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Biomedical subjects

G Bönner

Publications and source records attributed to G Bönner.

At least 91 records · Page 5Linked to original sources
PubMed1981

Measurement of kallikrein activity in urine of rats and man using a chromogenic tripeptide substrate. Validation of the amidolytic assay by means of bradykinin radioimmunoassay.

Urinary kallikrein activity in rats and man was measured by an amidolytic assay using the chromogenic tripeptide D-valyl-leucyl-arginine-p-nitroanilide (S 2266). The sensitivity of the assay permits the measurement of 3.5 to 250 mKU of purified porcine pancreatic kallikrein. The intraassay coefficient of variation was 1.6 +/- 0.3% and the interassay coefficient of variation 7.4 +/- 0.9%. No changes in kallikrein activity was found in urine samples kept for 7 days at 4 degrees C for 14 months at -20 degrees C. Repeated freezing and thawing reduced kallikrein activity. Kallikrein activity of the same urine samples was also estimated by means of a bradykinin radioimmunoassay, which determines the kinins released during incubation of urine with partially purified dog kininogen (kininogenase activity). The urinary kallikrein activity assayed by means of these two methods showed a high correlation with coefficients of r = 0.9134 for rat urine (p less than 0.0001) and r = 0.8002 for human urine (p less than 0.001).

Amides↗
PubMed1981

The renal kallikrein-kinin system in Brattleboro rats with hereditary hypothalamic diabetes insipidus. Missing relationship between antidiuretic hormone and the renal kallikrein-kinin system.

The activity of the renal kallikrein-kinin system was investigated in male Brattleboro rats homozygous for hypothalamic diabetes insipidus (DI); Long-Evans rats (LE) were taken as controls. In the rats with DI, urinary kallikrein excretion was lower (P less than 0.05) than in the LE rats. However, when related to total renal mass or to body weight, there was no difference between the two strains. Kallikrein activity in the renal cortex was similar in the Brattleboro and the LE rats. Antidiuretic hormone (vasopressin tannate) in a dose of 100 mU given once daily for 3 days had no effect on urinary kallikrein excretion in either of the strains. Water deprivation for 24 h resulted, also in both strains, in a similar reduction in urinary kallikrein excretion. The renal kallikrein-kinin system of LE rats and that of DI rats does not principally differ in basic activity, nor in response to the administration of vasopressin, nor to water deprivation.

Angiotensin II↗
PubMed1980

Ureteral contractions induced by rat urine in vitro: probable involvement of renal kallikrein.

Rat urine, even at a 1:10 final dilution in Tyrode's solution, stimulates contraction of the ureteral musculature in vitro. This effect can be ascribed to the presence of kallikrein or a kallikrein-like enzyme in urine. Isometric contractions of ureters were prevented by previous addition of aprotinin to the organ bath. Urine also lost its activity after inactivation of enzymes by heat or acid treatment.

Animals↗
PubMed1980

Increased kallikrein excretion in spontaneously hypertensive rats and its inhibition by 6-hydroxydopamine.

Urinary kallikrein excretion was studied in young, stroke-prone, spontaneously hypertensive rats (spSHR). Seven-week-old spSHR were found to excrete more kallikrein into the urine than normotensive Wistar Kyoto control rats (WKR). "Chemical sympathectomy", induced by 6-hydroxydopamine (6-OHDA) immediately after birth, resulted in normotensive blood-pressure levels and in a reduction of kallikrein in spSHR. In normotensive WKR, blood pressure and urinary kallikrein excretion were only slightly diminished by 6-OHDA. The results suggest a relationship between sympathetic activity and kallikrein excretion, being especially pronounced in spSHR, which have an elevated sympathetic activity.

Animals↗
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

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

[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↗
PubMed1979

A novel orally active converting-enzyme inhibitor YS 980: effects on blood pressure in spontaneously hypertensive rats.

1. The effects of long-term treatment with the angiotensin I converting-enzyme inhibitor YS 980 were examined in stroke-prone spontaneously hypertensive (sp-SH) rats. Development of hypertension was markedly blunted in the YS 980-treated animals. 2. Effective converting-enzyme inhibition was confirmed by significant increases in plasma angiotensin I (ANG I) and plasma renin concentration, inhibition of the pressor responses to intravenous ANG I and potentiation of the depressor responses to intravenous bradykinin. 3. Urinary free aldosterone excretion was decreased but no changes in urinary sodium and potassium excretion were observed. 4. The pressor responses to intravenous leucine-enkephalin were reduced. 5. The pressor responses to injection of ANG I and bradykinin into the lateral brain ventricle were unaltered. 6. We conclude that the antihypertensive action of YS 980 in sp-SH rats cannot be explained by the inhibition of the plasma renin-angiotensin system alone. Effects on other peptide systems must be considered.

3-Mercaptopropionic Acid↗
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↗