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L A Walker

Publications and source records attributed to L A Walker.

72 records · Page 4Linked to original sources
PubMed1987

Properties of spontaneous Enterobacter cloacae mutants with temperature-conditional derepression of type I beta-lactamase synthesis.

Spontaneous mutants, with temperature-conditional derepression of chromosomally-encoded Type I beta-lactamase synthesis, were derived from two independent clinical isolates of Enterobacter cloacae. At the permissive temperature (28 degrees C) the mutants' beta-lactamase activity was equivalent to that of their respective parents but at restrictive temperatures (above 40 degrees C) the activity increased many hundred-fold. The increased beta-lactamase expression correlated with reduced beta-lactam susceptibility. In temperature shift-up experiments, the initial rate of beta-lactamase synthesis closely paralleled that of the parent strains induced with cefoxitin. Maximal beta-lactamase activity in the mutants was attained after about 3 h growth at restrictive temperatures and was significantly higher than that of the cefoxitin-induced parents. However, the level was not as high as that observed in isogenic temperature-stable derepressed mutants, under the same conditions. All temperature-conditional mutants showed hyper-induction of beta-lactamase synthesis at permissive temperatures. Our findings are discussed in relation to a positive control model for regulation of Type I beta-lactamase synthesis in Ent. cloacae.

Anti-Bacterial Agents↗
PubMed1986

Renal response to pentobarbital anesthesia in rats: effect of interrupting the renin-angiotensin system.

The influence of interrupting the renin-angiotensin system on the renal hemodynamic response to barbiturate anesthesia was assessed in conscious, trained, chronically catheterized rats. Anesthesia induced by pentobarbital caused a marked reduction in mean arterial pressure, heart rate, glomerular filtration rate (GFR) and effective renal plasma flow (ERPF). Pretreatment of rats with captopril, an inhibitor of angiotensin I converting enzyme, prevented the impairment of renal hemodynamics by pentobarbital without restoring blood pressure. GFR remained at 100 to 110% of control values in captopril-pretreated rats receiving pentobarbital, but was reduced by pentobarbital (90-120 min after induction) to 75 +/- 5% in rats which did not receive captopril. ERPF showed similar changes. An antagonist of angiotensin II receptors, 1-sarcosine-8-isoleucine-angiotensin II, did not prevent the anesthesia-induced decrements in GFR and ERPF (GFR was reduced to 78 +/- 6% and ERPF to 68 +/- 4% at 90-120 min after pentobarbital). This failure of the antagonist of angiotensin II receptors to protect renal hemodynamics may have been due to its intrinsic agonist activity on the renal vasculature. This is suggested by the fact that, in captopril-pretreated rats, which maintained renal hemodynamics in response to pentobarbital, addition of 1-sarcosine-8-isoleucine-angiotensin II caused a reduction in GFR and ERPF and an elevated blood pressure. At 100 min after administration of pentobarbital, plasma renin activity was elevated compared to a conscious control group (3.57 +/- 0.42 vs. 1.94 +/- 0.34 ng angiotensin l/ml X hr, P less than .05). It is concluded that the renin-angiotensin system mediates an impairment of renal hemodynamics during pentobarbital anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1986

Effect of renal denervation on the antinatriuretic response to morphine administration in conscious rats.

The effect of surgical denervation on the antinatriuretic response to morphine was assessed in conscious rats prepared with arterial and venous catheters and bladder cannulas. In sham-operated animals, morphine sulfate (4 mg/kg i.v. plus 2 mg/kg X hr) caused a marked reduction in sodium excretion (650 +/- 218 vs. 2394 +/- 265 nEq/100 g X min in vehicle-treated animals; P less than .05). Although glomerular filtration rate was reduced, fractional excretion of sodium, expressed as a percentage of the filtered load, was also markedly decreased by morphine (0.62 +/- 0.18 vs. 1.51 +/- 0.15% in the vehicle group; P less than .05). The changes in sodium excretion were readily reversed by naloxone. In rats subjected to the renal denervation procedure, morphine had no effect on sodium excretion (1614 +/- 261 vs. 1926 +/- 520 nEq/100 g X min) or on fractional sodium excretion (1.92 +/- 0.50 vs. 1.41 +/- 0.37%). However, glomerular filtration rate was reduced by morphine as in the sham-denervated rats. Blood pressure and heart rate were not significantly affected by morphine in either group. The results suggest that morphine enhances renal tubular sodium reabsorption, at least in part, by a mechanism dependent on intact renal nerves. Because there was no evidence of generalized sympathetic activation (as judged by blood pressure and heart rate changes), the effect may be selective for the renal innervation.

Animals↗
PubMed1984

Natriuretic effect of naloxone in fasted, water-loaded rats.

