PubMed Health⌕ Search

Biomedical subjects

R Düsing

Publications and source records attributed to R Düsing.

At least 163 records · Page 9Linked to original sources
PubMed1981

Inner medullary osmolality and sodium concentration are decreased in rats during escape from DOCA-induced salt retention.

1. Papillary osmolality and sodium and potassium concentrations were determined in rats during a control period and during escape from the sodium-retaining effect of deoxycorticosterone acetate and compared with the changes observed after acute frusemide injection. 2. During escape, papillary osmolality [554 +/- 36 vs 754 +/- 42 mmol/kg of papillary water (H2O), P less than 0.005] and papillary sodium concentration (131 +/- 7 vs 182 +/- 8 mmol/kg H2O, P less than 0.001) were significantly decreased as compared with the control values, while papillary potassium concentration remained unchanged. 3. Frusemide decreased papillary osmolality to 538 +/- 41 mmol/kg H2O (P less than 0.005), papillary sodium concentration to 125 +/- 9 mmol/kg H2O (P less than 0.001) and papillary potassium concentration from 80 +/- 2 to 69 +/- 3 mmol/kg H2O (P less than 0.05). 4. The present results suggest that medullary portions of the distal tubule (probably the ascending loop of Henle) may represent one site of tubular sodium chloride rejection during escape from the sodium-retaining effect of deoxy-corticosterone acetate.

Animals↗
PubMed1981

Renal prostaglandins and water balance: studies in normal volunteer subjects and in patients with central diabetes insipidus.

1. In six healthy volunteer subjects polydipsic water loading significantly increased urine volume from 1203 +/- 242 (SEM) to 5072 +/- 320 ml/24 h (P less than 0.001) with a significant decrease in urinary osmolality. This increase in urine volume by more than fourfold was associated with a slight increase in urinary excretion of prostaglandin E2 from 466 +/- 66 to 1017 +/- 174 pmol/24 h (P = 0.05). 2. In five patients with central diabetes insipidus mean urine volume of 10 838 +/- 107 ml/24 h was reduced to 1205 +/- 204 ml/24 h (P less than 0.001) by treatment with 1-desamino-8-arginine vasopressin (desamino-[Arg8]vasopressin; 15 microgram/day) with a significant rise in urinary osmolality. Desamino-[Arg8]vasopressin treatment was associated with a significant increase of suppressed urinary excretion of prostaglandin E2 (PGE2) in four of these patients from 246 +/- 66 to 2643 +/- 677 pmol/24 h (P less than 0.01). 3. Concomitant treatment with indomethacin in addition to desamino-[Arg8]vasopressin significantly suppressed urinary excretion of PGE2 and significantly increased urinary osmolality as compared with treatment with desamino-[Arg8]vasopressin alone. 4. Desamino-[Arg8]vasopressin significantly increased urinary excretion of adenosine 3':5'-cyclic monophosphate (cyclic AMP). However, there was no further change in urinary excretion of cyclic AMP during concomitant indomethacin treatment. 5. The results suggest that urine flow itself is not an important determinant of urinary PGE2 excretion. In patients with central diabetes insipidus the urinary concentrating response to desamino-[Arg8]vasopressin is enhanced during inhibition of prostaglandin synthesis without changes in urinary excretion of cyclic AMP.

Adult↗
PubMed1980

The role of the prostaglandin system in the regulation of renal function in normal women.

The role of prostaglandins in the regulation of renal function was studied in seven healthy female volunteers taking a constant metabolic diet containing 59 meq of sodium and about 50 meq of potassium daily. Each subject underwent two renal clearance studies, during which vasopressin (priming dose, 200 mU; "sustainer," 200 mU/hour at 1 ml/min) was infused intravenously. The first clearance study served as the control; indomethacin (2 mg/kg/day) was given for seven days before the second clearance study to inhibit prostaglandin synthesis. Food and fluid were withheld for 12 hours before the studies. Urine was collected through an indwelling bladder catheter at 30 minute intervals. Glomerular filtration rate was estimated from inulin clearance and renal blood flow from para-aminohippurate (PAH) clearance. Indomethacin was associated with a significant increase in maximal urinary osmolality from 826 +/- 47 mosmol/kg H2) to 920 +/- 32 mosmol/kg H2O (P < 0.01). Minimal "free water" clearance was -1.40 +/- 0.02 ml/min before and -1.63 +/- 0.04 ml/min (P < 0.01) after the administration of indomethacin. Indomethacin did not affect urine flow, urinary sodium or potassium excretion, glomerular filtration rate or renal plasma flow. In addition, indomethacin did not affect the urinary excretion of cyclic adenosine monophosphate (AMP). Plasma arginine-vasopressin, measured in two subjects by radioimmunoassay, did not change with blockade of prostaglandin synthesis. It appears that prostaglandins antagonize the hydro-osmotic effect of antidiuretic hormone by an intrarenal mechanism, independent of changes in renal hemodynamics or cation excretion. This mechanism is probably mediated by an alteration in the water permeability of the collecting ducts. Since urinary cyclic AMP did not change during blockade of prostaglandin synthesis, whereas urinary osmolality increased, a change of vasopressin-dependent cyclic AMP production in the kidney was probably not reflected in urinary cyclic AMP.

