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Biomedical subjects

A Helber

Publications and source records attributed to A Helber.

At least 37 records · Page 2Linked to original sources
PubMed1980

Sodium-potassium-dependent ATPase activity in erythrocyte ghosts of patients with primary and secondary hypertension.

1. We have investigated the function of the Na+-K+ pump in the erythrocytes of patients with various types of hypertension by measuring the activity of ouabain-sensitive Na+-K+-dependent ATPase and ouabain-insensitive ATPase in the erythrocyte ghosts of these patients. 2. Mean Na+-K+-ATPase activity was increased threefold in six patients with Cushing's syndrome and hypertension (0.985 +/- SD 0.288 mumol of phosphate h-1 mg-1) compared with that in 49 control subjects (0.334 +/- 0.147 mumol of phosphate h-1 mg-1) (P < 0.0025), but not in four patients with primary aldosteronism (0.278 +/- 0.108 mumol of phosphate h-1 mg-1). 3. Na+-K+-ATPase activity slightly exceeded the control range in 57 patients with primary hypertension (0.410 +/- 0.245 mumol of phosphate h-1 mg-1; P < 0.025) and in 12 patients with renal hypertension (0.475 +/- 0.250 mumol of phosphate h-1 mg-1) (P < 0.025). 4. There was no difference in ouabain-insensitive ATPase between the controls and the different types of hypertension. 5. The data support the hypothesis of an activation of the Na+ pump in patients with glucocorticoid excess. This helps to explain previous observations of a redistribution of sodium and water to the extracellular compartment in experimental glucocorticoid-induced hypertension.

Adult↗
PubMed1980

Hypercholesterolaemia and hypertriglyceridaemia in patients with analgesic nephropathy.

Patients with analgesic nephropathy are reported to have a higher risk of atherosclerosis. One possible reason for this is a high incidence of hyperlipaemia in patients with analgesic nephropathy. In a retrospective study, serum cholesterol and serum triglyceride concentrations of patients with analgesic nephropathy and moderately restricted renal function were significantly higher compared to a control group with other renal diseases of similar age and degree of renal insufficiency. Hyperlipaemia in analgesic nephropathy is not explained by end-stage renal failure on one side or protein loss as in nephrotic syndrome on the other side. Some possible mechanisms for hyperlipaemia in analgesic nephropathy are discussed.

Adult↗
PubMed1980

Regulation of serum-progesterone in patients with essential hypertension.

Increased levels of progesterone in serum have been reported in male patients with essential hypertension (EH). We, therefore, investigated serum progesterone levels in relation to excretion of aldosterone after 4 days of low Na+ intake and 6 days following high Na+ diets, in 11 normotensive controls, 22 male patients with EH and 8 male patients with hypertension of renal origin (RH). In the group of normotensive controls, the concentration of progesterone in serum averaged 228 +/- 90 and 186 +/- 93 (mean +/- SD) pg/ml during low and high regimens of Na+ intake, respectively, despite a fall in the excretion of aldosterone from 22.8 +/- 9 to 1.8 +/- 1.4 microgram/24 h. Similarly, in patients with EH, serum progesterone remained unchanged during either low or high Na+ intake regimens: 197 +/- 73 and 219 +/- 83 pg/ml, respectively. In patients with RH, serum progesterone tended to be lower during both low and high Na+ diets: 167 +/- 61 and 185 +/- 72 pg/ml, respectively. In 5 normotensive controls, diurnal variations of progesterone and cortisol were significantly correlated (r = 0.726, p < 0.005). The results of the present study suggest, that progesterone is not involved in metabolism of Na+, either in normotensive or hypertensive male subjects. Correlation between circadian variations of progesterone and cortisol suggests, that progesterone levels are modified by ACTH secretion.

Adult↗
PubMed1979

Acid- and cryoactivation of renin in human plasma.

Inactive renin in normal human plasma was activated in vitro either by cryoactivation (incubation at 0 degrees C/-5 degrees C up to 3 months) or acid-activation (dialysis to pH 3.0 for 48 h followed by diaylsis to pH 7.5). Plasma-renin-concentration was similar after either activation procedure (96 +/- 50 microU/ml vs 100 +/- 43 microU/ml). There was no further significant acid-activable renin after cryoactivation. These data suggest that conversion of inactive to active renin by optimized procedures is complete. The term "total renin" for activation results under these conditions seems to be valid.

Dialysis↗
PubMed1979

[The saralasin test in the diagnosis of hypertension (author's transl)].

