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R Düsing

Publications and source records attributed to R Düsing.

At least 145 records · Page 8Linked to original sources
PubMed1985

Relation of endogenous digoxin-like immunoreacting activities to salt balance and renal function in man.

We have previously shown that a natriuretic factor which is present in a small molecular weight fraction (IV) of serum and urine from salt loaded animals and healthy subjects, respectively, inhibits the Na-K-ATPase enzyme in vitro and also binds to a specific digoxin antibody. In the present study digoxin-like immunoreacting activity (DLIA) was therefore determined in the serum of healthy volunteers during low (35 nmol/day) and high (greater than 400 mmol/day) sodium intake and of patients with chronic renal failure and serum creatinine concentrations ranging from 127 to 757 mumol/l. DLIA was determined with a radioimmunoassay for digoxin in native serum and in the salt (III) and post-salt (IV) serum fractions eluted from a Sephadex G-25 column. DLIA in native serum of healthy subjects was less than 0.125 ng/ml. After gel filtration DLIA eluted exclusively in the small molecular weight salt (F III) and post-salt (F IV) fractions. Whereas DLIA increased in F III and decreased in F IV, total DLIA in F III + IV slightly increased from 0.37 +/- 0.03 to 0.49 +/- 0.05 ng/ml (p less than 0.01) with the change from low to high sodium intake. DLIA in native serum of uremic patients ranged from 0 to 1.70 ng/ml and was detectable consistently only in patients with serum creatinine concentrations above 250 mumol/l. DLIA in F III which averaged 0.22 +/- 0.04 ng/ml and total activity which ranged from 0.11 to 0.88 ng/ml closely correlated with the degree of renal impairment (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Further studies on the mechanism of increased blood pressure during dietary linoleic acid deprivation.

The present studies investigate the changes in blood pressure and excretory renal function in rats during dietary linoleic acid deprivation. Four groups of animals were fed isocaloric diets containing 10 en % saturated fat and either 5 en % linoleic acid (groups I and III) or 5 en % oleic acid (groups II and IV). In addition, groups I and II received a chronic high intake of Na (greater than 5 mmol/day) while groups III and IV were Na restricted with an average Na intake of 0.7 mumol/day. Blood pressure significantly increased in the high salt, linoleic acid deprived group II and was unchanged in all three other groups of animals. De novo synthesis of prostaglandin E2 in rat kidney inner medullary homogenates in the four groups of animals at the end of the dietary protocol showed a marked dependency on Na balance with significantly (p less than 0.01) higher values in the Na restricted animals as well as on linoleic acid intake with significantly (p less than 0.01) higher values in the linoleic acid substituted animals. Urinary excretion of NaCl during acute expansion of the extracellular fluid volume with hypotonic saline was significantly impaired in the animals receiving oleic acid instead of linoleic acid. In a metabolic study, linoleic acid deprived animals retained Na from the first day of linoleic acid deprivation and blood pressure started to rise only after a substantial amount of Na had been retained. Our results show that linoleic acid deprivation suppresses renal arachidonic acid cyclooxygenase metabolism and impairs the renal ability to excrete an acute salt load. Impaired renal excretory function precedes the increase in blood pressure. Thus suppressed renal cyclo-oxygenase metabolism which impairs renal excretory function may be a crucial mechanism in the rise of blood pressure during dietary linoleic acid deprivation.

Animals↗
PubMed1983

The converting enzyme inhibitor captopril stimulates prostacyclin synthesis by isolated rat aorta.

In the present study, pretreatment of rats with captopril significantly stimulated prostacyclin (PGI2) synthesis by their isolated aorta. This effect was maximal at captopril doses of 1.0 mumol/kg body weight. When added directly into the incubation buffer, captopril at final concentrations of 50 and 500 nM also increased the synthesis of PGI2 by isolated rat aorta. Our results show that captopril stimulates PGI2 synthesis in vascular tissue and that this effect may be due at least in part to a direct action of this substance.

Angiotensin I↗
PubMed1983

Interaction of bemetizide and indomethacin in the kidney.

