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D Rouse

Publications and source records attributed to D Rouse.

At least 37 records · Page 2Linked to original sources
PubMed1991

TMB-8 prevents the hydroosmotic response to ADH in rabbit cortical collecting tubules.

Both AVP and dDAVP effect a transient increase in cytosolic free calcium (iCa2+) in cortical collecting tubule (CCT) cells. To investigate the physiological role of this increase in iCa2+, we examined the effect of TMB-8, a putative inhibitor of iCa2+ release, on the initial and sustained phase of AVP- and dDAVP-stimulated water permeability (Pf) in isolated, perfused CCTs. Pretreatment of tubules with TMB-8, 50 microM, suppressed the increase in osmotic water permeability (Pf) induced by 10 microU/ml AVP and dDAVP, but had no effect on the sustained phase of the response. When increased to 100 microM. TMB-8 inhibited the sustained phase of AVP action. A similar pattern was observed on AVP-stimulated adenyly cyclase activity in rabbit renal membranes. Pretreatment of tubules with 50 microM TMB-8 attenuated the initial increase in Pf in response to cholera toxin but not to 8-Br-cAMP or forskolin. There was no effect of this concentration of TMB-8 on the sustained phase of these agonists. These studies suggest that, in lower concentrations, TMB-8 inhibits the mobilization of iCa2+, which is important for the interaction of Gs with the catalytic unit of adenylyl cyclase and the initial increase in AVP-stimulated Pf. In higher concentrations, TMB-8 inhibits adenylyl cyclase activity directly.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

Vitamin B6 is effective therapy for nausea and vomiting of pregnancy: a randomized, double-blind placebo-controlled study.

Fifty-nine women completed a randomized, double-blind placebo-controlled study of pyridoxine hydrochloride (vitamin B6) for the treatment of nausea and vomiting of pregnancy. Thirty-one patients received vitamin B6, 25-mg tablets orally every 8 hours for 72 hours, and 28 patients received placebo in the same regimen. Patients were categorized according to the presence of vomiting: severe nausea (score greater than 7) or mild to moderate nausea (score of 7 or less). The severity of nausea (as graded on a visual analogue scale of 1-10 cm) and the number of patients with vomiting over a 72-hour period were used to evaluate response to therapy. Twelve of 31 patients in the vitamin B6 group had a pre-treatment nausea score greater than 7 (severe) (mean 8.2 +/- 0.8), as did ten of 28 patients in the placebo group (mean 8.7 +/- 0.9) (not significant). Following therapy, there was a significant difference in the mean "difference in nausea" score (ie, baseline - post-therapy nausea) between patients with severe nausea receiving vitamin B6 (mean 4.3 +/- 2.1) and placebo (mean 1.8 +/- 2.2) (P less than .01). In patients with mild to moderate nausea and in the group as a whole, no significant difference between treatment and placebo was observed. Fifteen of 31 vitamin B6-treated patients had vomiting before therapy, compared with ten of 28 in the placebo group (not significant). At the completion of 3 days of therapy, only eight of 31 patients in the vitamin B6 group had any vomiting, compared with 15 of 28 patients in the placebo group (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Clonidine inhibits fluid absorption in the rabbit proximal convoluted renal tubule.

Previous studies have shown that norepinephrine (NE) and the beta-adrenoceptor agonist, isoproterenol (I), enhance fluid absorption (JV) in isolated, perfused proximal convoluted tubule segments (PCT). Pretreatment of PCT with the beta-adrenoceptor antagonist, propranolol, inhibited the action of NE and produced a significant decline in JV, suggesting modulation of JV by both alpha- and beta-adrenoceptors. The present studies further characterize the alpha-adrenoceptor control of JV in isolated perfused PCT using specific agonists and antagonists. Basal JV declined significantly with the addition of the alpha 2-adrenoceptor agonist, clonidine (10(-4) M), to the bath; however, it was unchanged with the addition of the alpha 1-adrenoceptor agonist, methoxamine (10(-6) or 10(-4) M). With the addition of 10(-6) M isoproterenol JV increased significantly, and returned to control values with the subsequent addition of clonidine (10(-6) or 10(-4) M). Pretreatment of PCT with the alpha 2-adrenoceptor antagonist, yohimbine (10(-5) M), or with pertussis toxin (100 ng/ml) did not interfere with the stimulation of JV by isoproterenol, but abolished the inhibition of isoproterenol-stimulated JV by clonidine. Thus, clonidine inhibits JV in PCT via an alpha 2-adrenoceptor. This effect is mediated by a pertussis toxin inhibitable GTP-binding protein, but not one that is coupled to adenylyl cyclase.

