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Biomedical subjects

J Manitius

Publications and source records attributed to J Manitius.

51 records · Page 3Linked to original sources
PubMed1986

An investigation into the alpha-adrenoceptor mediating renal nerve-induced calcium reabsorption by the rat kidney.

An investigation was undertaken in pentobarbitone-anaesthetized rats to determine the sub-type of alpha-adrenoceptor responsible for the renal nerve-induced increases in the reabsorption of calcium and sodium by the tubules of the kidney. Stimulation of the renal nerves at low frequencies (0.8-1.5 Hz) did not change either renal blood flow or glomerular filtration rate but significantly reduced urine flow by 32%, calcium excretion by 36% and absolute and fractional sodium excretions by 36% and 22%, respectively. In the presence of the selective alpha 1-adrenoceptor antagonist prazosin, renal nerve stimulation (2-3 Hz) caused a significant reduction in renal blood flow of 7% but did not change either glomerular filtration rate, urine flow, calcium excretion or absolute and fractional sodium excretions. During administration of the selective alpha 1-adrenoceptor antagonist, idazoxan, renal nerve stimulation (1.0-1.5 Hz) significantly reduced renal blood flow by 4% and glomerular filtration rate by 7%; at the same time there were significant falls in urine flow of 43%, calcium excretion of 43% and absolute and fractional sodium excretions of 41% and 37%, respectively. These results show that low frequency renal nerve stimulation causes an anticalciuresis, independent of renal haemodynamics, which represents an increase in tubular reabsorption of calcium. This effect was blocked by prazosin but not idazoxan which is consistent with the mediation of alpha 1-adrenoceptors. The neurally-induced antinatriuresis also appeared to be dependent on the activation of alpha 1-adrenoceptors.

Animals↗
PubMed1986

A study in the rat of the renal actions of nitrendipine and diltiazem on the adrenergic regulation of calcium and sodium reabsorption.

In pentobarbitone-anaesthetized rats, intravenous administration of diltiazem at 5 micrograms kg-1 min-1 did not change blood pressure or renal blood flow but increased glomerular filtration rate by approximately 16%, urine flow by 85%, calcium excretion by 151% and absolute and fractional sodium excretions by 100% and 69%, respectively. A similar pattern of responses was obtained in renally denervated animals, except that calcium excretion did not change statistically. Diltiazem given at 20 micrograms kg-1 min-1 into renally innervated and denervated groups of animals depressed blood pressure between 15-17 mmHg but had no effect on renal haemodynamic or tubular function. Nitrendipine administered at 0.5 microgram kg-1 min-1 to renally innervated and denervated animals significantly depressed blood pressure in intact animals by 6 mmHg and in both groups did not change renal haemodynamics but caused similar increases in urine flow of between 79-98%, calcium excretion of between 87 and 125%, absolute sodium excretion of between 108 and 140% and fractional sodium excretion of between 83 and 170%. Infusion of nitrendipine at 1.0 micrograms kg-1 min-1 into intact or renally denervated animals decreased blood pressure by 18-20 mmHg and increased urine flow by 84-111%, calcium excretion by 85%, absolute sodium excretion by 81-137% and fractional sodium excretion by 52-102%. Stimulation of the renal nerves at low frequencies (0.8 to 1.5 Hz) caused minimal changes in renal haemodynamics but decreased urine flow by 27%, calcium excretion by 35%, absolute and fractional sodium excretions 32% and 36%, respectively. In different groups of animals given either diltiazem at 20 pg kg- I min' or nitrendipine at 0.5 pg kg'- min' or 1.0 fg kg'- min', a similar degree of renal nerve stimulation caused an identical pattern of excretory responses of similar magnitude to those obtained in the absence of drug. 4 The calciuretic, diuretic and natriuretic activities of diltiazem and nitrendipine were not dependent on renal nerves and probably represented a direct action on the tubular reabsorptive processes of these ions. The renal nerve-induced increases in tubular calcium and sodium reabsorption indicate that these alpha-adrenoceptor-mediated responses are not dependent on the inward movement of calcium

Animals↗
PubMed1985

The effect of dietary sodium loading on the kinetics of sodium excretion and blood pressure regulation in essential hypertensive men.