The effect of a single oral dose of 25 mg bemetizide on renal function without and with concomitant administration of the prostaglandin synthesis inhibitor indomethacin was investigated in ten healthy volunteers during sustained water diuresis. Bemetizide induced a significant increase in urinary sodium and chloride excretion from 196 +/- 30 and 163 +/- 28 mumol/min to 690 +/- 54 and 537 +/- 51 mumol/min (P less than 0.01). This effect occurred in the absence of changes in glomerular filtration rate, urinary excretion of phosphate or the delivery of chloride beyond the proximal nephron to the distal tubules (distal delivery) [(CH2O + CCl)/GFR . 100], but was associated with a significant decrease in distal fractional chloride absorption (DFACl) [CH2O/(CH2O + CCl)] from 0.84 +/- 0.02 to 0.63 +/- 0.02 (P less than 0.01). Bemetizide also increased urinary excretion of prostaglandin (PG) E2. Concomitant indomethacin administration significantly suppressed urinary excretion of PGE2 and markedly decreased urinary excretion of sodium and chloride during control and following bemetizide administration. Indomethacin had no effect on glomerular filtration rate, urinary excretion of phosphate, distal delivery or the urinary excretion of bemetizide but significantly increased DFACl both during control and after bemetizide administration. Our results show that bemetizide as a thiazide-diuretic acts in the diluting segments of the nephron. Indomethacin administration induces retention of sodium and chloride and blunts the renal effects of bemetizide via increased absorption in the diluting segments. The interaction of both drugs most likely represents a pharmacodynamic interaction.

Adult↗
PubMed1983

Dietary linoleic acid deprivation: effects on blood pressure and PGI2 synthesis.

The possible role of arachidonic acid metabolites in the regulation of arterial blood pressure was investigated in rats receiving 0, 5, or 9 energy (en) % linoleic acid in their diet (groups 1-3) over 6 wk. In group 1 animals, systolic arterial blood pressure significantly increased from 100.5 +/- 2.0 to 110.6 +/- 3.1 mmHg (P less than 0.01) after 6 wk of dietary linoleic acid deprivation, whereas no effect on blood pressure was observed in group 2 and 3 animals receiving dietary linoleic acid supplements. Generation of prostacyclin (PGI2)-like activity by isolated aorta from rats fed the different diets was determined using a platelet-aggregation bioassay following incubation of aortic tissue for 12, 15, and 30 min, respectively. In isolated aorta from rats fed the 5 en% linoleic acid, production of PGI2 was 55.9 +/- 1.2, 70.5 +/- 2.6, and 90.9 +/- 3.6 pmol/mg over the three incubation periods. In group 1 animals, a significant suppression of PGI2 generation to 35.4 +/- 1.5, 41.1 +/- 1.7, and 55.0 +/- 1.2 pmol/mg (P less than 0.005) was observed, whereas PGI2 production was unaltered in aortic tissue from group 3 animals. In contrast, plasma concentrations of circulating thromboxane B2 were highest in group 1 animals (2.15 +/- 0.38 pmol/ml) and measured 1.28 +/- 0.17 and 0.83 +/- 0.10 pmol/ml in group 2 and 3 animals, respectively. Our results demonstrate that dietary deprivation of the arachidonic acid precursor linoleic acid increases arterial blood pressure that is associated with a suppression of vascular PGI2 synthesis and, most likely, a secondary rise in circulating thromboxane concentrations.

Animals↗
PubMed1983

Substance P-induced changes in kidney function in the conscious rat: relation to the renal prostaglandin system.

Infusion of substance P into the renal artery was previously shown to cause a significant natriuresis which was associated with increased kallikrein excretion. Since the renal kinin and prostaglandin (PG) systems may be interrelated, the present study was performed to investigate the effects of substance P on renal function and its potential interaction with the renal PG system in the conscious rat. 24 female Sprague-Dawley rats were infused intravenously with substance P (1 ng . min-1 . kg-1 body weight) and the body weight was kept constant by an intravenous infusion of 0.45% saline. Substance P had no effects on arterial blood pressure, glomerular filtration rate (GFR) and 125I-hippuran clearance in the absence or presence of indomethacin (INDO). Basal UPGE2 V was unaltered by substance P infusion but was suppressed by INDO before and during substance P by 80 and 88%, respectively. Substance P raised urinary flow rate (V) by 105%, CH2O by 96%, UNaV by 378%, UKV by 48% and UPO4V by 147% (p less than 0.001). Although INDO significantly suppressed V, CH2O, and UNaV during all collection periods, it did not affect absolute UPO4V and UKV and the relative rise in V, CH2O, and UNaV induced by substance P. Thus, the diuretic and natriuretic effects of substance P are not mediated by renal PG, but are partially blunted by INDO through increased distal absorption of sodium and water, INDO has no effect on substance P-induced alterations in proximal tubular function.