Adenylate Cyclase Toxin↗
PubMed1990

Ongoing fetomaternal hemorrhage treated by serial fetal intravascular transfusions.

Nonimmune hydrops secondary to atraumatic, massive fetomaternal hemorrhage was diagnosed at 33.5 weeks' gestation by a maternal Kleihauer-Betke stain, confirmed by funipuncture. The initial fetal hematocrit was 6.5%. Kleihauer-Betke testing revealed a fetomaternal hemorrhage of approximately 230 mL. Fetal karyotype, total immunoglobulin M, and liver function tests were normal. Maternal parvovirus serology was negative. Treatment with two fetal intravascular transfusions provided only transient improvement because the fetomaternal hemorrhage proved to be unrelenting.

Adult↗
PubMed1990

Immune hydrops fetalis attributable to anti-HJK.

We describe a new low-frequency antigen as the cause of immune hydrops fetalis in a fetus presenting at 27 weeks with a hematocrit of 6%. The fetus was treated successfully by intravascular transfusion. This antigen, temporarily identified as HJK, has been detected in only one family.

Adult↗
PubMed1988

The mechanism of hypercalciuria in streptozotocin-induced diabetic rats.

Metabolic studies were performed in streptozotocin-induced diabetic (D) rats and normal control (C) rats to assess the role of hyperphagia in the hypercalciuria of diabetes. Urinary calcium excretion (UCaV) was significantly higher in D v C rats fed ad libitum. When D rats were pair-fed (calorie and mineral restriction) with C rats, UCaV declined but remained significantly higher than in C rats. When D rats were allowed their usual increased calorie intake but restricted to C rat mineral consumption, UCaV remained elevated. These findings suggested a tubular reabsorptive defect. In vivo microinjection studies were then performed to identify the site(s) of the tubular reabsorptive defect. Using 1.0 mmol/L Ca in the injectate, 45Ca recovery in the urine (CaR%) was significantly higher in D rats after intratubular injections into early and late proximal tubules and late distal but not early distal tubules. An additional load-dependent defect was revealed in the terminal nephron when the Ca concentration of the injectate was increased to 1.8 mmol/L. After early distal injection, CaR% was significantly increased in D v C rats. Infusion of PTH into thyroparathyroidectomized C and D rats enhanced Ca absorption to a similar degree but did not correct the reabsorptive defect in D rats. These results argue against a lack of end-organ responsiveness to PTH in diabetes or a low serum PTH level as the cause of the hypercalciuria. We conclude that hyperphagia contributes to the hypercalciuria of diabetes in the absence of increased Ca intake. Also, two tubular reabsorptive defects exist: one in the loop of Henle; the other, load-dependent in the terminal nephron.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1988

Presence of an unusual methanogenic bacterium in coal gasification waste.

Methanogenic bacteria growing on a pilot-scale, anaerobic filter processing coal gasification waste were enriched in a mineral salts medium containing hydrogen and acetate as potential energy sources. Transfer of the enrichments to methanol medium resulted in the initial growth of a strain of Methanosarcina barkeri, but eventually small cocci became dominant. The cocci growing on methanol produced methane and exhibited the typical fluorescence of methanogenic bacteria. They grew in the presence of the cell wall synthesis-inhibiting antibiotics d-cycloserine, fosfomycin, penicillin G, and vancomycin as well as in the presence of kanamycin, an inhibitor of protein synthesis in eubacteria. The optimal growth temperature was 37 degrees C, and the doubling time was 7.5 h. The strain lysed after reaching stationary phase. The bacterium grew poorly with hydrogen as the energy source and failed to grow on acetate. Morphologically, the coccus shared similarities with Methanosarcina sp. Cells were 1 mum wide, exhibited the typical thick cell wall and cross-wall formation, and formed tetrads. Packets and cysts were not formed.

Journal Article↗
PubMed1988

Calcifediol antagonizes PTH action on water and phosphate absorption in rabbit pars recta.

