[Effect of vasopressin on renin liberation in the rat kidney].
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Animals↗
Biomedical subjects
A Konrads
Publications and source records attributed to A Konrads.
[Kaposi's sarcoma (author's transl)].
Kaposi's sarcoma of the skin and an aplastic syndrome occurred together in a 51-year-old patient. Macroscopically livid papules and nodules were observed. Histomorphologically endotheliomatous cell proliferation with signs of infiltrative growth was found. Because of the aplastic pancytopenia cytostatic treatment of the Kaposi sarcoma was contraindicated. The patient finally died of vascular failure with haemorrhagic diathesis being manifest. Syntropy of Kaposi's sarcoma with malignant haematological diseases is known. However, association with aplastic anaemia has not been observed so far. The pathogenesis of Kaposi's sarcoma is unknown.
Anemia, Aplastic↗
[Sézory syndrome from the internist's viewpoint].
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Aged↗
[Sézary syndrome (author's transl)].
Morphological demonstration of the typical Sézary cell in peripheral blood confirmed the diagnosis of Sézary syndrome in a 64-year-old patient with generalized erythrodermia and typical histopathological skin changes. Enzymes and immunocytological membrane characteristics of Sézary cells changed in the course of the disease after cytostatic therapy. Polychemotherapy clinically led to transitory complete regression of skin changes. Reviewing the few published investigations it is found that the morphologically sufficiently defined Sézary cells are apparently not uniform cytochemically and immunocytologically in different patients.
Autopsy↗
Extrarenal prorenin and renin in anephric patients.
Active renin was detected in 6 of 7 anephric patients (mean value: 0.72 +/- 0.27 microU/ml, n = 7; normals: 19.7 +/- 2.4 microU/ml, n = 10), using an assay method without intrinsic acid- or cryoactivation. Prorenin, measured as the difference between plasma renin concentration (PRC) before and after acid-activation in vitro, was present in considerable amounts in all patients (32.4 +/- 3.5 microU/ml; normals: 80.7 +/- 9.7 microU/ml). PRC after cryoactivation at--5 degrees C during 1 week was insignificantly lower than after acid-activation in the patients. There was a linear correlation between PRC after either activation procedure (p less than 0.01). Supine or upright posture did not influence active or inactive renin in the anephric subjects. Our studies show that low but significant levels of active renin and a considerable amount of prorenin are detectable in anephric patients. The data suggest that prorenin in normal subjects in a significant proportion is of extrarenal origin. Orthostasis has no effect on extrarenal active or inactive renin.
Adult↗
The renin--kallikrein--prostaglandin system: plasma active and inactive renin and urinary kallikrein during prostacyclin infusion in man.
Renal prostaglandins are integrated with the kallikrein-kinin and renin-angiotension systems in a vasoactive hormone complex. Prostacyclin potently stimulates renin release from rabbit cortical slices and plasma renin activity rises in response to prostacyclin infusion in man. Prostaglandins also stimulate the production of kallikrein, a potential activator of renin in vivo. To investigate the mechanism of prostacyclin induced renin release, human volunteers were infused with prostacyclin 8ngKg-1min-1 and vehicle alone in random order. Despite a marked increase in plasma active renin during prostacyclin both plasma inactive renin and urinary kallikrein failed to alter from control values. Urinary sodium and volume were increased by prostacyclin. The stimulation of renin by intravenous prostacyclin is not mediated by activation of the kallikrein system.
Adult↗
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↗
Sézary syndrome: immunocytological and cytochemical variability of Sézary cells.
The characteristic large cells in the blood of a patient with Sézary syndrome underwent immunocytological and cytochemical changes during polychemotherapy, which caused transient regression of skin lesions. Tartrate-resistant acid phosphatase was demonstrable in a few cells only after chemotherapy; initially, only 2% T cells and 26% B cells could be demonstrated in the blood by immunocytological methods; after cytostatic therapy, 35% T cells but no B cells were detected.
Acid Phosphatase↗
[Alopecia in thyroid diseases: characteristic trichograms].
Trichograms from the parietal and occipital area were evaluated in 34 patients with thyroid diseases, which complained about hair loss. The followings findings can be regarded as characteristic for alopecia in thyroid diseases, being not related to the functional state of the thyroid gland: increase of dysplastic hairs over 50%, increase of broken hairs over 15% and strenghthening of these findings in the occipital area. Alopecia in thyroid diseases is not caused by changes within the hair cycle but probably by impaired hair quality.
Adult↗
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↗
Glycerol-induced acute renal failure in Brattleboro rats with hypothalamic diabetes insipidus.
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Acute Kidney Injury↗
Renin-activation by kallikrein: evidence for alkaline-activation of plasma renin.
Porcine pancreatic kallikrein leads to a significant activation of human plasma renin when incubated at pH 8.2. 'Endogenous' activation of plasma renin can be seen by incubation of plasmas at the same pH. Both 'endogenous' alkaline- and kallikrein-activation of plasma renin can be inhibited by aprotinin. Both, kallikrein- and 'endogenous' alkaline activation of plasma renin are significantly correlated to cryo- and acid-activation. We suggest that kallikrein-and 'endogenous' alkaline-activiation come close to the in vivo activation process.
Animals↗
[Kaposi's sarcoma and aplastic pancytopenia: simultaneous occurrence in a patient].