Animals↗
PubMed1982

Hemodynamic and hormonal responses to 8-arginine-vasopressin in healthy man: effects of indomethacin.

Previous investigations suggest that in a normotensive organism the vasopressor effect of 8-arginine-vasopressin (AVP) is very effectively buffered by cardiovascular reflex mechanisms. Exogenous AVP administration shows only small, transient increases in blood pressure in spite of continued AVP-infusion and high plasma AVP concentrations. The present study aims to clarify the mechanism of the observed transient blood pressure elevations which are often referred to as "tachyphylaxis". Our results in healthy subjects show a two phase response to exogenous AVP: an initial phase which is characterized by cardiac reflex mechanisms and a second phase during which a normalisation of the elevated total peripheral resistance occurs. Inhibition of prostaglandin synthesis with indomethacin almost completely attenuates this vascular counterregulation to exogenous AVP, thus providing evidence that a prostaglandin mediated vasodilation in response to AVP may be the underlying mechanism for "vasopressin tachyphylaxis". The role of the renin-angiotensin-system and the importance of different regional hemodynamic effects of AVP are discussed.

Adult↗
PubMed1982

Arachidonic acid metabolism in isolated rat aorta. Dependence of prostacyclin biosynthesis on extracellular potassium concentration.

Slices of rat aorta were incubated in Krebs-Ringer bicarbonate buffer for measurements of immunoreactive 6-ketoprostaglandin F1 alpha, thromboxane (TX) B2, prostaglandin (PG)E2, and PGF2 alpha, and in Tris buffer (pH 9.3) for determination of prostacyclin (PGI2)-like activity. No significant generation of TXB2, PGE2, or PGF2 alpha by rat aortic tissue could be detected. The time-dependent release of 6-keto-PGF1 alpha Krebs-Ringer bicarbonate buffer closely correlated with PGI2 generation in alkaline Tris buffer. During a 30-min incubation period, 6-keto-PGF1 alpha, release was 79.8 +/- 3.3 pmol/mg at a buffer potassium concentration of 3.9 mmol/liter and significantly increased by 23% to 98.3 +/- 8.5 pmol/mg (P less than 0.025) in the absence of potassium in the incubation medium. A smaller decrease in buffer potassium concentration to 2.1 mmol/liter and an increase to 8.8 mmol/liter did not significantly alter aortic 6-keto-PGF1 alpha release. Changes in the incubation buffer sodium concentration from 144 mmol/liter to either 138 or 150 mmol/liter at a constant potassium concentration of 3.9 mmol/liter did not alter the recovery of 6-keto-PGF1 alpha. Our results support the concept that PGI2 is the predominant product of arachidonic acid metabolism in rat aorta. They further show that PGI2 can be recovered quantitatively as 6-keto-PGF1 alpha under the present in vitro conditions. In addition, this in vitro study points to the potassium ion as a modulator of vascular PGI2 synthesis with a stimulation at low potassium concentrations.

Animals↗
PubMed1982

Prostaglandins participate in the regulation of NaCl absorption in the diluting segments of the nephron in vivo: effects of furosemide.

Various studies point to a role of the renal prostaglandin (PG) system in the regulation of renal NaCl excretion. In the present experiments, distal delivery of proximal tubular fluid (DD) [CH20 + CC1)/GFR x 100] and distal fractional chloride absorption (DFAC1) [CH20/(CH20 + CC1)] were studied in 6 healthy volunteers undergoing sustained water diuresis. Studies of renal function were performed during intravenous infusion of hypotonic (0.45%) saline and during additional treatment with indomethacin, furosemide and furosemide plus indomethacin. Hypotonic saline was infused at increasing rates of 0.09, 0.18, and 0.36 ml min-1 kg-1 body weight each for a 45-min period. DD over all three clearance periods averaged 8.27 +/- 0.71 ml min-1 100 ml-1 glomerular filtration rate (GFR) during saline infusion alone and was unchanged by indomethacin (8.09 +/- 0.63 ml min-1 100 ml-1 GFR). DFAC1 averaged 0.79 +/- 0.02 during saline and significantly increased to 0.87 +/- 0.01 (p less than 0.002) during concomitant indomethacin treatment. Increased NaCl absorption in the diluting segment during indomethacin was paralleled by a decrease in urinary excretion of chloride (UC1V) from 221 +/- 29 during control to 124 +/- 19 muEq/min (p less than 0.025) and in urinary excretion of PGE2 (UPGE2V) from 1.45 +/- 0.12 to 0.51 +/- 0.09 pmol/min (p less than 0.025). Furosemide increased UPGE2V to 2.94 +/- 0.34 pmol/min (p less than 0.05) and UC1V to 2,590 +/- 128 muEq/min (p less than 0.001). This effect was associated with an increase in DD to 26.70 +/- 1.33 ml min-1 100 ml-1 GFR (p less than 0.001) and a decrease in DFAC1 to 0.19 +/- 0.02 (p less than 0.001). Neither DD and DFAC1 nor UC1V were altered during furosemide+indomethacin as compared to furosemide in spite of a marked suppression of UPGE2V to 0.56 +/- 0.13 pmol/min. Our results support the concept that renal PG participate in the regulation of NaCl absorption in the diluting segments of the nephron. Furthermore, the tubular effects of furosemide appear not to be mediated by the PG system.

