Galanin affects vasopressin and oxytocin release from the hypothalamo-neurohypophysial system in haemorrahaged rats.

The effect of centrally administered galanin (Gal; 100 pM i.c.v.) on the hypothalamo-neurohypophysial storage as well as blood plasma level of vasopressin and oxytocin was estimated in haemorrhaged (1 ml per 100 g b.w.) male Wistar rats. Gal i.c.v. treatment did not alter vasopressin and oxytocin content both in the hypothalamus and neurohypophysis as well as their concentration in blood plasma of not haemorrhaged rats. Haemorrhage decreased the hypothalamic and neurohypophysial vasopressin and oxytocin storage but increased the neurohormones plasma level in animals injected with vehicle solution. During the haemorrhage, the increase in plasma vasopressin and oxytocin was inhibited in rats previously treated i.c.v. with galanin. The hypothalamic and neurohypophysial vasopressin as well as oxytocin content significantly increased in animals treated with galanin and subsequently haemorrhaged. These results suggest that galanin may have a regulatory role in the hypothalamo-neurohypophysial function especially under condition of hypovolemia.     

Effect of endothelin-1 on release of arginine-vasopressin from perifused rat hypothalamus

Endothelin-1 (ET-1) is an endothelium-derived vasoconstrictor peptide with potent pressor activity. We studied the effect of ET-1 on release of arginine-vasopressin (AVP) from perifused rat hypothalamus. ET-1 (10(-10) to 10(-8) M) significantly stimulated AVP release. The ET-1-induced AVP release was completely blocked in the presence of nicardipine. Our results suggest a possible involvement of ET in the regulation of AVP release.     

Galanin influences vasopressin and oxytocin release from the hypothalamo-neurohypophysial system of salt loaded rats.

Galanin is a peptide present in the nervous system and peripheral tissues which exerts a broad range of physiological functions. The influence of centrally administered galanin (Gal; 100 pM i.c.v.) on arginine vasopressin (AVP) and oxytocin (OT) content in the hypothalamus and neurohypophysis as well as on their blood plasma concentration was estimated in male Wistar rats drinking ad libitum 2% solution of natrium chloride per 48 hours. In euhydrated rats and subsequently applied i.c.v. with Gal a significant fall in the hypothalamic and neurohypophysial content of OT but not AVP was observed, however, without simultaneous changes in these neurohormones blood plasma concentration. On the contrary, i.c.v. injection of Gal to salt-loaded rats caused a marked raise in AVP and OT level in the hypothalamus and neurohypophysis with subsequent diminution of both neurohormones concentration in blood plasma. These results suggest that in euhydrated rats Gal has an inhibitory influence on the biosynthesis as well as axonal transport of OT, but not AVP. On the contrary, in salt-loaded rats galanin restricts secretion of both neurohormones into the systemic circulation.     

Centrally administered galanin modifies vasopressin and oxytocin release from the hypothalamo-neurohypophysial system of euhydrated and dehydrated rats.

Galanin (Gal) as a neuropeptide with widespread distribution in the central nervous system may be involved in the mechanisms of vasopressin (AVP) and oxytocin (OT) release from the hypothalamo-neurohypophysial system. Vasopressin and oxytocin content in the hypothalamus and neurohypophysis as well as plasma level of both neurohormones were studied after galanin treatment in euhydrated and dehydrated rats. In not dehydrated rats intracerebroventricular (i.c.v.) injections of Gal did not affect the hypothalamic and neurohypophysial OT content, however, distinctly increased plasma OT concentration. In the same animals Gal diminished the hypothalamic AVP content but was without the effect on neurohypophysial AVP storage; plasma AVP level then raised. Galanin, administered i.c.v. to rats deprived of water, distinctly inhibited AVP and OT release from the hypothalamo-neurohypophysial system. Simultaneously, plasma AVP and OT level was significantly diminished after Gal treatment in dehydrated rats. These results suggest that modulatory effect of galanin on vasopressin and oxytocin release depends on the actual state of water metabolism. Gal acts as an inhibitory neuromodulator of AVP and OT secretion under conditions of the dehydration but stimulates this process in the state of equilibrated water metabolism.     

