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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In examining the relationship between erythrocyte sodium, potassium, and blood pressure in Nigerians, we measured the erythrocyte sodium and potassium in 25 hypertensive and 34 normotensive subjects. Of the normotensive subjects, 15 had positive family histories of hypertension and 19 did not. The hypertensive subjects were older (50.1 +/- 1.7 years) than the normotensive subjects (25.4 +/- 0.7 years) (mean +/- SEM; P < .001). The mean arterial pressure in hypertensive subjects was higher (108.8 +/- 2.3 mm Hg), as expected, compared with normotensive subjects (86.98 +/- 1.62 mm Hg) (P < .001). The mean duration of hypertension in hypertensive subjects was 5.60 +/- 0.75 years. Erythrocyte sodium was higher in hypertensive subjects (9.57 +/- 0.19 mmol/L) compared with normotensive subjects (7.96 +/- 0.19 mmol/L) (P < .001). Among normotensive subjects, erythrocyte sodium was higher in those with a positive family history of hypertension (8.59 +/- 0.31 mmol/L) compared to those without such a history (7.47 +/- 0.18 mmol/L), and this was also statistically significant (P = .027). Erythrocyte potassium levels were similar in the hypertensive subjects (83.51 +/- 0.71 mmol/L), in normotensive subjects (81.86 +/- 0.81 mmol/L), and in those without a family history of hypertension (80.20 +/- 0.51 mmol/L) (P = .675). We observed a significant (P < .001) positive correlation between erythrocyte sodium and systolic (r = 0.99) and diastolic (r = 0.39) blood pressures. Our findings support the hypothesis that erythrocyte sodium is closely related to blood pressure and its nonracial genetic determinants.
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PMID:Intracellular sodium and blood pressure in Nigerians. 184 41

Recombinant human insulin-like growth factor I (rhIGF-I) was administered subcutaneously to 6 normal subjects and 2 patients with GH deficiency at a dose of 0.1 mg/kg for 7 consecutive days after breakfast. In normal subjects, plasma IGF-I levels increased from 217 +/- 22 ng/ml (Mean +/- SEM) to maximal levels of 581 +/- 6 ng/ml 4 h after the first administration of IGF-I. The blood glucose levels were statistically depressed 4 h after injection at 69 +/- 2 mg/dl. Similar plasma IGF-I and blood glucose profiles were observed after the seventh administration of IGF-I. The free form of IGF-I in plasma was 2.3 +/- 0.3 ng/ml in normal subjects and increased to maximal levels of 43.5 +/- 5.1 ng/ml 2 h after the first IGF-I administration. A similar pattern for the free form of IGF-I was observed after the seventh administration; however, the values obtained at 0, 1 and 2 h were greater after the seventh administration. In patients with G-deficiency, the plasma IGF-I and blood glucose profiles were similar to those observed in normal subjects, although the total IGF-I levels were low in these patients at all sampling points during the study. Slight decreases in serum insulin, uric acid, and creatinine were observed after the seventh administration of IGF-I. There were no changes in the excretion of urea nitrogen, creatine, creatinine, sodium, potassium, chlorine, calcium or C-peptide in the urine during the 7 days of IGF-I administration.
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PMID:Repeated sc administration of recombinant human insulin-like growth factor I (IGF-I) to human subjects for 7 days. 184 57

To compare the metabolic effects of indapamide (I) and hydrochlorothiazide (HCTZ) at equivalent hypotensive doses, 11 hypertensive patients (5 male, 8 black, aged 56 +/- 8 yr--mean +/- SEM) having serum uric acid concentrations greater than 8.0 mg/dL while receiving previous therapy with thiazides, received 28-day courses of placebo, indapamide (2.5 mg/d), and HCTZ (25 mg/d) in randomized, double-blind, double-crossover design. Supine and standing blood pressures, weight, pulse rates and sera were obtained after each 28 day period. Blood pressures and weights were lowered (P less than .001 and 0.01, respectively) equally by the diuretics: supine blood pressures fell from 168 +/- 4/104 +/- 2 (placebo) to 153 +/- 4/93 +/- 2 (HCTZ) and 155 +/- 4/94 +/- 2 mm Hg (I); standing blood pressures (after 2 minutes upright) also decreased: 171 +/- 5/104 +/- 2 (placebo) to 156 +/- 5/93 +/- 2 (HCTZ) and 157 +/- 4/94 +/- 2 mm Hg (I). There was a statistically significant difference (P less than .05) across treatments by analysis of variance in both uric acid and potassium concentrations: serum urate (in mg/dL) was lowest with placebo (7.1 +/- 0.3), and rose to 8.3 +/- 0.2 with HCTZ (P less than .001 compared with placebo by paired t test), and 8.1 +/- 0.2 with I (P less than .005 vs. placebo). The urate concentration with I was significantly lower than that with HCTZ (P less than .02), but the magnitude of the difference was small (0.2 mg/dL).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A double-blind, randomized, placebo-controlled comparison of the metabolic effects of low-dose hydrochlorothiazide and indapamide. 188 Feb 34

