Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of E. coli with the viruses T7 or T3 leads to a dramatic efflux of potassium ions. This ion efflux is caused by the virus particle since no concomitant protein synthesis is required. T7 mutants carrying deletions in the M-gene (Schweiger et al., 1975), however, yield virus particles disturbed in the ion release.
Mol Gen Genet 1976 Dec 08
PMID:E. coli membranes become permeable to ions following T7-virus-infection. 79 75

1. Whole-body retention and plasma values of 131I after a test dose were measured for up to 32 days in patients previously rendered athyreotic by surgery, and 131I treatment for thyroid carcinoma, and who were without detectable functioning tissue at the time of study. 2. About 99-8% of the administered 131I was rapidly excreted, consistent with renal iodide excretion. The remainder (about 0-2%) was eliminated slowly, with mean half-life 15 days; we call this the slow-turnover component. 3. By the sixth day after the 131I dose, very little [131I]iodide remained in the plasma. The average protein-bound 131I was only 0-0035% of dose/l, with mean half-life 14-1 days; 90% was non-extractable in butanol. Labelled albumin accounted for about 80% of the non-extractable fraction. 4. The distribution space estimated from the slow-turnover component and protein-bound 131I was 34 l, indicating that most of the slow-turnover component is extravascular. 5. Stable potassium iodide administration, starting 2 days after giving 131I, had no observable effect on the variables measured. 6. Impairment of renal function delayed [131I]iodide excretion and increased both slow-turnover component and plasma protein-bound 131I. 7. A simple model describing iodine kinetics in athyreotic individuals is suggested. It predicts that the slow-turnover component contains only about 4 micrograms of iodine and, since this is distributed widely in body tissues, it is unlikely to be of biological significance.
Clin Sci Mol Med 1977 Jul
PMID:A slow component of iodine turnover in athyreotic individuals. 87 23

1. In the perfused rat mesenteric vascular bed, the effects of angiotensin II, cortisol and prostaglandin E2 on the vascular responses to noradrenaline or potassium chloride were studied. 2. Angiotensin II in subpressor concentrations potentiated the vasoconstrictor response to noradrenaline and potassium chloride. This effect of angiotensin II was inhibited in the presence of indomethacin and prostaglandin E2. 3. Cortisol in physiological concentrations inhibited the potentiating effect of angiotensin II. 4. Prostaglandin E2 enhanced the vasoconstrictor response to noradrenaline. This effect was not abolished by cortisol. 5. These results suggest that some actions of angiotensin II and cortisol in vivo are mediated by the regulation of prostaglandin synthesis or release.
Clin Sci Mol Med 1977 Sep
PMID:Potentiation of pressor effects of noradrenaline and potassium ions in the rat mesenteric arteries by physiological concentrations of angiotensin II: effects of prostaglandin E2 and cortisol. 91 46

1. Renal lithium clearance in healthy men was elevated while the subject was reclining, decreased upon standing and increased upon lying down during 45-60 min tests. 2. Parallel changes in renal clearance of creatinine, sodium and potassium, and urine flow rate occurred in response to the changes in posture. 3. The findings demonstrate for the first time that posture is a factor that can influence lithium excretion. Control of posture during lithium excretion tests is recommended.
Clin Sci Mol Med 1976 Jul
PMID:Effect of posture on renal lithium clearance. 93 60

1. Twenty-three hypertensive patients were treated by sotalol, a pure beta-adrenergic receptor blocking agent. The drug produced a significant decrease of blood pressure in nineteen patients. 2. On average, cardiac index decreased but not significantly; heart rate decreased and stroke index increased significantly. Total peripheral resistance varied in both directions. 3. Sotalol determined a fall in plasma renin concentration (only significant in the high-renin group), a fall in plasma angiotensin II concentration and in urinary excretion rate of aldosterone accompanied by a rise in plasma potassium concentration. 4. The fall of blood pressure was not correlated with the decreases of renin and angiotensin II concentrations or excretion rate of aldosterone. However, in the placebo period plasma angiotensin II concentration was significantly correlated with total peripheral resistance; during sotalol treatment the variations of these two parameters seemed also to be correlated. 5. There was a poor correlation between decreases of cardiac output and of blood pressure; it was impossible to foresee the magnitude of the lowering of the blood pressure from the initial cardiac index. 6. The association of a diuretic with sotalol enhanced the hypotensive effect of the beta-receptor blocking drug, without significant increase of plasma renin and angiotensin II concentrations.
Clin Sci Mol Med 1976 Jul
PMID:Effect of sotalol on haemodynamics and renin-angiotensin-aldosterone system in hypertensive patients. 93 70

1. The mechanism of potassium transport across human distal colon was investigated in twenty-two individuals without evidence of bowel disease, by using a dialysis method in conjunction with measurements of the transepithelial potential difference (p.d.). 2. Whether potassium was absorbed or secreted depended on its initial concentration in the lumen. The potassium net flux was approximately zero when the luminal potassium concentration was between 30 and 50 mmol/l. 3. Potassium secretion rate was little affected by sodium absorption rate, or by the luminal sodium concentration or by the osmolality of the luminal solution. 4. Potassium secretion rate was increased by partial substitution of other cations for sodium, in the descending order Li greater than NH4 greater than Rb greater than Na. Potassium concentration increased on average to over 80 mmol/l when lithium was in the lumen. 5. The observed transepithelial p.d. was inadequate to account for the intraluminal potassium concentrations attained, the discrepancy being most marked when ammonium or lithium was in the lumen. It is suggested that some potassium is secreted by the epithelial cells and this component of the total potassium flux into the lumen is increased when rubidium, ammonium or lithium is substituted for sodium.
Clin Sci Mol Med 1976 Sep
PMID:Potassium transport across the distal colon in man. 96 58