Reports of the effects of calcifediol (25-hydroxycholecalciferol) on phosphate excretion, alone or with parathyroid hormone (PTH), or with adenosine 3',5'-cyclic monophosphate (cAMP), have been conflicting. The purpose of this investigation was to examine the effects on fluid and phosphate transport by the rabbit pars recta of calcifediol alone or with PTH. In tubule segments obtained from rabbits fed a normal diet, the addition of 10 or 30 nM calcifediol to the bath did not alter fluid absorption (Jv) or lumen-to-bath phosphate flux (JPil----b). However, pharmacological concentrations did inhibit Jv by 20.9 +/- 5.6% (100 nM, P less than 0.02) and 37.9 +/- 9.4% (1.0 microM, P less than 0.01) and JPil----b by 18.5 +/- 6.6% (100 nM, P less than 0.05) and 40.5 +/- 8.6% (1.0 microM, P less than 0.01). In the presence of 30 nM, 100 nM, or 1.0 microM calcifediol, neither 0.25 nor 1.0 U/ml PTH inhibited JPil----b. A modest decline in Jv did occur with 1.0 U/ml PTH in the presence of 30 nM and 100 nM calcifediol. Unlike calcifediol, when 10 nM calcitriol (1,25-dihydroxycholecalciferol) was present in the bath, 0.2 U/ml PTH significantly depressed Jv and JPil----b. To investigate the mechanism of action of high calcifediol concentration, measurement of the collected minus perfused tubule fluid chloride concentration difference was performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1987

Captopril inhibits the hydroosmotic effect of ADH in the cortical collecting tubule.

Previous studies have shown that captopril (CP) inhibits ADH-stimulated osmotic water permeability (Pf) in the toad bladder by potentiating endogenous bradykinin (BK). The present studies examine the effect of CP on ADH-stimulated Pf in isolated, perfused rabbit cortical collecting tubules (CCT). CP (10(-4) M) reversibly inhibited Pf, stimulated by maximal concentrations of ADH (10 microU/ml). Pretreatment of CCT's with 5 microM indomethacin, however, abolished the effect of CP. Inhibition of BK production by the kallikrein inhibitors, aprotinin and benzamidine, failed to enhance Pf stimulated by submaximal concentrations of ADH (2.5 microU/ml). Since ADH exerts its effects by activation of adenylyl cyclase (AC), further experiments were performed to identify the site at which CP inhibits this cascade. CP significantly inhibited forskolin (10(-4) M) stimulated Pf; however, it had no effect on cyclic AMP (10(-5) M) stimulated Pf, suggesting that the site of action is on the catalytic subunit or one of the GTP regulatory proteins of AC. To further localize the site of CP's action, CCT's were pre-incubated with pertussis toxin (0.5 microgram/ml) to inactivate the inhibitory, guanosine triphosphate (GTP) regulatory protein, Gi. In these tubules, CP failed to inhibit the action of ADH. We conclude that CP stimulates prostaglandin production which in turn activates Gi and inhibits AC activity. We further suggest that CP stimulates PG's directly, not via BK.

Animals↗
PubMed1985

Modulation of phosphate absorption by calcium in the rabbit proximal convoluted tubule.

Proximal convoluted (S2) and straight (S3) renal tubule segments were studied to determine the effect of Ca on lumen-to-bath phosphate flux (JlbPO4). Increasing bath and perfusate Ca from 1.8 to 3.6 mM enhanced JlbPO4 from 3.3 +/- 0.7 to 6.6 +/- 0.6 pmol/mm per min in S2 segments (P less than 0.001) but had no effect in S3 segments. Decreasing bath and perfusate Ca from 1.8 to 0.2 mM reduced JlbPO4 from 3.7 +/- 0.6 to 2.2 +/- 0.6 in S2 segments. These effects were unrelated to changes in fluid absorption and transepithelial potential difference. Increasing cytosolic Ca with a Ca ionophore, inhibiting the Ca-calmodulin complex with trifluoperazine, or applying the Ca channel blocker nifedipine had no effect on JlBPO4 in S2 segments. Increasing only bath Ca from 1.8 to 3.6 mM did not significantly affect JlbPO4. However, increasing only perfusate Ca enhanced JlbPO4 from 3.4 +/- 0.7 to 6.1 +/- 0.7 pmol/mm per min (P less than 0.005). Inhibition of hydrogen ion secretion, by using a low bicarbonate, low pH perfusate, both depressed base-line JlbPO4 and abolished the stimulatory effect of raising perfusate Ca. Net phosphate efflux (JnetPO4) also increased after ambient calcium levels were raised, ruling out a significant increase in PO4 backflux. When net sodium transport was abolished by reducing the bath temperature to 24 degrees C, JnetPO4 at normal ambient calcium was reduced and increasing ambient calcium failed to increase it, ruling out a simple physicochemical reaction wherein phosphate precipitates out of solution with calcium. The present studies provide direct evidence for a stimulatory effect of Ca on sodium-dependent PO4 absorption in the proximal convoluted tubule, exerted at the luminal membrane. It is postulated that Ca modulates the affinity of the PO4 transporter for the anion.

