Expression of the ammonia transporter proteins Rh B glycoprotein and Rh C glycoprotein in the intestinal tract.

Ammonia metabolism is important in multiple aspects of gastrointestinal physiology, but the mechanisms of ammonia transport in the gastrointestinal tract remain incompletely defined. The present study examines expression of the ammonia transporter family members Rh B glycoprotein (RhBG) and Rh C glycoprotein (RhCG) in the mouse gastrointestinal tract. Real-time RT-PCR amplification and immunoblot analysis identified mRNA and protein for both RhBG and RhCG were expressed in stomach, duodenum, jejunum, ileum, and colon.

Roles of interleukin 1 beta and tumor necrosis factor in lipopolysaccharide fever in rats.

The roles of interleukin 1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF) in lipopolysaccharide (LPS)-induced fever were investigated in the rat. We used antisera against IL-1 beta and TNF to determine whether we could alter the fever by blocking the action of these cytokines. The intravenous injection of antiserum IL-1 beta 3.

The effects of pentoxifylline on lipopolysaccharide (LPS) fever, plasma interleukin 6 (IL 6), and tumor necrosis factor (TNF) in the rat.

The purpose of these studies was to test whether pentoxifylline, a drug that can inhibit the production and action of cytokines hypothesized to be endogenous pyrogens (for example, interleukin 1 and tumor necrosis factor [TNF]), is antipyretic. We also tested the effects of pentoxifylline on plasma activities of interleukin 6 (IL 6) and TNF in response to an injection of a fever-inducing dose of lipopolysaccharide (LPS). Our results showed that a high dose of pentoxifylline (200 mg/kg) caused hypothermia in control rats and blocked LPS fever, while a low dose (50 mg/kg) did not have these effects.

The effects of psychological stress on plasma interleukin-6 activity in rats.

The purpose of this study was to determine the effects of a particular psychological stress, exposure to an open-field, on plasma IL-6 activity in rats. Plasma IL-6 activity was 40.6 +/- 7.

In vivo evidence that the rise in plasma IL 6 following injection of a fever-inducing dose of LPS is mediated by IL 1 beta.

Although it has often been speculated that Interleukin (IL) 1 alpha and IL 1 beta are circulating endogenous pyrogens (EP), there are few data demonstrating an elevation of these cytokines in the plasma of febrile animals. We hypothesized that IL 1 is released locally and may act to stimulate the release of another pyrogen, IL 6, which circulates to the brain to cause fever. The major purpose of the present study was to determine whether pretreatment of rats with antiserum to IL 1 beta, which attenuates lipopolysaccharide (LPS) induced fever, also results in an attenuation of the rise in plasma and cerebrospinal fluid (CSF) concentrations of IL 6.

Stress-induced rise of body temperature in rats is the same in warm and cool environments.

Several forms of psychological stress result in a rise in body temperature in rats. In this study, we report that rats housed at a low ambient temperature (11.1 degrees C) develop stress-induced rises in body temperature that do not differ from the responses seen when the animals are kept at a temperature within their thermoneutral zone (24.

Temperature regulation in biotelemetered spontaneously hypertensive rats.

Core temperature of the spontaneously hypertensive rat (SHR) was not found to be different from the core temperature of the control rat, the Wistar-Kyoto rat (WKY), when the rats were left undisturbed in their home cages. When the rats were exposed to a variety of stressful environments, including cage switching, exposure to an open field, and handling, both SHR and WKY rats showed an increase in temperature. For the set of rats supplied by Charles River, the SHR temperature response to the stress was identical to the WKY rats' temperature response.

Role of interleukin 6 in fever in rats.

The purpose of these studies was to assess whether interleukin 6 (IL-6) is an endogenous pyrogen, responsible for all or part of the fever caused by lipopolysaccharide (LPS) in rats. We have found that the core temperature (as measured by biotelemetry) rose significantly after intracerebroventricular (icv) injection of recombinant human IL-6. The same doses of IL-6, when administered intravenously or intraperitoneally, had no effect on body temperature.

Antiserum against tumor necrosis factor increases stress hyperthermia in rats.

Psychological stress (e.g., exposure to a novel environment) causes a rapid rise in body temperature in rats.

Antiserum against tumor necrosis factor enhances lipopolysaccharide fever in rats.

The role of tumor necrosis factor (TNF, cachectin), a putative endogenous pyrogen, was investigated by comparing fever and plasma TNF levels after the intraperitoneal and intramuscular injection of 10 micrograms/kg lipopolysaccharide (LPS) into male Sprague-Dawley rats and by neutralization of endogenous TNF using TNF antiserum. An intraperitoneal injection of LPS caused a biphasic fever that lasted approximately 6.5 h.

Net renal tubular reabsorption of zinc in healthy man and impaired handling in sickle cell anemia.

Zinc deficiency is a significant clinical finding in sickle cell anemia (SCA) and abnormalities of zinc handling such as hyperzincuria are present. The cause of increased urinary zinc excretion in SCA is not clear. To define the renal handling of zinc in SCA and in healthy subjects, we measured zinc (total and ultrafilterable plasma zinc, urine zinc) and creatinine clearance in eight healthy and seven SCA subjects.

Human circadian rhythms in temperature, trace metals, and blood variables.

The literature supports the concept that circadian changes in body temperature reflect changes in the thermoregulatory set point. We were interested in studying the relationship between the circadian rhythm in body temperature and 24-h variations in plasma concentrations of iron, zinc, circulating leukocyte counts, and plasma interleukin 1 (IL-1) activity. Eight healthy men were studied for two separate 48-h sessions.