Absorption↗
PubMed1982

The role of prostaglandins in diabetes insipidus produced by desoxycorticosterone in the dog.

To determine the role of renal prostaglandins (PGs) in the renal response to desoxycorticosterone acetate (DOCA), dogs were studied on a constant diet in which sodium intake was restricted (2.5 meq/day) or high (115 meq/day). On the restricted sodium intake, DOCA (25 mg/day im for 6 days) did not affect urinary volume, sodium, potassium, PGE2, or PGF2 alpha. On the high sodium intake, DOCA produced sodium retention for 1 day and a sustained increase in urinary potassium with a fall in serum potassium to 3.1 meq/liter. Urine volume increased from 574 +/- 50 to 1726 +/- 177 ml/day (P less than 0.001) with a fall in urinary osmolality from 1545 +/- 122 to 495 +/- 55 mosmol/ liter (P less than 0.001) as serum sodium increased from 149.0 +/- 1.0 to 152.5 +/- 0.3 meq/liter (P less than 0.025) by the sixth day of DOCA. Urinary PGE2 and PGF2 alpha were unchanged during the first 2 days of DOCA, then increased progressively from control values of 261 +/- 60 and 1143 +/- 144 ng/day ng/day, respectively, to 730 +/- 62 (P less than 0.005) and 3013 +/- 479 ng/day (P less than 0.01), respectively. Potassium repletion during continued DOCA treatment restored urinary volume, osmolality, PGE2 and PGF2 alpha, and serum sodium to control values. Treatment with indomethacin during DOCA-induced hypokalemia, polyuria, hypernatremia, and increased urinary PG, restored urinary PGs to control values, and corrected the polyuria and hypernatremia without a change in serum potassium. Thus, DOCA produced potassium depletion, polyuria, increased urinary PGs, and hypernatremia in dogs on a high sodium intake but not in those on a restricted sodium intake. As polyuria and hypernatremia were corrected either by potassium repletion, which corrected the supranormal renal synthesis of PGs, or by indomethacin, which inhibited their synthesis, renal water loss was presumably the result of an increase in renal PG synthesis, probably stimulated by potassium depletion.

Animals↗
PubMed1981

[Hepato-renal syndrome (author's transl)].

The hepato-renal syndrome is defined as potentially reversible functional renal failure associated with acute fulminant hepatitis or, more often, with advanced chronic liver failure. It is characterized by oliguria, azotemia, retention of sodium and water with formation of ascites, and hyponatremia. While urinary sodium concentration of less than 10 mEq/l reflects intact tubular sodium absorption, the kidney lacks the ability for adequate free-water generation. This condition must be separated from specific renal diseases which may arise during the course of intra-or extrahepatic diseases and which must be classified accordingly. Pathophysiological aspects of the hepa-to-renal syndrome include hemodynamic factors, such as changes in intrarenal blood flow distribution in the presence of elevated intrarenal and reduced peripheral vascular resistance. The functional relationship of vasoconstrictor, sodium retaining, and anti-diuretic hormones (e.g., renin-angiotensin, aldosterone, and vasopressin) to vasodilator, diuretic, and natriuretic hormonal factors (e.g., prostaglandins, kinins, and natriuretic hormone) may be altered as well. Finally, a pre- and intrahepatic spillover resulting in decreased endotoxin clearance must be considered. Due to the lack of understanding of their complex interactions, so far pharmacological and therapeutic approaches remained ineffective to correct at least some of these factors. Today, recovery from hepato-renal syndrome will, therefore, mainly depend on the course of the underlying liver disease.

Acute Kidney Injury↗