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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of insulin on the renal handling of sodium, potassium, calcium, and phosphate were studied in man while maintaining the blood glucose concentration at the fasting level by negative feedback servocontrol of a variable glucose infusion. In studies on six water-loaded normal subjects in a steady state of water diuresis, insulin was administered i.v. to raise the plasma insulin concentration to between 98 and 193 muU/ml and infused at a constant rate of 2 mU/kg body weight per min over a total period of 120 min. The blood glucose concentration was not significantly altered, and there was no change in the filtered load of glucose; glomerular filtration rate (CIN) and renal plasma flow (CPAH) were unchanged. Urinary sodium excretion (UNaV) decreased from 401 plus or minus 46 (SEM) to 213 plus or minus 18 mueq/min during insulin administration, the change becoming significant (P smaller than 0.02) within the 30-60 min collection period. Free water clearance (CH2O) increased from 10.6 plus or minus 0.6 to 13 plus or minus 0.5 ml/min (P smaller than 0.025); osmolar clearance decreased and urine flow was unchanged. There was no change in plasma aldosterone concentration, which was low throughout the studies, and a slight reduction was observed in plasma glucagon concentration. Urinary potassium (UKV) and phosphate (UPV) excretion were also both decreased during insulin administration; UKV decreased from 66 plus or minus 9 to 21 plus or minus 1 mueq/min (P smaller than 0.005), and tupv decreased from 504 plus or minus 93 to 230 plus or minus 43 mug/min (P smaller than 0.01). The change in UKV was associated with a significant reduction in plasma potassium concentration. There was also a statistically significant but small reduction in plasma phosphate concentration which was not considered sufficient alone to account for the large reduction in UPV. Urinary calcium excretion (UCaV) increased from 126 plus or minus 24 to 200 plus or minus 17 mug/min (P smaller than 0.01). These studies demonstrate a reduction in UNaV associated with insulin administration that occurs in the absence of changes in the filtered load of glucose, glomerular filtration rate, renal blood flow, and plasma aldosterone concentration. The effect of insulin on CH2O suggests that insulin's effect on sodium excretion is due to enhancement of sodium reabsorption in the diluting segment of the distal nephron.
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PMID:The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man. 112 Jul 86

In order to evaluate the possible role of vasoactive hormones in the mechanism of exaggerated sodium loss due to reduced renal mass we measured plasma concentration of atrial natriuretic peptide (ANP), aldosterone, plasma renin activity (PRA), plasma noradrenaline, and dopamine, in 12 children with advanced chronic renal failure (mean CIn 17.8 +/- 2.6, mean +/- SEM, CPAH 93.5 +/- 17 ml/min per 1.73 m2, FENa 7.0 +/- 0.95%). No patient had clinical signs of volume overload. Plasma concentrations of ANP were not significantly different from those of healthy age-matched controls (29.2 +/- 7.2 vs 23.2 +/- 3.1 fmol/ml) and did not correlate with urinary sodium excretion. Plasma concentrations of aldosterone, PRA and noradrenaline, were also within the physiological range, while plasma dopamine levels were elevated (260 +/- 36 vs 98 +/- 11 pg/ml, less than 0.001). Our data do not support the notion that ANP or the renin-aldosterone axis play a major role in the adaptation of remaining nephrons to maintain long-term sodium balance in normotensive children with chronic renal failure.
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PMID:Atrial natriuretic peptide and sodium homeostasis in chronic renal failure. 253 71

1. We studied the relationship between changes in glomerular filtration rate (GFR) determined as inulin clearance (CIn), and changes in renal blood flow (RBF), determined as p-aminohippurate clearance (CPAH), after the ingestion of a large (1.35 +/- SEM 0.04 g/kg, n = 9), moderate (1.08 +/- 0.03 g/kg, n = 10) or mild (0.55 +/- 0.02 g/kg, n = 8) protein load given as a meat meal. Control subjects (n = 10) received a carbohydrate meal. 2. CIn and CPAH increased after a protein meal. Two hours after eating the test meal, GFR levels were (mean +/- SEM) 160.0 +/- 13.8 (P less than 0.05), 141 +/- 7.69 and 127.8 +/- 9.07 ml/min in the groups that received a large, moderate and mild protein load, respectively. Peak CIn values after the meal were 211.6 +/- SEM 14.92 (P less than 0.001), 177.5 +/- 10.88 (P less than 0.01) and 129.0 +/- 8.72 ml/min after a large, moderate and mild protein load, respectively. 3. At peak GFR levels after the meal, filtration fraction (FF) (CIn X 100/CPAH) increased significantly (P less than 0.02) with the large and with the moderate protein load, but not with the mild protein load. 4. There was a significant (P less than 0.001) positive relationship between increments of FF and increments of CIn, but not CPAH, whether the values were expressed as post-meal/pre-meal ratios or as absolute changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship between glomerular filtration rate and renal blood flow at different levels of protein-induced hyperfiltration in man. 333 49

