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J A Dürr

Publications and source records attributed to J A Dürr.

8 recordsLinked to original sources
PubMed1994

Effect of bacitracin on the degradation of a vasopressin receptor ligand with high affinity for the V1 and V2 vasopressin isoreceptors.

We previously described a new iodinated vasopressin analogue (N epsilon-[125I]L-Tyr-[Lys8]-vasopressin) with high affinity for the vasopressin V1 and V2 isoreceptors. The aim of the present study was: i) to analyse the degradation pathway of N epsilon-[125I]L-Tyr-[Lys8]-vasopressin and (ii) to look for an effective inhibitor of radioligand degradation. N epsilon-[125I]L-Tyr-[Lys8]-vasopressin was processed in a temperature-dependent manner by crude cell membranes from LLC-PK1 cells. Only one degradation product was seen using RP-HPLC. The degradation product co-eluted with monoiodotyrosine. The stereoisomer, N epsilon-[125I]D-Tyr-[Lys8]-vasopressin, underwent the same degradation process. Bacitracin prevented degradation at doses as low as 40 mg/l without alterating the binding affinity.

Animals↗
PubMed1992

Internalization of V2-vasopressin receptors in LLC-PK1-cells: evidence for receptor-mediated endocytosis.

The mechanism of internalization of the vasopressin-receptor (V2-subtype) of LLC-PK1-cells, a pig renal tubular cell line, is unknown. We studied internalization utilizing a novel, highly specific vasopressin analogue ((125I)-[8-p(OH)-phenylpropionyl]-LVP, 2000 Ci/mmol). Scatchard analysis performed with membranes of LLC-PK1-cells revealed a Kd of 0.8 +/- 0.2 nM and a Bmax of 366 +/- 41 fmol/mg of protein. Degradation of the ligand was excluded by RP-HPLC-analysis. Internalization was proven by the acid-wash technique, quantitative light-microscopic autoradiography and electron microscopy. The ligand was internalized in a time- and temperature-dependent manner. At 4 degrees C, no uptake was found; at 22 degrees C, after 30 min of incubation, more than 50% of the radioligand was found inside the cell. Electron microscopy demonstrated that plasma-membrane bound vasopressin receptors are internalized by receptor-mediated endocytosis via coated pits.

Animals↗
PubMed1991

Aldosterone in congestive heart failure: analysis of determinants and role in sodium retention.

In patients with congestive heart failure (CHF), the role of aldosterone in the abnormal sodium (Na+) retention and the determinants of plasma aldosterone (PA) including plasma atrial natriuretic factor (hANF), plasma renin activity (PRA), and plasma potassium (K+) have not been fully elucidated. We therefore studied the effect of the specific aldosterone antagonist, spironolactone, on urinary Na+ and K+ excretion and plasma hormone responses in 6 Na(+)-retaining CHF patients. After withdrawal of diuretics 4 days prior to the study, the CHF patients were placed on a Na+ intake of 100 mmol/day for 9 days. Spironolactone, 200 mg p.o. bid, was administered for the last 4 days of the 9-day study period. PRA and norepinephrine increased with spironolactone treatment (both p less than 0.05). Plasma hANF before spironolactone was significantly elevated and decreased during spironolactone therapy (p less than 0.05). Urinary Na+ excretion significantly increased during spironolactone administration and the positive Na+ balance was reversed in the CHF patients. Moreover, the urine Na+:K+ concentration ratio significantly increased during spironolactone administration. Analysis of the relationship between PA, plasma K+, PRA, and plasma hANF indicated that PRA is the primary determinant of PA in patients with CHF. Thus, the present results indicate that the renin-angiotensin-aldosterone system is an important mediator of Na+ retention in CHF, as evidenced by the reversal of the positive Na+ balance with a specific aldosterone antagonist. This natriuretic effect can be demonstrated in the presence of potential antinatriuretic influences including stimulation of the renin-angiotensin and sympathetic nervous systems and a decrease in plasma hANF.

Aldosterone↗
PubMed1989

Role of hemodynamic factors in osmoregulatory alterations of rat pregnancy.

Plasma osmolality (Posmol) decreases in pregnancy, possibly because of hemodynamically mediated arginine vasopressin (AVP) secretion, i.e., inadequate vascular filling and/or decreased blood pressure. This hypothesis was tested in Sprague-Dawley rats treated on gestational days 1-18 or 13-18 with 1) deoxycorticosterone acetate (DOCA) + standard chow (0.5% Na), 2) vehicle + standard chow, or 3) high-Na (1.25%) diet. Renal sodium "escape" and suppression of the renin-aldosterone system suggested "effective volume expansion," yet Posmol was similar in all pregnant groups, 7-10 mosmol/kg below levels in virgin controls, and plasma AVP was unaltered. Apparent osmotic thresholds for AVP secretion, similar in control and DOCA-treated gravid animals, were 8-10 mosmol/kg below those of untreated virgin rats. Norepinephrine + DOCA, administered to gravid animals consuming normal or high-Na chow, increased blood pressure approximately 10% above control levels, but this also failed to alter Posmol. These data suggest that mechanisms other than hemodynamically mediated AVP secretion are responsible for the osmoregulatory alterations accompanying rodent pregnancy.

Animals↗
PubMed1987

Diabetes insipidus in pregnancy.

Diabetes insipidus (DI) and pregnancy may coexist and, when they do, present challenging diagnostic and therapeutic problems. Women with preexisting central DI usually experience increased thirst and require additional hormone replacement. Women with nephrogenic DI have an increased water turnover. Of interest is a group of women with transient DI of gestation. In some of these patients, central DI is brought to the fore by increases in water turnover during pregnancy as well as increments in the metabolic clearance of arginine vasopressin (AVP), especially near term. Others have a "vasopressin-resistant" form of the disease, which in one case followed by us appeared to be due to marked increments in circulating cystine-aminopeptidase (vasopressinase). This patient's DI was resistant to pitressin, but she concentrated her urine when given dDAVP. Her vasopressinase levels 2 weeks postpartum were still several-fold those of normal term gravidas. Her DI remitted, and she concentrated her urine appropriately 2 months postpartum. This article reviews the different forms of DI peculiar to pregnancy.

Arginine Vasopressin↗
PubMed1987

Pregnancy: an overfill or underfill state.

With pregnancy, the expansion of plasma and extracellular fluid volume, increased cardiac output, and increased glomerular filtration rate (GFR) and renal blood flow (RBF) are compatible with primary renal sodium and water retention with secondary enlargement of the vascular compartment (overfill hypothesis). Alternatively, a primary enlargement of the vascular compartment (eg, prostaglandin-mediated vasodilation and placental arteriovenous shunting) with secondary renal sodium and water retention (underfill hypothesis) is supported by the activation of the renin-angiotensin-aldosterone (RAA) system, resetting of vasopressin release and thirst to a lower plasma osmolality, and a further stimulation of the RAA system and vasopressin when pregnant rats' water intake is maintained at a level of a virgin rat fluid intake, diminished BP and increased cardiac output in the first trimester, and worsening of hyponatremia with sodium restriction in the pregnant but not the virgin rat. With the underfill hypothesis, normal sodium and water excretion with mineralocorticoid escape could be mediated by hormonally induced increases in GFR and RBF associated with pregnancy. The nature of such a hormone effect of pregnancy to enhance renal hemodynamics remains to be defined.

Animals↗