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Biomedical subjects

G Bönner

Publications and source records attributed to G Bönner.

At least 73 records · Page 4Linked to original sources
PubMed1985

Direct hypotensive action of intravascular bradykinin in man.

To investigate the cardiovascular effects of bradykinin (BK), the peptide was injected into 6 normotensive volunteers in the supine position. BK was given intravenously as a bolus in a dose of 0.001-7.5 microgram BK/kg body weight. Intraarterial blood pressure decreased dose related in a range of 0.25-1.0 microgram BK/kg body weight. Pretreatment with 2 X 50 mg indomethacin or 80 mg propranolol as well as changes in oral salt intake (from 10 to 300 mmol Na+/day) had no effect on the blood pressure-lowering effect of BK. Captopril (25 mg) potentiated the effect of BK 20- to 50-fold. In primary hyperaldosteronism, renal kallikrein activity and absolute vascular reaction to BK was increased. The results showed clearly that in man, similarly as in rats, BK lowers blood pressure by direct vasodilation and acts independently of prostaglandins, beta-receptors or salt intake.

Blood Pressure↗
PubMed1985

Haemorheology in adolescent hypertensives.

Fifty-three untreated borderline hypertensives and 73 normotensives were randomly selected from 1342 adolescents (age range 23-27 years) who were examined in 1975, 1976 and 1980 in an epidemiological study. Blood pressure was 127.2 +/- 1.0/79.0 +/- 0.8 mmHg in normotensives and 147.2 +/- 1.6/93.7 +/- 1.1 mmHg in hypertensives (P < 0.001). Erythrocyte deformability was measured with a positive pressure filter system (pore diameter 5 microns) at 37 degrees C. Erythrocyte deformability was significantly increased in hypertensives with a value of 1.77 +/- 0.05, compared with 1.64 +/- 0.04 in normotensives (P < 0.05). No difference in apparent whole blood viscosity, haematocrit and plasma fibrinogen was measurable between the groups. Although plasma noradrenaline and adrenaline concentration at rest and after 3 min standing were not different, excretion of urinary catecholamines was significantly elevated in hypertensives with 155.0 +/- 3.3 micrograms/24 h (normotensives: 100.7 +/- 5.3 micrograms/24 h; P < 0.001).

Adolescent↗
PubMed1984

Cardiovascular and adrenal sensitivity to angiotensin II in essential hypertension.

Regulation of aldosterone secretion by sodium chloride is impaired in a group of essential hypertensives: high-salt diet fails to suppress aldosterone in these patients despite low renin values. The mechanism of this impaired regulation of aldosterone has not been clarified so far. We tested the sensitivity of aldosterone secretion and blood pressure to A II in 20 normotensive controls (aged 20-60, MAP 92 +/- 3 mm Hg), in ten normotensives with one or two parents with hypertension, and in 21 patients with essential hypertension (aged 17-65, MAP 119 +/- 4 mm Hg). After a period of 6 days on high-salt intake (300-320 mEq Na+/day), A II (0.1, 0.5, 1.0 and 2.0 ng/kg/min) was infused, each concentration for 30 min. According to aldosterone excretion during sodium loading, patients were divided into group A with complete suppression (n = 12, aldosterone excretion 3.6 +/- 0.4 microgram/day) and in group B with insufficient suppression (n = 9, aldosterone excretion 15.5 +/- 2.3 micrograms/day). Despite similarly low plasma renins, rise of serum aldosterone levels during A II infusion was significantly higher in group B patients than in group A patients and normotensive controls. Rise in mean arterial blood pressure, however, brought about by graded A II infusion was similar in both groups of hypertensives and in normotensive controls. The results demonstrate an increased adrenal sensitivity to A II in a subgroup of essential hypertensives only. A similar adrenal hypersensitivity to A II found by others in patients with hyperaldosteronism due to adrenal hyperplasia supports the hypothesis that the same mechanism underlies both disorders.

Adolescent↗
PubMed1984

The influence of isotonic saline administration on the urinary excretion of kallikrein in rats.