Chronic effects of lead on the renin-angiotensin system.

This paper reviews the chronic effects of lead exposure on the renin-angiotensin system in experimental animals and human beings. In rats, when lead exposure is begun several weeks after birth in doses that cause blood lead concentrations (PbB) of 30 to 40 micrograms/dL, the result is an increase in basal plasma renin activity (PRA) and renal renin concentration, with no change in the metabolic clearance of renin; this is presumptive evidence for increased renin secretion. PRA is also increased in 1-month-old animals whose exposure to lead (in doses that raise PbB to 9 micrograms/dL) was begun in utero.

Effects of chronic infusion of lipopolysaccharide on food intake and body temperature of the rat.

Unrestrained male Sprague-Dawley rats were infused for seven days with a low (2.45 micrograms/hr) or high (9.81 micrograms/hr) concentration of E.

Increased vasodilator responses to acetylcholine in psychosocial hypertensive mice.

Responsiveness to endothelium-dependent (acetylcholine and A23187) and endothelium-independent (nitroprusside and 8-bromo cyclic guanosine 3',5'-monophosphate [cGMP]) vasodilators was examined in two vascular preparations from hypertensive and normotensive mice. CBA Agouti mice were made hypertensive by exposure to social stress in a complex population cage. After 2 months, the hindquarter vascular bed was pump-perfused at a constant flow with plasma substitute to evaluate changes in perfusion pressure, and helical strips of aorta were suspended in muscle baths for measurement of isometric force generation.

Further evidence that stress hyperthermia is a fever.

Exposure of rats to an open-field results in a rapid rise in body temperature. Fifty-four percent of this rise in body temperature was blocked by intracerebroventricular administration of the antipyretic drug sodium salicylate. Intraperitoneal administration of indomethacin, a potent blocker of prostaglandin production, also attenuated the stress-induced hyperthermia to the same degree.

Hyperthermia induced by open-field stress is blocked by salicylate.

Psychological stress results in a rise in body temperature. Here we report that in rats, hyperthermia induced by open-field stress can be blocked by administration of the antipyretic drug sodium salicylate. These data suggest that this rise in body temperature is a true fever, perhaps mediated by prostaglandins.

Effect of centrally administered interleukin-1 and endotoxin on food intake of fasted rats.

We have previously shown that interleukin-1 (IL-1), a polypeptide known to mediate many aspects of the acute phase response to infection, suppresses food intake when injected intraperitoneally into fasted rats. IL-1 acts at the level of the hypothalamus to induce fever. In view of the large number of peptides that have been shown to alter food intake as well as body temperature when injected intracerebroventricularly (ICV), we hypothesized that the receptor site for the anorexigenic activity of IL-1 would be located in a central nervous site bathed by the cerebrospinal fluid.

Suppression of food intake during infection: is interleukin-1 involved?

Loss of food appetite is a common manifestation of acute infectious illness and is believed to contribute to the negative nitrogen balance and loss of body weight that is seen during infection. The frequency with which anorexia occurs with infection suggests that it may be part of the acute phase response. In the present experiments, food intake of fasted rats was suppressed following injection of interleukin-1, a polypeptide that mediates many host responses to infection.

The role of fever in appetite suppression after endotoxin administration.

In order to test the hypothesis that fever, and not some other aspect of the acute phase response, decreases food intake after administration of endotoxin, food intake of rats was studied under conditions of 1) fever, 2) antipyresis, and 3) endotoxin tolerance. Injection of endotoxin resulted in a significant elevation in rectal temperature and a significant reduction in food intake. Administration of the antipyretic drug sodium salicylate to endotoxin-injected animals lowered rectal temperatures to control levels, but food intake was still suppressed.

Clearance of renin in unanesthetized rats: effects of chronic lead exposure.

These experiments studied the influence of chronic lead exposure on the steady-state clearance of exogenous homologous renin in unanesthetized, unrestrained rats. Relative to time controls (TC), rats chronically exposed to 500 ppm lead in drinking water had significantly elevated basal plasma renin concentrations (PRC) (Pb = 12.0 +/- 1.

Effects of lead on the secretion and disappearance of renin in rabbits.

The disappearance rate of renin from plasma was evaluated in both acutely and chronically lead-exposed rabbits. In addition, the effects of lead (Pb) on in vitro renin secretion were determined with rabbit renal cortical slices. Rabbits acutely exposed to Pb (0.

Insulin is a physiological inhibitor of urinary zinc excretion in anesthetized dogs.

Renal clearance experiments were performed on anesthetized dogs to determine the role of insulin in regulation of urinary zinc excretion. Intravenous infusion of somatostatin (2 micrograms/min) increased zinc excretion by approximately 100%, in association with 67% decreases in the plasma concentrations of both insulin and glucagon. Infusion of insulin (30 mU X kg-1 X min-1) along with the somatostatin maintained plasma insulin constant and completely eliminated the somatostatin-induced hyperzincuria; indeed, a small decrease in zinc excretion invariably occurred.

Effect of parathyroid hormone on renin secretion.

The ability of parathyroid hormone (PTH) to increase renin secretion was investigated in pentobarbital-anesthetized dogs. An intravenous infusion of bovine PTH 1-34, at the dose of 0.028 microgram/kg-1 min-1 increased renin secretion by 149% (501 +/- 105 to 1249 +/- 309 ng hr-1 min-1); renin secretion returned to control values during the recovery period.