meclofenamate did not increase the urine osmolality after water deprivation. These results make unlikely the hypothesis that the polyuria of potassium-deficiency, is the result of enhanced renal synthesis of prostaglandins with subsequent antagonism of the hydro-osmotic effect of vasopressin. Male animals consistently excreted less PGE2 than female animals.

Animals↗