The effects of moderate, chronic (5 days) potassium depletion on cardiac function were assessed in 14 normokalemic and 13 hypokalemic open chest, anesthetized dogs. Cardiac responses to intravenous bolus injection of 2.5 micrograms/kg body weight epinephrine (10 normokalemic and 11 hypokalemic dogs) and to rapidly increased preload (8 dogs in each group) were evaluated. Hypokalemic dogs received a low potassium diet plus chlorthalidone. Plasma potassium levels were lower (p less than 0.001) in the hypokalemic dogs (3.2 +/- 0.1 mEq/liter [mean +/- SEM]) than in the normokalemic dogs (4.1 +/- 0.1). The inotropic response to epinephrine was lower in hypokalemic than in normokalemic dogs, the response of the maximal rate of rise of left ventricular pressure was 20% greater (p less than 0.03) and the response of the peak rate of change of ejection power was 60% greater in the normokalemic dogs. The relaxation response to epinephrine (the maximal rate of fall of left ventricular pressure) was 33% lower (p less than 0.02) in hypokalemic dogs. Responses to rapid volume expansion were impaired by hypokalemia; maximal stroke volume index was 31% lower (p less than 0.01), maximal cardiac index was 26% lower (p less than 0.01) and the peak response to the maximal rate of filling was 51% lower (p less than 0.01). There were no differences in basal cardiac function. Therefore, modest potassium depletion within the clinical range impaired the contractile and relaxation responses to epinephrine and preload and impaired rapid filling.
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PMID:Chronic hypokalemia and the left ventricular responses to epinephrine and preload. 189 55

Calcium glycerophosphate (CaGP) was tested as an alternative to calcium gluconate (CaGluc) and potassium mono- and dibasic phosphate (KPhos) as a source of Ca and P in total parenteral nutrition (TPN) solutions for piglets. Four-day-old piglets were infused for 7 days with a TPN solution that provided either 4.2 mmol Ca and 2.1 mmol P/kg/24 h as CaGluc and KPhos (the maximum quantities that can be provided using these sources), or 15.0 mmol Ca and 15.0 mmol P/kg/24 h as CaGP. Ca and P retentions were more than six times greater (p less than 0.01) in the piglets receiving CaGP (14.5 +/- 0.2 vs 2.2 +/- 0.3 mmol Ca/kg/24 h and 13.3 +/- 0.4 vs 2.4 +/- 0.1 mmol P/kg/24 h) (Mean +/- SEM). The ratio of Ca to fat-free dry weight, an indicator of bone mineralization, was significantly higher (p less than 0.05) in the humerus (174.8 +/- 2.2 vs 147.2 +/- 6.7) and femur (158.3 +/- 4.8 vs 130.1 +/- 7.8) in the CaGP group. This study showed that CaGP is efficiently used as a source of Ca and P in TPN solutions for piglets. The results suggest that the use of CaGP as the source of Ca and P in TPN solutions may prevent the development of the undermineralized bone seen in low-birth weight infants nourished intravenously.
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PMID:Calcium glycerophosphate as a source of calcium and phosphorus in total parenteral nutrition solutions. 190 52

We were able to confirm previous studies demonstrating that administration of thyroxine is capable of ameliorating the severity of acute nephrotoxic renal failure in the rat. Nephrotoxic acute renal failure was induced by the subcutaneous injection of potassium dichromate (6.25 mg/kg) into Sprague-Dawley rats. Twenty-four hours after this injection, rats received an intraperitoneal injection of either thyroxine (80 micrograms/kg body wt) or normal saline. Forty-eight hours after the potassium dichromate injection, renal clearance studies were performed. Inulin clearance was significantly higher in the thyroxine-treated than in the saline-treated acute renal failure rats: 1.12 +/- 0.13 (SEM) mL/g versus 0.75 +/- 0.07 mL/min/g kidney wt (P = 0.025). Thyroxine treatment also effected an increase of p-aminohippuric acid extraction from 0.23 +/- 0.03 to 0.33 +/- 0.02 (P = 0.011) and a decrease in the fractional excretion of sodium from 0.38 +/- 0.21 to 0.11 +/- 0.03% (P = 0.037 by Mann-Whitney U test). In order to investigate one potential mechanism of the beneficial effect of thyroxine we studied renal tubular regeneration in this model of acute renal failure. Renal cortical uptake of labeled thymidine into DNA was significantly increased 48 h after the injection of potassium dichromate, and thyroxine administration further enhanced this repair process: 53.9 +/- 3.6 versus 81.4 +/- 5.3 dpm/200 pg of DNA (P = 0.0033).
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PMID:The beneficial effects of thyroxine on nephrotoxic acute renal failure in the rat. 193 36