A 49 year old patient developed simultaneously a histologically verified Kaposi's sarcoma and an idiopathic aplastic pancytopenia. An association of these perhaps virus-induced diseases has not been reported until now. Consequences concerning the diagnostic approach of changes in peripheral blood cells in patients with Kaposi's sarcoma are delineated. Changes in peripheral blood and bone marrow in patients with Kaposi's sarcoma are discussed.
Biopsy↗
Effects of vasopressin and its deamino-D-arginine analogue on renin release in the isolated perfused rat kidney.
The direct action of arginine-vasopressin (AVP) and its deamino-D-arginine analogue (DDAVP) on renin release (RR) has been studied in isolated rat kidneys perfused with an electrolyte solution at constant pressure in a single-pass system. AVP and DDAVP infused at various concentrations (80 to 2100 pg/ml and 80 to 8700 pg/ml, respectively) reduced volume and increased osmolality of urine in a dose-dependent way. High doses of AVP reduced renal perfusate flow and glomerular filtration rate while DDAVP had no effect on renal haemodynamics. When vasoconstrictor doses of AVP or high concentrations of DDAVP were infused, "basal" RR remained unchanged. However, when RR had been stimulated by infusion of isoproterenol, vasoconstrictor doses of AVP as well as high doses of DDAVP which did not increase renal vascular resistance diminished RR by about 30% (P less than 0.01, and P less than 0.05, respectively). These results suggest that the inhibition of RR by vasopressin is not related to its vasoconstrictor action.
Animals↗
Role of cyclic AMP in the regulation of renin release from the isolated perfused rat kidney.
The role of cyclic AMP in the regulation of renin release (RR) was studied in isolated rat kidneys, which were perfused at constant pressure in a single-pass system with a modified Krebs-henseleit solution. Isoproterenol (IP) (2 x 10(-9) to 2 x 10(-6) M) and 3-isobutyl-1-methyl-xanthine (IBMX) (4 x 10(-7) to 7 x 10(-5) M) induced a dose-dependent increase of renal perfusate flow, glomerular filtration rate and urinary sodium excretion. RR was stimulated up to 10-fold above control values within 5 min. At the lowest concentrations IP stimulated RR, but did not affect renal haemodynamics. When IP and IBMX were administered concomitantly, a supraadditive stimulation of RR was observed. Dibutyryl-cAMP (db-cAMP) and 8-Br-cGMP (10(-6) to 10(-4) M) produced a similar dose-dependent vasodilation and natriuresis, but differed in their action on RR. Within 15 min after the start of the infusion, db-cAMP increased RR up to 4-fold, whereas 8-Br-cGMP was without an effect. These results suggest that IP, IBMX and db-cAMP stimulated RR by increasing the concentrations of cAMP in the epitheloid cells and independently of changes in renal haemodynamics and sodium excretion.
1-Methyl-3-isobutylxanthine↗
Effect of saralasin and serum in myohaemoglobinuric acute renal failure of rats.
1. In rats deprived of food and water for 24 h acute renal failure was produced by the intramuscular injection of glycerol. Eight hours later plasma urea concentration had increased threefold despite a small rise in urine volume. Plasma concentrations of renin and renin substrate were elevated. 2. When saralasin, a competitive antagonist of angiotensin II, was infused for 8 h after glycerol injection, urine volume and plasma urea were similar to values in rats that had received an infusion of saline. 3. Administration of rat serum (4.5 ml h-1 kg-1) for 4 h suppressed plasma renin concentrations, but plasma urea increased to the same extent as in rats without serum. 4. When saralasin and serum were infused at the same time, urine volume, urine osmolality and solute excretion increased and the rise of plasma urea was diminished. 5. Saralasin has a protective effect against glycerol-induced acute renal failure only when volume is replaced concomitantly.
Acute Kidney Injury↗
Renal vasoconstriction in glycerol-induced acute renal failure. Studies in the isolated perfused rat kidney.
1. Acute renal failure was produced in rats by the intramuscular injection of glycerol (6.1 mol/l 10 ml/kg). Either 2 or 4--6 h later the right kidney was isolated and perfused for 1 h with an electrolyte solution containing a gelatin preparation (Haemaccel, 35 g/l) at pressures between 90 and 100 mm Hg in a single-pass system. 2. In kidneys taken from rats with acute renal failure renal vascular resistance was markedly increased immediately after the start of the perfusion as compared with control kidneys taken from untreated rats. During the following 30 min of perfusion the resistance progressively decreased and, at 1 h of perfusion, was similar to that in control kidneys or only moderately elevated. 3. Despite the reduction of renal vascular resistance glomerular filtration rate was still markedly increased immediately after the start of the perfusion as compared with control kidneys taken from untreated rats. During the following 30 min of perfusion the resistance progressively decreased and, at 1 h of perfusion, was similar to that in control kidneys or only moderately elevated. 3. Despite the reduction of renal vascular resistance glomerular filtration rate was still markedly impaired after 1 h of perfusion and fractional reabsorption of sodium and water as well as the secretion of p-aminohippurate were diminished. Renal venous renin concentration and renin release were lower in kidneys taken from rats with acute renal failure than in the control experiments. 4. These results suggest that the increase in renal vascular resistance and the stimulation of renin release after injection of glycerol in vivo are the consequence of extra- rather than intra-renal mechanisms.
Acute Kidney Injury↗
Vasopressin and renin in glycerol-induced acute renal failure in the rat.
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Acute Kidney Injury↗