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)

1. The relationships between the renin-angiotensin-aldosterone system, sodium and potassium balance and systolic blood pressure were studied during development of moderate (160-180 mmHg; clip i.d. 0.25 mm) and severe (200-230 mmHg; clip i.d. 0.20 mm) renal hypertension in rats with an undisturbed contralateral kidney. 2. In severely hypertensive rats renin activity in the peripheral plasma increased from day 9, by which time the systolic blood pressure was elevated to 160-180 mmHg. The rate of total corticosteroid and aldosterone production in vitro increased from day 14 and plasma renin substrate concentration increased from day 24. In moderately hypertensive rats, none of these changes occurred. 3. During the first 10 days after the application of 0.25 and 0.20 mm clips, sodium and potassium retention/g gain in body weight were higher than in sham-operated controls. During the next 10 days, the positive balance stabilized in animals with a 0.25 mm clip whereas, in animals with a 0.20 mm clip, sodium and potassium balance returned to the level of the sham-operated controls through increased renal losses. Despite these changes the systolic pressure rose further in animals with a 0.20 mm clip. 4. The initial sodium retention could be a factor in the early rise of blood pressure and could account for the delay in the rise of peripheral plasma renin activity. The subsequent loss of the retained sodium and potassium during the development of severe hypertension could have facilitated the rise in peripheral plasma renin activity, but did not initiate this rise.
Clin Sci Mol Med 1975 Jan
PMID:Changes in the renin-angiotensin-aldosterone system and in sodium and potassium balance during development of renal hypertension in rats. 116 91

1. The influence of dietary sodium intake on the glomerular filtration rate (GFR/nephron) and potassium and phosphate excretion was examined at three stages of progressive chronic renal failure produced in rats by sequential partial nephrectomies. 2. The adaptive increased sodium excretion per nephron in the control group receiving a constant sodium intake did not occur in the experimental group that had a gradual reduction of dietary sodium in direct proportion to the fall in GFR. 3. Despite the difference in sodium excretion, the increase in GFR/nephron, the daily variation in the amount of potassium and phosphate excreted, the increase in potassium and phosphate excretion per unit nephron, and the plasma potassium and phosphate concentrations were the same in the two groups. 4. The concept of 'autonomous adaptation' in chronic renal failure is presented.
Clin Sci Mol Med 1975 Sep
PMID:Effect of proportional reduction of sodium intake on the adaptive increase in glomerular filtration rate/nephron and potassium and phosphate excretion in chronic renal failure in the rat. 117 35

1. Body weight was measured through forty consecutive illnesses in seventeen patients with oedema in association with chronic bronchitis and hypoxia. All patients were taking diuretic drugs at the time. 2. Body weight increased little as peripheral oedema and a raised jugular venous pressure appeared. The subsequent weight-loss during treatment was usually greater than the pre-treatment weight-gain. Body weight increased slowly in convalescence to equal or exceed hospital admission weight without a deterioration of general health or reappearance of oedema. 3. Total body water, exchangeable sodium and exchangeable potassium were measured in patients after treatment of the acute illness and clearance of oedema and again in six patients of the group 2-3 months later in convalescence. Total exchangeable sodium was normal or slightly reduced after treatment of oedema and in convalescence between recurrent acute illnesses. Even when gross oedema was present exchangeable sodium was substantially increased in only one of three patients studied at this stage. Total exchangeable potassium was invariably severely depressed. 4. Large changes of body tissue weight without comparable change in exchangeable sodium support previous evidence that oedema in hypoxic bronchitis is not simply a further form of congestive cardiac failure. 5. It is suggested that at least some of the tissue loss in acute exacerbations is a direct result of hypoxaemia and similar to that observed at high altitude. Part of the oedema fluid is thought to be derived from intracellular water released during dissolution of tissue matrix.
Clin Sci Mol Med 1975 Oct
PMID:Body weight and body water in chronic cor pulmonale. 119 92

1. Sodium and potassium transport rates in human leucocytes were measured in vitro at different external potassium concentrations. 2. At nominally zero external potassium concentrations, the ouabain-sensitive sodium efflux was reduced to less than 20% of its maximum value. There was evidence that under these conditions a ouabain-sensitive sodium-sodium exchange occurs. 3. Both total and ouabain-insensitive potassium influx increased with increasing external potassium concentration. The ouabain-sensitive potassium influx showed saturation. 4. Ouabain-insensitive potassium efflux was also stimulated by increasing the external potassium concentration, suggesting significant potassium-potassium exchange at physiological external potassium concentrations.
Clin Sci Mol Med 1975 Nov
PMID:The effect of external potassium concentration on leucocyte cation transport in vitro. 119 96

1. The effect of modifying potassium intake on arterial plasma renin activity, angiotensin II and aldosterone concentrations, renal blood flow and their responses to exogenous angiotensin II has been assessed in twenty-six normal subjects. 2. Reduced potassium intake was associated with a significant increase in circulating renin activity and angiotensin II concentration and a significant reduction in renal blood flow. Conversely, a high potassium intake was associated with a significant increase in plasma aldosterone concentration and renal blood flow without alteration in plasma renin activity or angiotensin II concentration. 3. Reduced potassium intake decreased both the renal vascular and the adrenal response to infused angiotensin II. Conversely, an increased potassium intake enhanced the responsiveness of both systems. 4. The results suggest an important influence of potassium-induced renin-angiotensin system responses on both the renal vasculature and adrenal glomerulosa cell in normal man.
Clin Sci Mol Med 1975 Dec
PMID:The influence of potassium on the renal vasculature and the adrenal gland, and their responsiveness to angiotensin II in normal man. 120 82