In 15 conscripts, venous plasma potassium was followed during exercise on a training bicycle before and after 10 weeks of moderate physical training and a putative relationship with skeletal muscle Na,K-ATPase was evaluated. Peak plasma potassium concentration obtained at exhaustion was 6.1 +/- 0.2 and 5.6 +/- 0.2 mmol l-1 (mean +/- SEM, n = 14, P less than 0.05) before and after training, respectively. Throughout the exercise period and within the first minutes of rest plasma potassium concentration was 0.2-0.5 mmol l-1 higher before than after training. Neither peak values nor peak rises in plasma potassium concentration before nor after training were correlated to the 3H-ouabain binding site (Na,K-ATPase) concentration in vastus lateralis muscle. The results indicate that net loss of potassium from the skeletal muscle pool during exercise is reduced after training, that the heart during exercise may be exposed to a smaller rise in plasma potassium concentration after training than before, and that moderate improvement of capacity to clear extracellular potassium during exercise may be due to increased activity of existing Na,K-pumps in resting skeletal muscle fibres. This may reduce muscle fatigue, increase physical performance and explain the paradoxical observation that, despite an increased catecholamine response, there is a reduced risk of cardiac events after training.
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PMID:Exercise-induced hyperkalaemia can be reduced in human subjects by moderate training without change in skeletal muscle Na,K-ATPase concentration. 196 26

In a randomised, double-blind, crossover study, single oral doses of cromakalim, a potassium-channel activator, or placebo were given to 23 patients with nocturnal asthma. There was a significant reduction (p less than 0.005) in the early morning fall in forced expiratory volume in 1 s (FEV1) after 0.5 mg cromakalim (fall 9.8% [SEM 3.2%]) compared with placebo (18.5 [2.8]%). In a repeat dosing study, administration of 0.25 mg and 0.5 mg cromakalim on 5 consecutive nights to a further group of 8 asthmatic subjects significantly reduced the early morning fall in FEV1 from 28.7 (6.5)% after placebo to 19 (4.2)% after 0.25 mg and 14.9 (6.5)% after 0.5 mg. Potassium-channel activators may be useful in the treatment of asthma, especially for nocturnal symptoms.
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PMID:Attenuation of nocturnal asthma by cromakalim. 197 34

Some properties of the alveolar epithelial barrier during transalveolar transport of water and solutes were studied in normal humans and patients with sarcoidosis by means of the transalveolar capillary concentration gradients of various solutes. A total of 9 normal control subjects (Group A) and 60 sarcoidosis patients, 52 with an evolving disease (Group B) and 8 recovered (Group C), underwent bronchoalveolar lavage (BAL). The second aliquot of fluid was used to measure urea, glucose, potassium, and albumin, which were also investigated in plasma. Urea was used to determine the volume of alveolar epithelial lining fluid (AELF volume). Results are expressed as the ratio of solute concentration in AELF over that in plasma (A/P ratio). In Group A there were clear concentration gradients of glucose, potassium, and albumin between the AELF and plasma, as the A/P ratios of glucose, potassium, and albumin were 0.02 +/- 0.006 (mean +/- SEM), 3.2 +/- 0.34, and 0.04 +/- 0.008, respectively. In Group B the A/P ratios of glucose (0.21 +/- 0.02, p less than 0.001) and albumin (0.17 +/- 0.02, p less than 0.001) were significantly increased but that of potassium remained unchanged (2.9 +/- 0.2). The A/P ratios of these various solutes were independent of chest x-ray typing. The albumin but not the glucose A/P ratio was correlated with the percentage of lymphocytes recovered from BAL (p less than 0.02); however, there was no correlation between the albumin A/P ratio and the CD4+/CD8+ T lymphocyte ratio. In group C there was a striking contrast between the albumin A/P ratio, which was normal, and the glucose A/P ratio, which was clearly elevated despite a normal lymphocyte count.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose, K+, and albumin concentrations in the alveolar milieu of normal humans and pulmonary sarcoidosis patients. 202 21

Sodium polystyrene sulfonate (SPSS) is commonly administered for the acute and chronic treatment of hyperkalemia. Its oral intake is complicated by poor compliance due to multifaceted reasons. We therefore analyzed a method of reducing potassium (K) in formula by pretreatment with SPSS. If effective, this would bypass complications of enterally administered SPSS and provide low-K formula. Thirteen formulas and nutritional supplements were pretreated with SPSS to determine if one could bind K and provide formulas with decreased K contents. Using an SPSS concentration of 1 g/l mEq K in the formula, 62 +/- 2.6% (P less than 0.01, mean +/- SEM) of the K was removed in 30 min, while the sodium (Na) concentration was increased by 234 +/- 37% (P less than 0.01). Analysis suggests that the disproportionate increase in Na is due to exchange for calcium (Ca) and magnesium (Mg), interaction with proteins, and Na suspended with SPSS in the formula. Thus, SPSS pretreatment of formula is an effective method of making low-K formula, but the increase in Na exceeds the K reduction. Attention to possible complications of increased Na intake as well as decreased Ca and Mg intake is warranted.
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PMID:Pretreatment of formula with sodium polystyrene sulfonate to reduce dietary potassium intake. 202 33


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