The influence of naloxone (10 mg/kg i.p.) on water and electrolyte excretion was assessed in water-loaded rats subjected to fasting or fasting and refeeding. In fed animals, naloxone had no effect on water or electrolyte excretion compared to saline injected controls. However, during fasting, which has been shown to activate endogenous opioid systems, naloxone had a marked natriuretic effect (43 +/- 10 vs. 11 +/- 4 muEq/100 g X 2 h, p less than 0.05). Naloxone increased the sodium excretion to a level not significantly different from fed animals. Potassium and water excretion were not significantly changed compared to saline injected rats. The results suggest that fasting activates a naloxone-sensitive mechanism for sodium retention, perhaps by increasing the release of endogenous opioid peptides, and that refeeding inhibits this mechanism.

Animals↗
PubMed1984

Antinatriuretic effect of acute morphine administration in conscious rats.

The renal response to the acute administration of morphine was examined in conscious, chronically catheterized, nonhydrated rats. After control clearance periods, morphine sulfate was injected i.v. at 4 mg/kg followed by an infusion of 2 mg/kg X hr. Morphine caused an increase in urine flow which was variable in magnitude and duration. The initial diuresis was not maintained despite continued morphine administration and replacement of lost fluid. Compared to vehicle treatment morphine also induced marked sodium and chloride retention which was sustained throughout the 2-hr infusion period. There were no changes in blood pressure or heart during the clearance periods, although an initial transient hypotension and bradycardia were observed with morphine injection. There were no changes in glomerular filtration rate which could account for the antinatriuresis. Naloxone pretreatment blocked all of the observed renal responses. The results indicate that morphine exerts its effects on electrolyte excretion by enhancing renal tubular sodium or chloride reabsorption rather than changes in systemic hemodynamics or glomerular filtration rate. In a separate series of experiments, urine osmolality, osmolar clearance and free water clearance were estimated. All rats receiving morphine transiently excreted a hypotonic urine (minimum 183 +/- 23 mOsmol/kg of H2O) with a reduction in osmolar clearance and a sharp increase in free water clearance. These findings are consistent with a temporary inhibition of vasopressin release by morphine.

Animals↗
PubMed1983

Renal hemodynamics in conscious rats: effects of anesthesia, surgery, and recovery.

The influence of barbiturate anesthesia and minor surgical incisions on renal function was assessed in trained, chronically catheterized rats. In addition, renal hemodynamic changes during recovery from ether anesthesia and surgery were examined. Administration of pentobarbital in the chronic animals was associated with a marked reduction in arterial pressure (108 +/- 5 vs. 85 +/- 2 mmHg, P less than 0.01), renal blood flow (8.28 +/- 0.50 vs. 6.20 +/- 0.53 ml X min-1 X 100 g body wt-1, P less than 0.01), and glomerular filtration rate (1.30 +/- 0.10 vs. 0.97 +/- 0.11 ml X min-1 X 100 g body wt-1, P less than 0.01). Responses to Inactin were essentially identical. Small skin incisions during barbiturate anesthesia caused blood pressure to rise, but did not significantly change renal function parameters from already reduced values. In rats studied 2 h after ether anesthesia and surgical placement of catheters, arterial pressure was elevated compared with the same rats studied 4-7 days later (127 +/- 3 vs. 109 +/- 3 mmHg, P less than 0.005). Renal blood flow (5.80 +/- 0.37 vs. 8.90 +/- 0.93 ml X min-1 X 100 g body wt-1, P less than 0.01) and glomerular filtration rate (0.81 +/- 0.07 vs. 1.05 +/- 0.08 ml X min-1 X 100 g body wt-1, P less than 0.001) were markedly depressed during the recovery from surgery. It is concluded that barbiturate anesthesia depresses renal function in rats. This impairment should be considered when interpreting experiments that must be performed under anesthesia. In addition, the "conscious" preparation commonly used for renal studies in rats, i.e., one involving experimentation 2-3 h after ether anesthesia and surgery, is associated with a severe depression of renal hemodynamics.

Anesthesia, General↗
PubMed1982

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Animals↗
PubMed1981

Dose-dependent stimulation of renal prostaglandin synthesis by deamino-8-D-arginine vasopressin in rats with hereditary diabetes insipidus.

It has been postulated that renal prostaglandins (PGs) function as negative feedback inhibitors of the action of antidiuretic hormone (ADH), implying a correlation between levels of ADH and the rate of renal PG synthesis. These studies have evaluated the relationship between renal PG synthesis and hormone levels in rats with hereditary diabetes insipidus, a species devoid of circulating ADH. Since vasoconstrictor agents can stimulate renal PG synthesis by mechanisms unrelated to antidiuretic activity, deamino-8-D-arginine vasopressin (dDAVP) was utilized for replacement therapy instead of arginine vasopressin, which has considerable pressor activity. dDAVP was administered by S.C. implanted osmotic minipumps to obtain steady states of dDAVP at different dose levels. As indices of renal PG synthesis, urinary excretion of PGE2 and PGF2 alpha were measured by gas chromatography-mass spectrometry. PGE2 excretion, although increased by dDAVP treatment, was not correlated with dose of dDAVP. However, PGF2 alpha excretion was highly correlated with dose of dDAVP (r = 0.97, P less than .01). The sum (PGE2 + PGF2 alpha), which may more accurately reflect total medullary PG synthesis, was also significantly correlated with dose of dDAVP (r = 0.98, P less than .001). It is concluded that dDAVP stimulates renal PG synthesis in a dose-related fashion. This occurs at doses which bring urine osmolality into the normal physiological range. Furthermore, it is shown that stimulation of renal PG synthesis by arginine vasopressin is not due primarily to its pressor action. These experiments also provide evidence that urinary PGE2 and PGF2 alpha excretion can vary independently.

