Prostanoid generation in early stages of acute pancreatitis: A role for nitric oxide
Daniel ClosaGeorgina HotterNeus PratsO. BulbenaJoan Roselló‐CatafauLaureano Fernández‐CruzEllen Gelpí
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Keywords:
Eicosanoid metabolism
Prostanoid
Eicosanoid metabolism
Prostanoid
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Cyclic guanosine monophosphate
Pancreatic Islets
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The effects of chronic neonatal hyperthyroidism in rats on the ontogenic pattern of serum corticosterone and growth hormone (GH) were studied. Thyroxine (T4) treated and saline injected rat pups were sacrificed under basal and stress conditions. In comparison to saline control animals, daily T4 administration (0.4 micrograms/gram body weight) produced a sustained elevation in basal corticosterone levels by day 12 and a significant elevation of serum corticosterone in response to stress by day 4. The serum GH levels in non-stressed animals were moderately decreased in response to T4 administration as compared to saline injected animals with a greater reduction in GH measured in samples obtained from stressed animals. The results indicate that chronic T4 administration influences the developmental pattern of serum corticosterone and GH under both non-stress and stress conditions.
Corticosterone
Basal (medicine)
Chronic Stress
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We investigated the effects of thyroid status on nitric oxide synthase (NOS) gene expression in the rat hypothalamic paraventricular (PVN) and supraoptic nuclei (SON). Propylthiouracil (PTU)-induced hypothyroidism in male rats produced a highly significant reduction in NOS gene transcripts in the PVN and SON, as assessed by quantitative in situ hybridization histochemistry with a specific oligodeoxynucleotide probe. The addition of T3 (40 micrograms/kg) to the PTU-containing diet completely prevented the reduction in NOS transcripts. Hyperthyroidism, induced by adding 160 micrograms/kg T3 to the food, more than doubled the prevalence of NOS transcripts in the PVN and SON after a similar time. Up-regulation of NOS gene transcripts induced by the osmotic stimulus of chronic salt loading was markedly attenuated by PTU-induced hypothyroidism. These results demonstrate a major effect of thyroid status on regulation of NOS gene expression in the hypothalamus.
Propylthiouracil
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The studies reported herein were conducted to confirm that the pituitary gland is involved in maintaining growth hormone (GH) resistance in rats with insulin-dependent diabetes mellitus (IDDM) and to determine whether the adrenocorticotropic hormone (ACTH)-adrenal cortical axis is responsible. The rats were made diabetic by injecting streptozotocin (85 mg/kg body wt) IP once daily on two consecutive days. They were then injected with 15 IU Insulin SC twice daily on two consecutive days to enable them to survive hypophysectomy or adrenalectomy. Intact nondiabetic (NonDb), diabetic (Db), hypophysectomized diabetic (HxDb), and adrenalectomized diabetic (AxDb) rats were injected twice daily with 50 μg porcine (p) GH or with 0.9% saline for 2 weeks following the surgeries. Serum glucose levels of the saline-injected Db, HxDb, and AxDb rats were significantly greater than those of the NonDb rats by 106%, 65% and 49%, respectively. However, the levels in the HxDb and AxDb animals were significantly lower than those of the Db group by 20% and 28%, respectively. Injections of pGH into NonDb rats increased serum glucose concentrations by 38%, over their saline-treated controls, and by 29% in AxDb rats. This diabetogenic effect of GH was not seen in any other group. Administration of pGH to Db rats failed to increase body weight gain, tail growth, tibial epiphysial plate width, or serum IGF-I concentration over saline-injected controls. By contrast, HxDb and AxDb rats injected with pGH showed significant increases in all four growth parameters. Total serum IGF-I concentrations in AxDb rats injected with pGH equaled those in NonDb controls. To determine whether the lack of corticosterone (B) in the AxDb rats was responsible for the reduced hyperglycemia and restored responsiveness to pGH, AxDb rats were given B in their drinking water at 5 or 25 μg/ml. Administration of B reduced the beneficial effects of adrenalectomy by restoring hyperglycemia and growth impairment, and partially restored resistance to the pGH injections. These studies confirm that the pituitary contributes to diabetic growth impairment and show that the ACTH-adrenal cortical axis is primarily responsible for the GH-resistant state that develops in rats with IDDM.