Acute saline loading is known to increase kallikrein excretion. To clarify whether this is a specific stimulatory effect or rather a non-specific wash-out, pentobarbital anesthetized rats were loaded thrice (5 min infusions) at 40 min intervals with a volume of 150 mM NaCl equal to 5% of their body wt. The effect of such a load on the central venous pressure was studied in a separate group of rats. Control animals did not receive the infusions. Kallikrein excretion (amidolytic assay) increased with the first, but decreased with the subsequent saline administrations. The rise observed after the first load lost significance when kallikrein excretion was related to that of creatinine. The reduction observed after the second and third infusions remained significant even when expressed per mg of creatinine. Thus, saline load induced kallikrein "stimulation" is due to a non-specific wash-out. Similar transient enhancements of central venous pressure were observed after each of the three loads. This, together with the unchanged creatinine excretion (except for the rise seen after the first load) indicate that the lack of kallikrein stimulation after the second and third loads was not due to the appearance of heart failure. Saline loaded rats had a renal kallikrein activity at the end of the experiment which did not differ from that of controls. Plasma aldosterone concentration was reduced in saline infused rats, and it correlated with the kallikrein excretion when both, NaCl loaded and control rats, were taken into account.

Animals↗
PubMed1984

The renal kallikrein-kinin system in spontaneously hypertensive rats.

In male spontaneously hypertensive rats (SHRSP) of the stroke prone strain (Okamoto) and in normotensive Wistar-Kyoto rats (WKY) urinary kallikrein excretion was investigated at different age and at drug-induced diuresis. In rats of both strains from 7th till 19th week of age urinary kallikrein excretion increased with age. In SHRSP of 7th till 11th week of age kallikrein excretion was higher than in WKY rats, while it was lower in the 48-week-old SHRSP. No correlation was found between urinary kallikrein excretion and systolic blood pressure. In SHRSP and WKY rats a similar daily rhythm of kallikrein excretion in urine was found being high in the early morning and low in the afternoon. Kallikrein excretion correlated significantly with urine volume. The loop diuretic bumetanide (4 and 40 mg/kg) induced diuresis and natriuresis in both strains, however more marked in the WKY rats than in the SHRSP. Urinary kallikrein excretion, however, showed in both strains the same biphasic course with a short lasting increase and a secondary decrease. Thus, in the average urinary kallikrein excretion was not effected by the drug. Prolonged treatment with furosemide over 5 days (125 mg/kg) resulted in an increase in kallikrein excretion in urine, more pronounced in the WKY rats than in the SHRSP. The observed results suggest that renal kallikrein-kinin system is not involved in the development of spontaneous hypertension as a pathogenetic factor, but rather is influenced by other factors like hormone interactions, i.e. mineralocorticoids and catecholamines, as well as renal function and acute changes in urine flow.

Angiotensin II↗
PubMed1984

Steroid induced changes of the renal kallikrein-kinin system in rats.

In male Sprague-Dawley rats the influence of salt loading (1% NaCl), deoxycorticosterone acetate (2 X 15 mg/kg/day resp. 250 mg/kg sc), corticosterone (2 X 20 mg/kg/day sc) and adrenocorticosterone (0.5 mg/kg/day tetracosactid sc) on the activity of renal kallikrein and renal renin activity was investigated. Salt loading lowered renal kallikrein activity, deoxycorticosterone stimulated its activity and in combination they had no effect on renal kallikrein activity. The time course of kallikrein stimulation by deoxycorticosterone showed no relationship to the escape phenomenon of the kidney from the sodium retaining effect of the mineralocorticoid hormone. Reduction of endogenous mineralocorticoid hormones by adrenalectomy caused a marked reduction of urinary and renal kallikrein activity. Corticosterone suppressed the activity of the renal kallikrein-kinin system at the same time as the reduction in urinary aldosterone excretion. Adrenocorticotrophin caused the same decrease in the activity of renal kallikrein as corticosterone. Urinary aldosterone excretion, however, was significantly stimulated. Thus, the known positive correlation between kallikrein and aldosterone was missing. In all experiments the urinary excretion of kallikrein correlated highly with the kallikrein activity measured in renal cortical tissue. However, no correlation was found between kallikrein and urine volume or urinary excretion of sodium and potassium. In our experiments no relationship between the activity of the renin-angiotensin system and that of the renal kallikrein-kinin system was observed. Furthermore, no clear relationship was found between systemic blood pressure and the activity of the renal kallikrein-kinin system.