Production of acetaldehyde from ethanol byCandida utilis

Summary Ethanol-adaptedCandida utilis efficiently converted ethanol to acetaldehyde, a chemical feedstock of recognized importance. Acetaldehyde which has a low boiling point (21°C) readily evaporates and is easily recovered, thus this bioconversion could provide an energy saving process for efficient recovery of a useful product from low concentrations of ethanol.     

Effects of veratridine on Ca fluxes and the release of oxytocin and vasopressin from the isolated rat neurohypophysis

Uptake of radioactive calcium, 45Ca efflux, and hormone release from the isolated rat neurohypophysis were monitored in vitro after the addition of veratridine to the incubation medium. Veratridine dramatically increased hormone release, but the release was not sustained and had declined by about 90% after 2 h. Removal of external Na+ prevented hormone release as did addition to the incubation medium of tetrodotoxin or the calcium antagonists D600 and Mn2+ ions. Veratridine increased 45Ca uptake into the isolated neurohypophysis and the increase could be prevented by addition of tetrodotoxin or D600 to the medium. Efflux of 45Ca was not changed by addition of veratridine. The results underline the importance of both Na+ and Ca+2 channels in the regulation of secretion of neurosecretory products.     

Catecholamines in the tissues and blood of rats after administration of acetaldehyde and ethanol

Acetaldehyde alone and in combination with acute and chronic ethanol intoxication has been studied for its effect on the concentration of epinephrine and norepinephrine in different brain areas, in the heart muscle, in adrenals and blood plasma of rats. Acetaldehyde is shown to enhance the epinephrine and norepinephrine levels in the brain areas which are non-specific for neuromediation of the mentioned catecholamines. The joint administration of acetaldehyde and ethanol increased the epinephrine concentration in adrenals probably due to the effect of acetaldehyde. On the contrary, the norepinephrine concentration in the heart decreased because of the action of ethanol. The authors' data show that acetaldehyde becomes an inductor of the mechanisms of hormone-mediator dissociation, thus altering the functions of vegetative-adrenal system. The results of the investigation support the hypothesis that acetaldehyde plays a significant role among pathogenic factors of ethanol intoxication, since it changes in a special way the catecholamine concentration in the brain and in peripheral tissues.     

Kinetics of ethanol and acetaldehyde release suggest a role for acetaldehyde production in tolerance of rice seedlings to micro-aerobic conditions

BACKGROUND AND AIMS: This paper examines the basis of the greater tolerance of an indica rice cultivar FR13A to complete submergence compared with relatively intolerant japonica rice CT6241. We study whether this superior tolerance is related to its greater tolerance to O2 shortage and to an ability to run a more favourable rate of alcoholic fermentation during and after O2 deprivation. METHODS Fermentation products were analysed using sensitive laser-based photoacoustics at high time resolution to establish patterns and rates of ethanol and acetaldehyde emission by intact rice seedlings exposed to micro-aerobic (0.05-0.5 % O2) or zero O2 supply, and also during their return to air. Oxygen and CO2 emission or uptake was also quantified. KEY RESULTS: In the dark, no acetaldehyde and ethanol emission was observed until external O2 concentration in a gas phase decreased to 相似文献   

Artifactual production and recovery of acetaldehyde from ethanol in urine

Ethanol (1575 mg/L) incubated with fresh urine from healthy, ethanol-free subjects yields acetaldehyde. The concentration of acetaldehyde depends upon temperature, time of incubation, and pH. In samples made hypertonic with sodium chloride (200 mg/mL) and in samples filtered through 0.45-micron membranes, acetaldehyde production was not decreased. L-Ascorbic acid (0.1 mg/mL) added to normal pooled urine caused a threefold increase in acetaldehyde production but thiourea (7.6 mg/mL) stopped it. This suggests that the oxidation of ethanol to acetaldehyde is catalyzed by the semidehydroascorbate peroxy radical of ascorbic acid. Recovery of acetaldehyde added to urine was less than 100% over the pH range 1.5 to 10. Relative to blood, artifactual production of acetaldehyde from ethanol in urine is more easily controlled and is up to an order of magnitude less but corrections for the variables above are still required.     