Hypophysectomy
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Abstract We have investigated the effects of food deprivation on nitric oxide synthase (NOS) transcript levels in the rat paraventricular (PVN) and supraoptic nuclei (SON), using in situ hybridization histochemistry. Food deprivation for 48 h significantly and consistently reduced NOS transcript prevalence by approximately 50% in both sites. Since there is considerable evidence for an important role of 5‐HT in feeding behaviour, we then examined the effect of food deprivation on NOS gene expression in the PVN following para ‐chlorophenylalanine (PCPA)‐induced hypothalamic 5‐HT depletion. As starvation causes central down‐regulation of the thyroid axis, changes in thyrotropinreleasing hormone (TRH) and pituitary thyrotrophin (TSH) transcript prevalence were used as internal controls. PCPA pretreatment (200 mg/kg body weight as a single daily dose ip for 2 days) had no significant effect on basal levels of NOS, TRH or TSH transcripts, or on the effect of a subsequent 48 h fast, which significantly reduced all three. These results show for the first time, that food deprivation for 48 h significantly reduces NOS gene expression in the rat PVN and SON. Secondly, that basal levels and the fasting‐induced reductions in the prevalence of NOS, TRH and TSH transcripts were not affected by PCPA‐induced hypothalamic 5‐HT depletion. Therefore, at least under the experimental conditions used here, 5‐HT does not appear to be involved in setting baseline levels—or in the starvation‐induced inhibition of NOS or thyroid axis gene expression in the PVN.
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The sequential metabolism of eicosanoids by AA oxygenases confers biological properties that may have significant functional implications. Further, the interpretation of the effects of cyclooxygenase inhibitors on eicosanoid, dependent mechanisms needs to be reevaluated. Previously, if cyclooxygenase inhibitors affected the biological action of AA, it was considered to be due to elimination of a prostanoid-mediated component. This interpretation is no longer valid if a cell or tissue has significant P450 and cyclooxygenase activity. The cellular proximity of the P450-dependent monooxygenases and cyclooxygenase, described in tubules, interstitial cells, and blood vessels, may confer a unique ability of AA metabolites to coordinate tubular and vascular function.
Prostanoid
Eicosanoid metabolism
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The changes in the levels of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) in the neurointermediate lobe of the pituitary (NIL) following hypertonic saline administration were examined in rats. The plasma osmotic pressure in rats receiving 2% NaCl for 8 days was greatly increased. Plasma AVP concentration in rats receiving 2% NaCl for 8 days were significantly higher than in control rats (566% of the control level). Plasma corticosterone was significantly higher in the saline-treated rats than in controls, whereas plasma ACTH was not significantly different. The pituitary ACTH concentration was much higher in the saline-treated rats than in controls. CRH in the NIL was increased significantly by saline treatment (419% of the control concentration), whereas the CRH in the paraventricular nucleus and median eminence of control and saline-treated rats did not differ significantly. The AVP in the NIL fell greatly in saline treated rats. The extract from both control and saline-treated rats showed a major peak for immunoreactive CRH, with a retention time identical to that of rat CRH. However, the peak was much higher in the extract from saline-treated rats. The immunoreactive AVP peak was greatly reduced in saline-treated rats. These results suggest that hypertonic saline administration increases the CRH in the NIL and causes AVP hypersecretion and/or hyperfunction of magnocellular-NIL CRH might be responsible for pituitary-adrenal stimulation in saline-treated rats.
Hypertonic saline
Median eminence
Corticosterone
Corticotropin-releasing hormone
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The effect of N-acetylserotonin (NAS) on serum levels of thyroid-stimulating hormone (TSH) in the male rat was investigated. In the first experiment, NAS and carrier were injected intraperitoneally into rats. The animals were sacrificed 30 and 60 min after injection. It was found that NAS (100 micrograms/rat) significantly depressed serum TSH 60 Min after injection when compared with saline-injected controls. In another experiment in which samples were obtained from rats at 0, 30, 60, 90 and 120 min after injection, significant decrease in serum TSH was observed at all time intervals after NAS (100 micrograms/rat) injection while no such difference was observed in the saline-injected groups. It is suggested that NAS may exert an inhibitory effect on TSH secretion.
Thyroid-stimulating hormone
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