Animals↗
PubMed1980

Determination, source, metabolism, and functional role of renal prostaglandins.

A brief review of prostaglandin (PG) bio-chemistry of the kidney is presented. Methods of assessing renal PG synthesis are discussed and pitfalls pointed out. A role of renal PGs in renin release and water metabolism of man is shown. Experiments are described which form the basis for a hypothesis which postulates a role for renal cortical prostacyclin in renin release.

Animals↗
PubMed1978

Redistribution of intrarenal blood flow following ADH administration: lack of inhibition by blockade of prostaglandin in cyclooxygenase.

The effect of prostaglandin synthesis inhibition on the redistribution of renal cortical blood flow in response to antidiuretic hormone (ADH) was examined using radioactive microspheres in water loaded, thiopental-anesthetized dogs. Microsphere injections were made during a control and an ADH infusion period (0.35 mU/kg/min following a 20 mU/kg bolus) both before and after indomethacin pretreatment (8 mg/kg intravenously). Urinary prostaglandin E2 (PGE2) excretion in each period was measured by gas chromatography-mass spectrometry. ADH caused a marked redistribution of flow toward inner cortical zones from 19 +/- 1 to 25 +/- 2 ml/min (mean +/- SE, p less than 0.01). Fractional flow to inner zones was also significantly increased. Indomethacin pretreatment had no effect on the ADH-induced redistribution (17 +/- 2 vs. 24 +/- 2 ml/min, p less than 0.01), although urinary PGE2 excretion was suppressed by indomethacin by 60%. It is concluded that prostaglandins do not mediate the redistribution of intrarenal blood flow accompanying ADH administration.

Animals↗
PubMed1978

Antidiuretic hormone increases renal prostaglandin synthesis in vivo.

Studies demonstrating the antagonism by prostaglandins (PGs) of antidiuretic hormone (ADH) action led to the proposal that renal medullary PGs may act to attenuate the physiologic effects of ADH via a negative-feedback loop. Therefore, we examined urinary PG excretion, an indicator of renal PG synthesis, in rats with hereditary diabetes insipidus (DI) utilizing gas chromatography-mass spectrometry. The DI rats, devoid of ADH, excrete much less prostaglandin E2 (PGE2) than normal Long-Evans rats (39 +/- 5 vs. 228 +/- 53 ng/24 h, means +/- SE, P less than 0.005). DI and normal rats were treated for 35 days with ADH while separate groups of DI and normal controls received vehicle only. The ADH treatment increased urinary PGE2 excretion in DI rats to 233 +/- 35 ng/24 h whereas PGE2 excretion was unaffected by vehicle treatment. ADH treatment in normal rats similarly increased PGE2 excretion from 215 +/- 49 to 410 +/- 63 ng/24 h (P less than 0.05). To determine whether the rise in PGE2 excretion is the result of the rise in papillary osmolality, we subjected DI rats to dehydration, which increased urine osmolality from 130 +/- 10 to 302 +/- 12 mosmol/kg H2O but left urinary PGE2 unaffected. We conclude that ADH stimulates renal medullary PGE2 synthesis in vivo.

Animals↗
PubMedDate not supplied

Changes in the pulse wave form with flow through vessels with repetitive saccular dilatations and stenosis.

Several patients with fibroplasia of the renal arteries without significant stenosis were found to have surgically reversible renal hypertension. The hypothesis is advanced that receptors in the kidney may respond to altered wave form by causing an increase in blood pressure. Various models of normal and pathological renal arteries were made and tested in a pulse duplicator. A discrete harmonic analysis was made of input and output waves. The results indicate that nodular, non-stenotic models significantly alter the systolic rise in perfusion pressures to the kidney. Therefore, irregularity of vessel lumen without stenosis may be sufficient to alter organ function.

Diverticulum↗
PubMedDate not supplied

Determination of heavy metals and pesticides in ginseng products.

Medicinal plants may carry residuals of environmentally persistent pesticides or assimilate heavy metals in varying degrees. Several factors may influence contaminant accumulation, including species, level and duration of contaminant exposure, and topography. As part of a program for assessment of the quality of herbal medicines, we have analyzed 21 over-the-counter ginseng (Panax ginseng) products in various dosage forms. Chromium, mercury, and arsenic were undetectable above their limits of detection in both liquid and solid samples; while cadmium, lead, and nickel were present in the majority of samples. The chlorinated pesticide levels varied widely. In most samples, the total concentration of pesticides was below 100 ppb; while in 5 samples the total concentration exceeded 100 ppb.

Arsenic↗