Uraemia was induced in pigs by ligation of the renal vascular pedicle, and uraemic plasma was analysed for glucagon and glucagon-related peptides. A preponderance of large molecular weight (Mr) components comprising glicentin and moieties of slightly lower Mr was found, accounting for 73 +/- 3% (mean +/- SEM, n = 12) of the total plasma glucagon-like immunoreactivity. Comparisons with glicentin 1-61, produced by controlled, stepwise, consecutive digestion of purified natural glicentin with carboxypeptidases (carboxypeptidase A followed by carboxypeptidase B, and again by carboxypeptidase A and B), gel filtration, ion exchange chromatography, reverse phase HPLC and radioimmunoassays for the glucagon sequences 6-15 and 19-29 and for the glicentin sequence 12-30 all indicate that glicentin 1-61 constitutes approximately 57% of the large Mr glucagon-related peptides found in uraemia in pigs.
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PMID:Glicentin 1-61 probably represents a major fraction of glucagon-related peptides in plasma of anaesthetized uraemic pigs. 374 26

Simultaneous renal clearances of inulin (CIN), p-aminohippurate (CPAH), and creatinine (CCR) were measured in hydrated mares (6 ponies and 2 horses). The CIN and CPAH were determined during steady-state infusion at 3 different infusion rates. A 6-fold change in plasma IN concentration did not produce alteration in CIN, nor was there a difference between the ponies and horses (P greater than 0.2). The overall average (mean +/- SEM) was 190.6 +/- 5.89 ml . min-1 . 100 kg of body weight-1. There was no difference noted between simultaneous CIN and CPAH. Clearance of PAH remained essentially constant during the change in plasma PAH from 0.33 mg/dl to 5.27 mg/dl. The extraction ratio of PAH for the nonanesthetized pony was 0.966. Effective renal plasma flow (CPAH) of the pony exceeded that of the horse.
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PMID:Renal function of the pony and the horse. 707 82

Experimental and clinical studies have demonstrated a positive relationship between hyperlipidemia and rate of progression of renal disease, suggesting that lipids can induce or aggravate glomerular injury mainly by interacting with mesangial cells. Nevertheless, recently has been demonstrated that increased cholesterol levels can also induce endothelial cell dysfunction. Thus, since endothelium is known to play a major role in modulating the vascular tone, we have tested the possibility that hypercholesterolemia impairs the renal hemodynamics in patients with active nephrotic syndrome and elevated serum cholesterol levels. In this single-blind, nonrandom study, 12 patients were treated with pravastatin (group T, treated, n = 12) and 8 with placebo (group C, controls, n = 8). The controls were studied after the pravastatin group had been completed. Before starting the treatment the patients underwent basal determinations including routine laboratory investigations and PAH and inulin clearances. The same determinations were repeated after 48 h, and 6 and 12 weeks from the beginning of the treatment. The study at 48 h was performed to see if pravastatin had a direct, cholesterol-independent effect on renal function. The following basal results were reported (mean +/- SEM; group T vs. group C): serum cholesterol (mmol/l) 9.7 +/- 0.4 vs. 9.1 +/- 0.3 (NS); proteinuria (g/24 h): 6.2 +/- 0.2 vs. 7.0 +/- 0.7 (NS); PAH clearance (ml/min): 353 +/- 21 vs. 385 +/- 31 (NS); inulin clearance (ml/min): 62.5 +/- 7.7 vs. 67 +/- 9.3 (NS). After 48 h, no changes were observed in both groups. Subsequently, in group T, the following percentage changes of basal levels were observed: serum cholesterol -21.4 +/- 3.2% at 6 weeks (p < 0.05) and -34.9 +/- 3.2% at 12 weeks (p < 0.01); inulin clearance +3 +/- 3.7% at 6 weeks (NS) and +9.3 +/- 2.9% at 12 weeks (p < 0.05); PAH clearance +7 +/- 3.1% at 6 weeks (p < 0.05) and +21.2 +/- 5.5% at 12 weeks (p < 0.01). By contrast, no significant changes of these parameters occurred in group C at any time, so that the percent changes of baseline values of CPAH were significantly greater in group T (at 6 weeks: p < 0.05; at 12 weeks p < 0.005). These results indicate that the reduction of cholesterol is associated with a significant increase in renal plasma flow, thus, suggesting that hypercholesterolemia may actually impair the renal hemodynamics. We speculate that this effect may contribute to increase the risk of ischemic acute renal failure in nephrotic patients and, along with changes induced in the mesangium by other mechanisms, to contribute to the progression of renal disease.
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PMID:Effects of hypercholesterolemia of renal hemodynamics: study in patients with nephrotic syndrome. 883 3