Adult↗
PubMed1980

Effects of moderate short-term potassium depletion in normal humans. The role of prostaglandins.

The role of prostaglandins (PG) in the effects of potassium (K+)depletion was studied in six normal women. A mean K+-deficit of 220 mEq was induced with and without concomitant treatment with indomethacin (150 mg/day). Mean serum K+ concentration decreased from 4.2 +/- (S.E.) 0.1 to 3.2 +/- 0.1 mEq/L without indomethacin and from 4.1 +/- 0.1 to 3.2 +/- 0.1 mEq/L with indomethacin. "Supine" and "upright" plasma renin activity (PRA) and plasma norepinephrine concentration (NE) were unaltered by K+ -depletion alone but decreased with indomethacin. Plasma aldosterone (PA) was suppressed during K+-depletion (control: 7.2 +/- 2.6 ng/dl supine, 19.3 +/- 8.1 ng/dl upright; K+-depletion: 2.6 +/- 0.3 ng/dl supine, 5.5 +/- 1.3 ng/dl upright) and was paralleled by a decrease in urinary aldosterone. K+- depletion decreased urinary PGE2 from 667 +/- 133 to 343 +/- 60 ng/day (P less than 0.025) without a change in PGF2 alpha. The dose of exogenous angiotensin II (A II) which increased diastolic blood pressure by 20 mm Hg (pressor dose) was 7.1 +/- 1.4 ng/kg/min during control and increased to 11.0 +/- 0.7 ng/kg/min during K+-depletion (P less than 0.05). Indomethacin increased the sensitivity to A II both during control (pressor dose: 4.9 +/- 0.6 ng/kg/min) and K+ - depletion (pressor dose: 6.0 +/- 1.0 ng/kg/min). These results indicate that in healthy subjects, moderate short-term K+-depletion does not affect PRA or NE but decreases production of aldosterone and PGE2 by the kidney. The changes in vascular sensitivity to exogenous A II during K+-depletion and indomethacin and the decreases in plasma NE and PRA during indomethacin may be explained by changes in vascular vasodilator PG.

Aldosterone↗
PubMed1980

Prostaglandin-independent protection by furosemide from oliguric ischemic renal failure in conscious rats.

In 38 conscious rats divided into seven groups, acute unilateral ischemic renal failure was induced by 1 hour of complete occlusion of the left renal artery while the contralateral kidney remained intact. Renal excretory function of the left kidney was monitored up to 144 hours after ischemia and revealed a typical course of oliguric renal failure with oligoanuria persisting for more than 48 hours. Urinary osmolality and sodium concentration became plasma isotonic after release of renal artery occlusion and approximated control values on day 6 after ischemia. In nine rats, the i.v. infusion of furosemide before (6 microgram/min/100 g body wt) and after (12 microgram/min/100 g body wt) renal artery occlusion protected the ischemic kidney from oligoanuria with endogenous creatinine clearance of 0.42 +/- 0.11 ml/min/g kidney wt 5 hours after ischemia. Tubular absorption of sodium and water was at least partially preserved 36 hours after ischemia when infusion of furosemide was stopped. The loop diuretic significantly (P less than 0.01) increased total urinary prostaglandin (PG) E2 excretion before and after renal artery occlusion; and 5 hours after ischemia, PGE2 excretion from the ischemic kidney significantly exceeded that from the intact kidney (P less than 0.05). Indomethacin (1 mg/100 g body wt) administered in six animals markedly suppressed control PGE2 excretion (P less than 0.05) as well as the furosemide-induced rise in urinary PG excretion before and after ischemia but did not modify the protective effect of the diuretic in this experimental model. Inhibition of PG synthesis, however, reduced urinary flow rate and sodium and potassium excretion of the contralateral intact kidney and almost completely prevented its compensatory rise in creatinine clearance. The results indicate that mechanisms other than the intrarenal prostaglandin system must be considered to mediate the protective effects of furosemide in acute ischemic renal failure.

Animals↗
PubMed1980

Immunoreactive substance P in human plasma: response to changes in posture and sodium balance.

1. In healthy volunteers plasma concentrations of immunoreactive substance P were measured in response to changes in posture and dietary salt intake. 2. In 14 subjects plasma immunoreactive substance P was 168 +/- 31 pmol/l when subjects were supine and 401 +/- 51 pmol/l (P less than 0.001) when they were ambulant. 3. Measurement of supine plasma immunoreactive substance P at 6 h intervals gave a mean value of 240 +/- 39 pmol/l at 14.00 hours and a lowest value of 76 +/- 9 pmol/l at 02.00 hours. 4. In eight healthy subjects plasma immunoreactive substance P rose only slightly from 169 +/0 41 pmol/l, on a sodium intake ad lib., to 244 +/- 45 pmol/l by day 4 of dietary sodium restriction (35 mmol/day) and significantly fell to 51 +/- 20 pmol/l (P less than 0.001) by day 4 of high sodium intake (350 mmol/day). 5. Although exogenous substance P was shown to be natriuretic in dog and rat, the present results do not favour a role of endogenous substance P as a circulating natriuretic factor in man.