Changes in the blood of Wistar rats in acute poisoning with ethanol and acetaldehyde

1. The purpose of the study was to investigate the effect of ethanol and acetaldehyde on the erythrocyte and leucocyte system of Wistar rats. 2. Administration of the ethanol or acetaldehyde caused a considerable drop in the number of erythrocytes, haemoglobin level and haematocrit value in rats. 3. The mean erythrocyte volume was smaller after only 0.5 hr of exposure to ethyl alcohol. 4. The solutions used caused changes in the leucocyte system expressed in distinct neutrophilic leucocytosis. 5. Changes in the leucogram were reflected in the increase in the leucocyte index. 6. The degree of intensity of changes in both the erythrocyte and leucocyte system point to the greater toxicity of ethyl alcohol intoxication than is the case of acetaldehyde in a toxically corresponding dose (i.e. 0.5 and 5 g/kg body wt respectively).     

Co-transport of sex hormone-binding globulin/SHBG with oxytocin in transport vesicles of the hypothalamo-hypophyseal system.

The intrinsic expression of sex hormone binding globulin (SHBG) in magnocellular hypothalamic neurons, in part co-localized with either vasopressin or oxytocin, was recently described. This study is focused on the ultrastructural localization of SHBG in the hypothalamo-neurohypophyseal pathway in rats. Immunostaining for SHBG in the hypothalamic perikarya was increased by colchicine treatment, indicating that the steroid-binding globulin is subject to rapid axoplasmic transport along with the classical posterior lobe peptides. With immunoelectron-microscopic double labeling, we found co-localization of oxytocin and sex hormone binding globulin in a portion of the large dense-core vesicles in paraventricular and supraoptic perikarya and in axonal varicosities in the median eminence and in the posterior lobe. Our observations show that SHBG is processed, transported and stored along with oxytocin suggesting that SHBG is released from nerve terminals in the posterior lobe, the median eminence and possibly the brain similarly to and in conjunction with oxytocin.     

Absence of negative feedback by oxytocin on release from magnocellular neurones in conscious rats.

Peripheral administration of vasopressin (VP) was previously shown to exert a negative feedback influence on its own release and on the release of oxytocin (OT). In this study we examined the possible influence that OT has on the function of hypothalamic magnocellular neurones. Oxytocin was administered intraperitoneally and its effects on release from VP neurones and from OT neurones were determined as indexed by plasma concentrations of vasopressin-associated neurophysin ([VP-RNP]) and oxytocin-associated neurophysin ([OT-RNP]) under basal conditions and conditions of high plasma osmolality (Posm) induced by acute salt loading. Studies were performed on conscious, chronically instrumented Long-Evans rats. Oxytocin (1 nmol or 10 nmol) dissolved in 1 mL of 0.9% saline was administered intraperitoneally to animals 1 h before they received an intravenous infusion of hypertonic saline over 60 min at a rate designed to raise Posm by approximately 0.75 mosmol.min-1. Intraperitoneal injection of vehicle or 1 nmol of OT did not significantly alter [VP-RNP], [OT-RNP], or basal Posm. Administration of 10 nmol OT also had no effect on [VP-RNP] or [OT-RNP], but this dose of peptide significantly lowered basal Posm (299 +/- 2 to 290 +/- 2 mosmol/kg H2O, p less than 0.001). Both doses of OT did not significantly alter the responsiveness of VP neurones to hyperosmotic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Plasma and liver amino acids in rats after administration of ethanol or acetaldehyde

The changes in the level and pattern of free amino acids in plasma and liver after ethanol or acetaldehyde intoxication has been investigated in rats. After administration of 30% (w/v) ethanol, 6 g kg-1, or 1.5% (w/v) acetaldehyde, 0.3 ml kg-1, for 4 weeks we found a decrease in plasma and liver branched-chain amino acids and an increase in plasma aromatic amino acids and methionine. The results are analogous to those found in studies of damaged liver.