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Biomedical subjects

A Konrads

Publications and source records attributed to A Konrads.

At least 19 recordsLinked to original sources
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↗
PubMed1983

A new working formulation of non-Hodgkin's lymphomas. A retrospective study of the new NCI classification proposal in comparison to the Rappaport and Kiel classifications.

Two hundred thirty cases of malignant non-Hodgkin's lymphomas were reclassified in a retrospective study according to the New Working Formulation for Clinical Usage of the NCI as compared to the Rappaport and Kiel classifications. The reproducibility for the individual schemes this study was 81% (Rappaport), 79% (Kiel), and 85% (New Working Formulation). In keeping with the results of the NCI international study, all lymphomas were subdivided into 3 prognostic groups: (1) low-grade malignancy (6.0 years median survival); (2) intermediate-grade malignancy (3.5 years median survival); and (3) high-grade malignancy (1.4 years median survival). The NCI-proposed New Working Formulation for Clinical Usage is thus recommended as practical and unprejudicing classification scheme for general application; however, its usefulness as tool for translating one classification scheme into another appears limited.

Europe↗
PubMed1983

Radioimmunoassay of arginine-vasopressin in human plasma: development and clinical application.

A sensitive and specific radioimmunoassay for the measurement of arg-vasopressin (AVP) in human plasma is described. Recovery of added AVP from plasma was about 65-70%. An acetone extraction step was necessary to prevent unspecific blank effects. Sensitivity of the assay is 0.5 pg AVP/ml plasma. In normally hydrated subjects AVP-concentration ranged from 0.7 pg/ml to 5.8 pg/ml and showed a good correlation with plasma osmolality. In patients with complete diabetes insipidus (D.i.) AVP-values were below the sensitivity limit of the method and they were subnormal when D.i. was incomplete. There was no increase of AVP-concentration during fluid restriction in patients with complete or incomplete D.i. In subjects with psychogenic polydipsia AVP-values were normal and dehydration produced adequate rises of plasma AVP. In patients with SIADH (Schwartz-Bartter-syndrome) AVP-values were greatly enhanced (greater than 10 pg/ml) when correlated to plasma osmolality (less than 170 mosmol/kg H2O).

Adult↗
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

Antihypertensive effects of captopril and saralasin in essential and renal hypertension.

The antihypertensive effect of captopril and its mechanism of action were studied in patients with essential and renal hypertension. In mild essential hypertension (n = 12), during monotherapy with captopril (50 to 450 mg, 4 to 12 weeks) blood pressure was normalized in seven, improved in two and remained unchanged in three patients, plasma levels of active and acid-activatable inactive renin significantly increased and angiotensin II decreased, whereas no consistent changes in urinary kallikrein excretion occurred. In severe renal (n = 14) and essential (n = 9) hypertension, blood pressure was normalized in eight (seven with renal hypertension), improved in seven and unchanged in eight patients, when captopril (50 to 450 mg, 3 to 15 months) was added to the antihypertensive medication. In one patient with stenosis in a transplanted renal artery reversible renal failure occurred during captopril therapy possibly because of a steep initial decrease in blood pressure, although a toxic effect of the drug cannot be excluded. In another series of 12 renal and 8 essential hypertensive patients, a significant correlation between the acute effect of captopril (within 90 minutes) an saralasin on blood pressure was demonstrated (r=0.71, p less than 0.001). The change in blood pressure after either drug was significantly related to the initial plasma renin concentration. In conclusion, captopril seems to be an effective antihypertensive agent in essential and renal hypertension. Renal function should be monitored during captopril therapy. Our studies suggest that captopril decreases blood pressure by inhibiting the vasopressor action of the renin-angiotensin system.

Angiotensin II↗
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

[Management of treatment-resistant hypertension: comparison of the antihypertensive effect of endralazine and minoxidil (author's transl)].

In 16 fo 20 patients with treatment-resistant hypertension endralazine, combined with beta-receptor blockers and diuretics, significantly lowered mean arterial blood pressure from 198/112 mmHg to 148/88 mmHg. The initial dose of endralazine was 2.5 mg three times daily. After this the dosage was increased, at the three to six-day intervals according to antihypertensive action and side effects, to a maximum of 50 mg daily in steps of 5.0--7.5 mg per dose. - In a second series of eleven additional patients with treatment-resistant renal hypertension the blood-pressure lowering effect of hydralazine and minoxidil was compared in an open cross-over trial. The result was in favour of hydralazine. Sodium and water retention was slightly less marked with endralazine. Sleep disorders, increased frequency of feeling cold, moderately severe flushing with red checks and feeling hot occurred but rarely with endralazine and regressed during the period of observation.

Adolescent↗
PubMed1981

Renin release after furosemide and ethacrynic acid in man. Evidence for neural reflex control mechanisms.

The mechanisms of renin release after furosemide (F) and ethacrynic acid (EA) in man were examined. We evaluated whether acute volume shifts within the low pressure system after F induce renin release via neural pathways. Immersion in a water-bath or beta-blockade reduced the increase of plasma renin concentration after F but not after EA. It is concluded that acute renin release after F but not after EA in man is partially due to neurally mediated reflexes originating from volume receptors in the cardiopulmonary area.

Adult↗
PubMed1981

Effects of furosemide and orthostasis on active and inactive renin in normal and anephric man.

We investigated active and inactive (acid-activatable) plasma renin in anephric and in normal persons. In anephric patients (n = 15) plasma concentration of active and inactive renin was 1.15 +/-- 0.2 and 40.7 +/- 7.1 microunits ml, respectively; angiotensin II (n = 13) was 14.5 +/- 1.9 pg/ml. Furosemide (n = 10), 40 mg i.v., and upright posture (n = 8) did not change active or inactive renin in the anephric state. In normal men, furosemide (n = 9) within 15 min increased active renin from 29.9 +/- 5.8 to 82.4 +/- 14.8 microunits/ml (P less than 0.001), while inactive renin slightly but not significantly decreased from 136.3 +/- 29.9 to 121.1 +/- 19.2 microunits/ml; orthostasis (n = 15) within 4 h stimulated active renin (P less than 0.001) and slightly raised inactive renin (P less than 0.05). Both furosemide and orthostasis increased (P less than 0.001 each) the proportion of active renin in normal persons. Studies in one patient within 24 h after bilateral nephrectomy indicated half-life to be 30-60 min for active and 2-4 h for inactive renin. Thus, we detected low levels of active renin and considerable amounts of inactive renin and angiotensin II in anephric patients. Our data suggest that about 30% of inactive renin in normal plasma is of extrarenal origin. The stimulation of active renin by furosemide and orthostasis is bound to the presence of the kidney. Our studies provide indirect evidence that both manoeuvres may stimulate the conversion of inactive to active renin within the human kidney.

Adult↗