Adult↗
PubMed1979

Prolactin in primary aldosteronism.

1. This study was done to examine the possibility that escape from the sodium retention produced by aldosterone may be associated with an inhibition of prolactin secretion. Plasma prolactin concentrations were determined in seven patients with adrenal adenoma and aldosteronism, before and after unilateral adrenalectomy, at a time when they were in balance on a sodium intake of 109 mmol/day. 2. After operation, plasma aldosterone was normal [before operation, 52.7 +/- 12.1 (supine), 64.6 +/- 9.1 ng/dl (upright); after operation, 6.8 +/- 1.5 (supine), 11.1 +/- 3.0 ng/dl (upright)], while plasma prolactin remained unchanged [before operation, 19.6 +/- 2.8 (supine), 15.5 +/- 3.3 ng/ml (upright); after operation, 23.8 +/- 2.3 (supine), 11.1 +/- 3.0 ng/ml (upright)]. 3. Our results do not support a role for prolactin in the renal response to aldosterone in man.

Adrenalectomy↗
PubMed1979

Effects of aprotinin on renal function and urinary prostaglandin excretion in conscious rats after acute salt loading.

1. Aprotinin, a potent kallikrein inhibitor, was given to conscious rats with and without expansion of the extracellular fluid volume with isotonic saline. 2. In non-expanded rats aprotinin had no effect on arterial pressure, glomerular filtration rate (GFR), hippuran clearance, urinary flow rate, absolute sodium and potassium excretion or free-water clearance. 3. In volume-expanded rats aprotinin significantly reduced GFR, hippuran clearance, urine volume (V) UNaV, UKV and Cwater/GFR without effect on systemic arterial pressure. 4. Urinary immunoreactive prostaglandin E2 excretion significantly increased during the expansion phase but returned to below the control range during stable extracellular fluid volume expansion. 5. Aprotinin significantly suppressed urinary immunoreactive prostaglandin E2 excretion in non-expanded rats and in volume-expand rats during the expansion phase, but not during stable expansion. 6. The results suggest that the kallikrein-kinin system may contribute to changes in renal function during extracellular volume expansion. This action may not necessarily be associated with changes in renal prostaglandin E2 activity.

Animals↗
PubMed1978

Effects of inhibition of prostaglandin-synthesis on renal electrolyte excretion and concentrating ability in healthy man.

In five healthy subjects inhibition of prostaglandin (PG)-synthesis with indomethacin did not significantly alter glomerular filtration, urinary flow rate or sodium and potassium excretion during control urine collection periods or i.v. hypertonic saline infusion. Saline administration was accompanied by a fall in urinary PGEI-excretion from 0.58 +/- 0.14 to 0.26 +/- 0.09 ng/min (p less than 0.05). While indomethacin had no effect on basal urinary osmolality (Uosm), renal concentrating ability following hypertonic saline or i.v. administration of 100 mU lysine-vasopressin significantly increased in the presence of indomethacin with Uosm rising from 805 +/- 25 to 970 +/- 53 mosm/L (p less than 0.01) and from 839 +/- 47 to 996 +/- 62 mosm/L (p less than 0.01), resp. Since this was not accompanied by respective changes in urinary excretion of cyclic adenosine monophosphate (cAMP) mechanisms other than PG-antagonism of vasopressin, such as decreased medullary washout of solute, may contribute to enhanced renal concentrating ability following inhibition of PG-synthesis with indomethacin.

Adult↗
PubMed1978

Antihypertensive effect of volume depletion: interrelation with renal prostaglandins.

Since the original studies of Patak et al. in 1975 revealed that the antihypertensive and natriuretic effects of furosemide were markedly blunted or abrogated by indomethacin in both normotensive and hypertensive man, it has been postulated that the ameliorative effects of furosemide in human essential hypertension might be mediated by release of intrarenal prostaglandins. To study the direct effects of furosemide on prostaglandin biosynthesis and release, slices of rabbit renal medulla were incubated in Krebs-Ringer bicarbonate buffer, glucose 10 mM, 1-14C-arachidonic acid (AA) 10 microM, HSA /g/100 ml, 30 min 37 degrees C. Measurements were made of radioactive AA leads to PGE2, and total endogenous immunoreactive PGE2 production (iPGE2) with and without the addition of furosemide (10 microgram/ml) to the media. In the absence of furosemide AA leads to PGE2 was 73 +/- 22 nmol/30 min/g and in the presence of furosemide it fell to 30 +/- 4 nmol/30min/g. iPGE2 was 33 +/- / ng/30 min/mg and decreased to 25 +/- 3 mg with furosemide. These results indicate that the natriuresis and antihypertensive effect of furosemide in vivo, which is associated with a significant increase in urinary PGE2, is not the result of a direct stimulation of furosemide on prostaglandin synthesis but may result from a decrease in PGE metabolism, conversion to another biologically active prostaglandin or possibly be a reflection of events secondary to a direct effect of furosemide on renal hemodynamics and electrolyte excretion.

Aldosterone↗