The kinetics of urinary sodium excretion defined as the rate of urinary sodium excretion during five-days oral sodium loading was investigated in 12 male patients with essential hypertension. The change in blood pressure under oral 200 mmol/24 h NaCl intake correlated inversely with the rate of urinary sodium excretion (r = -0.60, p less than 0.05), but did not significantly depend on the change in the absolute amount of excreted sodium. The rate of sodium excretion correlated directly with preload glomerular filtration rate (GFR) (r = 0.63, p less than 0.05), effective renal plasma flow (ERPF) (r = 0.78, p less than 0.01) and inversely with renal vascular resistance (RVR) (r = 0.67, p less than 0.01). The fall of renal plasma flow at moderate increment in the filtration fraction under sodium loading correlated directly with the rate of urinary sodium excretion (r = 0.73, p less than 0.01). The results suggest that: 1) the rate of sodium excretion is a more important factor in blood pressure regulation than the ability of the kidney to excrete the entire sodium load; 2) renal haemodynamics plays an indirect role in blood pressure regulation.

Adult↗
PubMedDate not supplied

Hypertensive nephropathy - an increasing clinical problem.

Arterial hypertension-related renal damage is an increasingly common problem recently, because approximately 25% of patients currently treated with dialysis were hypertensive before renal replacement therapy was started. Hypertension is also known as a metabolic disease, while carbohydrate, purine and lipid disturbances are the features of this syndrome. On the other hand, the progression of renal disease depends on the extent of tubulointerstitial injury. For this reason, we undertook a study to evaluate the relationship between excretion of the markers of tubular damage (NAG) and some parameters of carbohydrate, purine and lipid metabolism in untreated essential hypertension. Both healthy volunteers (n = 15) aged 32. 6+/-7.8 and essential hypertensives (n = 25) aged 37.24+/-11.39 underwent the same tests. These tests were performed at 2-day intervals: intravenous glucose tolerance test with 0.5 g/kg b.w. as 40% glucose solution and oral fructose load test with 1.0 g/kg b.w. Area under glucose curve (GA) and serum uric acid post-fructose (PUAA) were calculated. Fasting: insulin, total cholesterol and LDL, triglycerides, free fatty acids (FFA) and urine excretion of NAG, albumin were determined. Glomerular filtration rate was estimated as creatinine clearance. Hypertensives showed statistically higher BMI (p<0.007), NAG (p<0.02), total cholesterol (p<0.01), LDL (p<0.007), FFA (p<0.007), insulin (p<0.01), PGA (p<0.01) and PUAA (p<0.03). NAG excretion correlated positively with WHR (r = 0.40), MAP (r = 0.47) and PUAA (r = 0.47) in hypertensives only. We presume that tubular injury at an early stage of renal damage in patients with essential hypertension could be a part of metabolic syndrome X.

Acetylglucosaminidase↗
PubMedDate not supplied

The relationship between insulin, glucose and serum uric acid and their contribution to the progression of renal damage in patients with primary glomerulonephritis.

It is known that some metabolic disturbances may modify the progression of renal disease including primary glomerulonephritis, but the role of purines in this process is still unknown. To investigate this, 13 untreated patients with primary glomerulonephritis were followed up for a mean of 17.6 months to analyze the changes in proteinuria and glomerular filtration rate. On entering the study, each patient was given an oral glucose tolerance test and an oral fructose load test. The areas under the glucose (PGA), insulin (PIA) and uric acid (PUAA, post-fructose) curves were calculated. Glomerulonephritic patients were found to have a statistically higher response to fructose than controls (782 +/- 219 vs 518 +/- 154, P < 0.005). Multiple regression analysis showed that PGA, PIA and PUAA were independently related to changes in proteinuria and glomerular filtration rate during the natural course of the disease. This preliminary study suggests that purine metabolism may modulate the progression of renal disease in proteinuric patients.

Administration, Oral↗
PubMedDate not supplied

[Evaluation of the effect of d,l-carnitine on lipid metabolism of patients after prolonged dialysis].

An effect of carnitine (Bicarnesine) on lipid metabolism in 14 patients treated with prolonged dialyses has been analysed. Carnitine has been administered orally in the dose of 30 mg/kg b.w. three times per week for 8 weeks and every day for the next 8 weeks. Carnitine, total triglycerides, total and HDL cholesterol, and glucose have been determined in serum. Blood lipoproteins have been assayed with electrophoresis in agarose gel. Total and free carnitine concentrations increased by 3.5 times within 16 weeks. Triglycerides level did not change significantly in all examined patients except a group of 6 patients with baseline hypertriglyceridemia, in which a significant but transient decrease in triglycerides level has been noted after 4 weeks of treatment. At the same time, normalization of blood lipoproteins has been observed. In the eighth week, a transient decrease in HDL-cholesterol has been noted. Result suggest, that carnitine despite an increase in total and free carnitine blood levels did not regulate lipid metabolism disorders. Moreover, its administration to patients treated with prolonged dialyses seems to be unfavourable due to several adverse reactions.

Adult↗