Absorption↗
PubMed1984

Calcium transport in the rabbit superficial proximal convoluted tubule.

Calcium transport was studied in isolated S2 segments of rabbit superficial proximal convoluted tubules. 45Ca was added to the perfusate for measurement of lumen-to-bath flux (JlbCa), to the bath for bath-to-lumen flux (JblCa), and to both perfusate and bath for net flux (JnetCa). In these studies, the perfusate consisted of an equilibrium solution that was designed to minimize water flux or electrochemical potential differences (PD). Under these conditions, JlbCa (9.1 +/- 1.0 peq/mm X min) was not different from JblCa (7.3 +/- 1.3 peq/mm X min), and JnetCa was not different from zero, which suggests that calcium transport in the superficial proximal convoluted tubule is due primarily to passive transport. The efflux coefficient was 9.5 +/- 1.2 X 10(-5) cm/s, which was not significantly different from the influx coefficient, 7.0 +/- 1.3 X 10(-5) cm/s. When the PD was made positive or negative with use of different perfusates, net calcium absorption or secretion was demonstrated, respectively, which supports a major role for passive transport. These results indicate that in the superficial proximal convoluted tubule of the rabbit, passive driving forces are the major determinants of calcium transport.

Animals↗
PubMed1984

The effect of hypocalcemia on renal bicarbonate absorption.

The effect of hypocalcemia on renal bicarbonate absorption (RHCO3/GFR) was examined in bicarbonate-loaded dogs. Following the infusion of ethylene-bis(oxyethylenitrilo)tetraacetic acid (EGTA) in intact dogs, RHCO3/GFR fell from 23.8 +/- 0.7 to 20.8 +/- 0.6 (p less than 0.005) and in thyroparathyroidectomized (TPTX) dogs from 25.6 +/- 1.44 to 23.6 +/- 2.15 (p less than 0.025). By contrast, infusion of EGTA which had been titrated with calcium had no effect, RHCO3/GFR being 27.7 +/- 1.14, control and 28.5 +/- 0.38, during EGTA (p less than 0.05). Hypocalcemia also significantly depressed the renal absorption of phosphate. There were no effects on renal hemodynamics or electrolyte excretion. These studies suggest that plasma-ionized calcium may play a role in regulating renal bicarbonate and phosphate absorption.

Animals↗
PubMed1984

Potassium retention in membraneless thymus lymphocyte nuclei.

Nonionic detergents, Triton X-100 and Brij 58, removed lipoid membranes of suspended thymus lymphocytes within 5 minutes. The mobilization and solubilization of cytoplasmic and nuclear proteins occurred much faster (less than 5 minutes) with Triton X-100 treatment than with Brij 58 treatment (less than 10 minutes). In Triton X-100 treated cells the loss of K+ was complete within 5 minutes whereas with Brij 58 treatment the K+ loss was not complete after 10 minutes. Thus, the high concentration of K+ and the low concentration of Na+ in the nuclei can remain near normal for minutes in the absence of membrane structures. If the ions were in free solution within the cells, disruption of membrane integrity should lead to equilibration of the ions with external media within seconds. The decrease of K+ in the Brij 58 treated cells with exposure time was correlated with the solubilization of the proteins. These results support the view that K+ and Na+ are not freely dissolved in the cellular water, but are co-compartmentalized with proteins inside the living cell.

Animals↗