Adrenalectomy↗
PubMed1983

Effect of changes in perfusion pressure on renal and urinary kallikrein in the isolated perfused rat kidney.

Kallikrein activity in urine and in the renal cortex of the isolated rat kidney, perfused at constant pressure, decreased, while renal perfusate flow, glomerular filtration rate, excretion of sodium and of potassium and urine flow remained unchanged. Abrupt changes in perfusion pressure resulted in corresponding changes in renal perfusate flow, glomerular filtration rate, excretion of sodium and of potassium and urine flow. Urinary kallikrein increased little and transiently only, each time perfusion pressure was elevated. At the end of the experiments, a marked decrease in kallikrein activity in the renal tissue was found. From these results, it might be concluded that the excretion of kallikrein from the isolated perfused rat kidney resulted in a marked depletion of kallikrein stores in the kidney, probably due to an insufficient kallikrein synthesis.

Animals↗
PubMed1982

[Primary hyperaldosteronism: differentiation between aldosterone-producing adenoma and idiopathic adrenocortical hyperplasia (author's transl)].

The regulation of aldosterone secretion by sodium restricted and enriched diet was assessed in 21 patients with primary aldosteronism for differentiation between unilateral aldosterone-producing adenoma and adrenocortical hyperplasia causing autonomous aldosterone hypersecretion. Compared to 10 patients with idiopathic adrenocortical hyperplasia, urinary aldosterone excretion after 4 days of sodium restricted diet was significantly higher in 11 patients with established adenoma (41.3 +/- 16.3 micrograms/24 h vs 19.8 +/- 8.5 micrograms/24 h; P less than 0.005). After six days of sodium loading these differences became even more obvious (35.3 +/- 14.0 micrograms/24 h vs 12.7 +/- 3.7 micrograms/24 h; P less than 0.0005). Sodium excretion did not influence aldosterone secretion in the adenoma group. In patients with hyperplasia both parameters showed a negative correlation (r = -0.522; P less than 0.001). Differentiation without overlap between both patient groups was achieved by comparison of the quotient of aldosterone excretion and serum potassium level during sodium enriched diet.

Adenoma↗
PubMed1982

Effect of dihydralazine on the renal kallikrein-kinin system of the rat.

Dihydralazine (0.1 mg/kg), injected intravenously into male Sprague-Dawley rats, caused a decrease in mean arterial blood pressure and an increase in renal plasma flow, while urine volume remained unchanged. Dihydralazine had no effect on kallikrein excretion in the urine and on kallikrein activity in the renal cortex. No correlation was found between renal kallikrein and either renal plasma flow or mean arterial blood pressure. The excretion of kinins in the urine rose markedly after the administration of dihydralazine; no correlation between urinary kinins and urinary or renal kallikrein was observed. Dihydralazine had no influence on the kininogen content of blood-free renal cortex. The enzymatic activity of kininase II in renal cortex was not impaired by dihydralazine. It is suggested that the increased formation of kinins within the kidney could be involved in the vasodilating and blood pressure lowering effect of dihydralazine.

Animals↗
PubMed1982

Renal kallikrein activity and urinary kallikrein excretion in rats with experimental renal hypertension.