The saralasin test was performed in 68 hypertensives. A clear-cut dependence of the test results on initial plasma-renin concentration and particular sodium balance was demonstrated. Because of this dependence the saralasin test should be performed only under constant conditions. A mild stimulation of the renin-angiotension system by salt restriction to a mean sodium excretion of 50 mmol daily and 80 mg furosemide by mouth 12 hours before the test seems best. In this way essential and renovascular hypertension could be distinguished with considerable reliability (P less than 0.001). Among patients with essential hypertension one could clearly separate those with high plasma-renin concentration from those with a normal or low one. Among patients with renovascular hypertension those with haemodynamically significant renal artery stenosis could with high probability be distinguished from those with non-effective stenosis. A positive saralasin test without testing the function of the normal contralateral kidney does not provide an indication for operation.

Adult↗
PubMed1979

[Sodium-potassium-adenosine triphosphatase-activity in red cell ghosts of patients with essential hypertension (author's transl)].

Increased sodium concentration and high influx of Na22 are reported in erythrocytes of patients with essential hypertension. It was speculated, that these findings are due to a disturbed transport for sodium across red cell membranes. We found a significantly increased activity of the ouabainsensitive Na-K-ATP'ase in red cell ghosts of 27 patients with essential hypertension compaired with 32 normotensive controls. There existed no difference in Mg-ATP'ase-activity between the two groups. These findings suggest an increased activity of the Na-pump in red cell membranes of patients with essential hypertension.

Erythrocyte Membrane↗
PubMed1979

[Improved interpretation of renal-vein-renin-ratio by simultaneous determination of renal 131I-hippuric-acid-clearance-ratio in patients with renovascular hypertension (author's transl)].

In patients with unilateral vascular kidney disease and hypertension, ratio of renal-vein-renin was compared with 131I-Hippuric-acid clearance and change in blood pressure during Saralasininfusion. The ratio of renal-vein-renin was positively correlated with the ratio in renal plasma flow between the kidneys in all patients studied. The ratio of renins therefore is a result of two factors: The difference in renin secretion and the difference in blood flow in the two kidneys. In patients with angiotensin independent hypertension renin-ratios up to 2.0 were found without relevance to elevated blood pressure. When the difference in renal blood flow between both kidneys was small, even a slight difference in renal vein renin indicated hypertension related to increased renin secretion. Renin-ratios in the critical range between 1.5 and 2.5 should only be interpreted in respect to a similar ratio in renal blood flow.

Adult↗
PubMed1978

[Hypertension and multiple renal arteries. Comparative studies on the frequency of multiple renal arteries in hypertensive patients and normotensives].

The frequency of multiple renal arteries in 394 aortographies was found to be 29.2%. The results were then grouped according to the indication for the investigation and according to the recorded blood pressure readings into a hypertensive and a normotensive group. Comparison of these two groups showed no significant difference in the frequency of multiple renal arteries. There were also no significant differences comparing double and multiple arterial supply of one kidney or one-sided or double occurrence of multiple renal arteries.

Aortography↗
PubMed1978

Pharmacokinetic and pharmacodynamic studies of infusions with [Sar 1, Val5, Ala8] angiotensin II (saralasin).

A modification of the infusion test with saralasin, an angiotensin II antagonist for the detection of renin-dependent high blood pressure was studied in renal hypertensive rats and in normotensive and hypertensive subjects. Infusion was started at a rate of 0.01 microgram/kg x min saralasin and the dose was increased ten-fold at 15 min intervals. A significant fall of diastolic blood pressure was observed at the dose of 0.1 microgram/kg x min in renal hypertensive rats, in healthy subjects treated with diuretics, and in patients with renovascular hypertension (saralasin responders). Plasma concentrations of angiotensin I, angiotensin II and of saralasin as well as plasma renin activity were measured. At the lowest infusion rate of 0.01 microgram/kg x min, saralasin plasma levels were 40-fold higher than plasma angiotensin II levels. The decrease in arterial blood pressure occurred at lower doses of saralasin than the increase of plasma renin due to inhibition of feedback on the renin secreting cells. It is concluded that if the saralasin test is performed by a stepwise increase of the infusion rate, potentially dangerous complications such as hypo- or hypertensive reactions can be avoided. The diagnostic reliability is improved by such a procedure since false positive and false negative responses may be prevented. The pressor effect of saralasin in non-renin dependent patients is an advantage since it causes a more marked difference of blood pressure change between saralasin responders and non-responders.

Angiotensin I↗
PubMed1976

[The effect of clonidine on renin-release (author's transl)].

In patients with primary hypertension, intravenous administration of 150 mug Clonidin caused a decrease in arterial pressure, renin activity, RPF, GFR and electrolyte excretion. Activation of intracerebral adrenergic alpha-receptors and diminished sympathetic outflow seem to be responsible for the decrease of renin release.

Adult↗