1. To study the effects of chloride depletion, without sodium depletion or change in plasma tonicity, on renal excretion of sodium and water, a single exchange peritoneal dialysis was performed in rats against a solution of glucose (15 g/1) containing either NaCl (150 mmol/l, control) or NaHCO3 (150 mmol/l, experimental); KHCO3 (4mmol/l)was added to both solutions. All rats were prepared before dialysis by a low NaCl diet for 10 days. 2. Peritoneal dialysis against NAHCO3 consistently produced a negative sodium and water balance compared with dialysis against NaCl. Despite this, subsequent electrolyte balance for 3 days showed that chloride-depleted rats excreted significantly more sodium and water and had a reduced urinary osmolality as compared with control animals. Increased sodium and water loss were unexplained by osmotic or bicarbonate diuresis. Kaliuresis was seen in the chloride-depleted rats but muscle potassium was not significantly depressed. 3. With sodium and water loss and continued renal chloride conservation, plasma chloride rose on the average from 88 mmol/l after dialysis against NaHCO3 to 100 mmol/l (control 104 mmol/l) at 72 h. Concomitant with this increase in plasma [C1-], on the third day after dialysis, during hydropenia, urinary osmolality and papillary [Na+] were not different from control cencentrations. 4. It is postulated that chloride depletion and/or hypochloraemia leads to diminished chloride transport in the loop of Henle and that this causes reduced sodium transport into the medulla, impaired concentration ability and inappropriate urinary sodium loss.
Clin Sci Mol Med 1976 Oct
PMID:Chloride depletion and hypochloraemia as a cause of renal sodium and water loss in the rat. 97 76

1. Two women with severe hypokalaemic alkalosis were investigated by means of muscle biopsy before and at the end of 2 and 3 weeks respectively of intense therapy with potassium chloride. 2. The muscle biopsy material was analysed for water, electrolytes, adenine nucleotides, phosphocreatine, free creatine, pyruvate, lactate, glycogen and free amino acids. The extra- and intra-cellular distribution of water, electrolytes and amino acids was calculated by the chloride method. 3. Both patients showed a marked loss of intracellular potassium and an increase in intracellular sodium concentration. The muscle magnesium content was also slightly decreased. After repletion with potassium chloride, muscle sodium and potassium became normal. 4. The contents of creatine phosphate, ATP, ADP, AMP, lactate and pyruvate were within normal limits, but the phosphocreatine/total creatine ratio was reduced. After repletion, a small change in the apparent creatine-phosphokinase equilibrium had occurred, suggesting a minor increase in intracellular pH. 5. The concentrations of the basic amino acids, lysine, arginine and ornithine were increased far above normal. The intracellular accumulation of arginine was much higher than the increase in lysine concentration and histidine concentration was normal. This differs from findings in potassium-depleted rats, where the intracellular lysine concentration is much higher than arginine concentration and histidine is high as well. After potassium repletion the intracellular concentration of ornithine, lysine and arginine became normal in one case and decreased considerable in the other. An increased intracellular concentration of glutamate and glutamine was also observed after potassium repletion.
Clin Sci Mol Med 1976 Dec
PMID:Influence of severe potassium depletion and subsequent repletion with potassium on muscle electrolytes, metabolites and amino acids in man. 107 Apr 23

1. Erythrocyte membrane permeability to sodium and potsssium ions was studied in 8-10 weeks spontaneously hypertensive rats (SHR, Kyoto/Wistar strain), normotensive Wistar and Sprague-Dawley rats. 2. The rate of 22Na efflux from the erythrocytes and the rate constant of Na/Na exchange were considerably greater in SHR than in normotensive Wistar and Sprague-Dawley rats. This difference remained the same in rats adrenalectomized 7 days before the experiment. The maximum difference in the constants was found when the sodium-potassium pump was blocked by ouabain. 3. The accumulation of 42K in the erythrocytes of SHR (the sodium-potassium pump being blocked) took place at a considerably slower rate, and the K+ wash-out into a potassium-free medium was faster than that in the normotensive Wistar and Sprague-Dawley rats. 4. These results indicate a higher permeability of the erythrocyte membrane of SHR for Na+ and K+, compared with normotensive Wistar and Sprague-dawley strains. It is suggested that this may reflect a more widespread cell-membrane defect, which could serve as a general cause for activating the mechanisms maintaining high blood pressure.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Evidence of altered permeability of the erythrocyte membrane for sodium and potassium ions in spontaneously hypertensive rats. 107 99

1. Urinary kallikrein, sodium, potassium and water excretion, and plasma renin activity were measured before and during the reversal of experimental hypertension produced by unclamping the renal artery in rats. 2. Kallikrein excretion decreased significantly after unclamping, suggesting that it does not play a significant role in the reversal of hypertension. 3. A decrease in plasma renin activity coupled with a slight increase of sodium excretion was observed, indicating that these might participate in the reversal of hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Urinary kallikrein and plasma renin during the reversal of renovascular hypertension in rats. 107 24


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