1. Rats were made hypertensive by ligating the aorta between the origins of both renal arteries. Sham-operated animals served as controls. Urinary and renal kallikrein activities, as well as plasma and renal renin activities, were measured 8 and 90 days after surgery. 2. Blood pressure was 155 +/- 6 mmHg on day 8 after aortic ligature and 142 +/- 6 mmHg on day 90; in controls pressures were 107 +/- 3 and 110 +/- 5 mmHg respectively. 3. Eight days after aortic ligature, kallikrein activity in the ischaemic kidneys was about 6.5 times, and in the non-ischaemic kidneys almost 2 times, that in controls. After 90 days the kallikrein activity was reduced to one-half of that in the controls in the ischaemic kidneys and it was normal in the contralateral. 4. The urinary kallikrein excretion of hypertensive rats was about one-third of that of the controls at both 8 and 90 days after aortic ligature. 5. The plasma renin activity in hypertensive rats was approximately seven times that in control animal 8 days after aortic ligature and did not differ from the control value after 90 days. Renin activity in the kidneys showed the same pattern as in other models of renovascular hypertension: elevation in the ischaemic kidney and reduction in the non-ischaemic one.

Animals↗
PubMed1982

Characterization of a group of essential hypertensives with impaired regulation of aldosterone.

The pattern of aldosterone excretion during high sodium intake in 100 patients with essential hypertension allowed the differentiation of two groups: in the majority of patients (group A, n = 64) aldosterone excretion was suppressed below 6 micrograms/day similar to the normotensive control group. In a second group (group B, n = 36), aldosterone remained above the control range despite forced sodium loading. In group B, serum potassium was significantly lower than in patients of group A (3.81 +/- 0.44 meq/l vs. 4.26 +/- 0.57 meq/l, p less than 0.001). The blood pressure lowering effect of spironolactone (200 mg/d) was more pronounced among patients in group B. Plasma renin values tended to be lower in group B compared to patients with suppressed aldosterone. Infusion of Angiotensin II (0.1 - 2 micrograms/kg/min) led to a similar relative rise of plasma aldosterone levels in both groups despite higher baseline values in group B. The exact mechanism of the impaired regulation of aldosterone in a subgroup of patients with essential hypertension remains to be elucidated.

Adenoma↗
PubMed1981

Changes in renal and urinary kallikrein activity by mannitol-induced osmotic diuresis.

1. Osmotic diuresis was induced in male Sprague-Dawley rats by a 30% (w/v) mannitol solution injected three times at 15-min intervals. Kallikrein excretion increased for a short period after the first two injections, but, despite marked diuresis, the increment of kallikrein excretion after the second injection was less marked than after the first and no enhanced kallikrein excretion was observed after the third injection of mannitol. 2. Urinary kallikrein excretion correlated only with urinary potassium excretion. No correlation was found with either urine volume or urinary sodium excretion. 3. At the end of the osmotic diuresis kallikrein activity was significantly reduced both in the urine and in the renal cortex. At that time plasma aldosterone concentration was slightly greater in the mannitol-treated than that in the control group, but the difference did not reach statistical significance. 4. In this experiment no relationship was observed between the activity of the renal kallikrein-kinin system and the plasma aldosterone concentration. 5. The transient increase in urinary kallikrein excretion is interpreted as a wash-out effect of renal kallikrein, which is followed by a diminished kallikrein activity in urine and in renal cortex.

Aldosterone↗
PubMed1981

Effects of sodium loading, desoxycorticosterone acetate, and corticosterone on urinary kallikrein excretion.

In male Sprague-Dawley rats, changes in kallikrein activity in urine were produced by high sodium intake (1% saline as drinking fluid for 14 days), and administration of desoxycorticosterone acetate (DOCA, 15 mg/kg s.c. for 5 days), and of corticosterone (2 x 0.2 or 2 x 20 mg/kg s.c. daily for 5 days). Salt loading caused a decrease in urinary kallikrein excretion (p less than 0.005), while DOCA produced an increase (p less than 0.001). While corticosterone, administered in the low dose, had no effect on urinary kallikrein excretion, the high dose, given for 5 days, diminished kallikrein excretion to about half the basal value (p less than 0.001). Simultaneously, the excretion of aldosterone decreased to about one third the amount measured in the corresponding control rats.

Aldosterone↗