1. In order to study the effect of overhydration on body potassium, experiments were performed on pair-fed rabbits, one of which was maintained continuously on vasopressin and given extra water (60-90 ml day-1 kg-1) for 6-8 days, while the other served as control. 2. Overhydrated rabbits excreted significantly more potassium (53%) in their urine than control rabbits and accumulated a mean potassium deficit of 65-0 mmol, significantly higher than the mean value of 37-1 mmol in the control rabbits. 3. In the overhydrated rabbits, potassium fell significantly in both erythrocytes, from 266 to 173 mmol/kg of dry cells, and also in muscle, from 435 to 341 mmol/kg of fat-free dry solids. Neither changed significantly in the control animals. 4. Overhydration in the presence of vasopressin leads to potassium depletion in the rabbit and a similar phenomenon might be expected in man. Potassium depletion due to overhydration might account for the hypokalaemia and reduction in exchangeable potassium observed in some patients with the syndrome of inappropriate secretion of antidiuretic hormone.
Clin Sci Mol Med 1975 Dec
PMID:Potassium depletion induced by vasopressin and overhydration in the rabbit. 120 83

1. The relations between the concentration of plasma uric acid and urinary excretion of aldosterone, sodium and potassium, were studied in ten healthy males on a diet containing 160 mmol of sodium and 90 mmol of potassium per day. 2. Plasma uric acid correlated positively with aldosterone excretion and this correlation was statistically independent of sodium and potassium excretion. 3. Plasma uric acid correlated positively with potassium excretion and negatively with the urinary sodium/potassium ratio. There was no significant simple correlation with sodium excretion but the partial correlation of plasma uric acid and sodium excretion was negative and significant when excretion of aldosterone and potassium were held constant.
Clin Sci Mol Med 1975 Dec
PMID:Plasma uric acid concentration related to the urinary excretion of aldosterone and of electrolytes in normal subjects. 120 92

1. The concentration of potassium in the erythrocytes and the plasma of forty-one normal subjects and twenty-five diabetic patients was measured and the results were used to calculate the total amount of potassium in the erythrocyte mass and the total amount of potassium in the plasma. The total body potassium was measured in a whole-body monitor. 2. In normal subjects a close correlation was found between total erythrocyte potassium and total body potassium and also between total plasma potassium and total body potassium. 3. The regression relation between total body potassium and total erythrocyte potassium in normal subjects was used to predict the total body potassium in diabetic patients. There was reasonable agreement between the measured and predicted total body potassium but there was poor agreement between the measured total body potassium and that predicted from the patient's height and age or height and age or height, weight and age.
Clin Sci Mol Med 1976 Jun
PMID:The relation between potassium in body fluids and total body potassium in healthy and diabetic subjects. 127 54

1. The effect of interleukin-1 (IL-1) was studied on voltage-activated ion currents of the identified central neurons of Helix pomatia L. using a two-microelectrode voltage clamp. The voltage-activated inward current (ICa) was decreased, whereas the outward current (I(net) K) was increased by IL-1. 2. IL-1 affects both the transient and the delayed rectifying potassium currents. The IL-1 modulatory effect on the voltage-activated ion currents was voltage and dose dependent. The threshold concentration for IL-1 was 2 U/ml. 3. The proposed modulatory effect of IL-1 appears to have more than one site of action on the neuron membrane ion channels. 4. Rabbit anti-human IL-1 polyclonal antiserum eliminated the IL-1 effects on the voltage-activated inward and outward currents. This is the first report demonstrating a direct effect of IL-1 modulation of voltage-activated ion currents on neurons of mollusks.
Cell Mol Neurobiol 1992 Oct
PMID:Modulation of voltage-activated ion currents on identified neurons of Helix pomatia L. by interleukin-1. 128 56

Previous current-clamp work has shown that dihydropyrazole insecticides block sodium channels in tonic sensory receptors and in axons depolarized by high K+ external solutions and that hyperpolarization removes the block [Pestic. Sci. 28:389-411 (1990)]. Voltage-clamp studies on internally perfused crayfish giant axons were done to confirm and extend these observations. At -100 mV dihydropyrazoles had little effect on the sodium current, but at more depolarized potentials they blocked it from either face of the membrane. The onset of block following a holding potential change or during wash-in of a dihydropyrazole was very slow, with a time constant of several minutes, and, although block could be removed with a similar time course by hyperpolarization, the effects of the insecticides could not be reversed by prolonged washing. Dihydropyrazoles did not affect delayed rectifier potassium currents in the axon. The voltage-dependent block could be described as a uniform shift of the steady state (slow) sodium inactivation (S infinity) curve in the direction of hyperpolarization, indicative of selective binding to inactivated states of the channel. Using hyperpolarizing prepulses to remove slow inactivation, block of sodium channels by dihydropyrazoles could be measured directly at holding potentials as positive as -50 mV, and it could be demonstrated that block saturated near -70 mV, consistent with a dependence on slow inactivation. The data were fit to a model tha assumes the dihydropyrazole binds to the slow-inactivated state of the channel on a one to one basis. Dissociation constants obtained from this analysis were similar to those obtained from analysis of inhibition of the binding of [benzoyl-2,5-3H]-batrachotoxinin A 20-alpha-benzoate by the same dihydropyrazoles. In axons whose fast or slow inactivation gates had been removed by N-bromoacetamide or trypsin, respectively, dihydropyrazoles still blocked sodium current, indicating that dihydropyrazoles can block the channel as well as enhance the normal slow inactivation process.
Mol Pharmacol 1992 Jan
PMID:Slow voltage-dependent block of sodium channels in crayfish nerve by dihydropyrazole insecticides. 131 Jan 38


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