摘要:

Immunoreactive β-endorphin (ir-β-END) concentrations were measured in the hypophysial portal plasma of the male rat under urethane anesthesia. On the basis of immunochemical studies and gel fitration chromatography it appears that ir-β-END in rat hypophysial portal plasma is primarily β-endorphin (β-END) and not β-lipotropin (β-LPH). In addition, much of the ir-β-END in portal plasma may be of pituitary origin since acute hypophysectomy resulted in approximately an 80% decrease in the portal plasma concentration of ir-β-END. Nevertheless, in anesthetized animals that had been hypophysectomized acutely, portal plasma concentrations of ir-β-END were still 5 times those in systemic plasma, indicative of hypothalamic secretion of the peptide. The administration of morphine sulfate (3 mg/kg, i.v.) resulted in a decrease of ir-β-END concentrations from 3,157 ± 547 pg/ml to 1,044 ± 250 pg/ml. This effect was blocked by naltrexone (1 mg/kg, s.c.) pretreatment. Capsaicin (10 µg), which, when infused into the lateral cerebral ventricle of the rat, has been shown to decrease the amount of β-END in the hypothalamus, but not elsewhere in the central nervous system, selectively decreased the concentration of ir-β-END in portal plasma without changing systemic ir-β-END concentrations. These studies indicate that ir-β-END in portal plasma is probably β-END which is derived from neurons in the hypothalamus. Moreover, it is concluded that the regulation of the release of ir-β-END from these neurons involves opiate receptor mechanisms. The inhibitory influence of opiates on ir-β-END secretion may be indicative of a classical feedback regulation of ir-β-E

ISSN:0028-3835    

DOI:10.1159/000124589

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The regulation of pituitary vasopressin (VP) receptor concentration was investigated in rats with antero-lateral cuts (ALC) placed around the hypothalamus, as well as in Brattleboro homozygotes (HO) that genetically suffer from a lack of AVP. Hypothalamic ALCs caused a reduction in (3H)-AVP binding, while counteracting the dramatic fall in binding that normally occurs after adrenalectomy. Surprisingly, in HO rats, long-term adrenalectomy did cause pituitary AVP receptor number to decrease to an extent similar to that seen in normal rats. However, the receptor disappeared twice as rapidly in heterozygote controls than in HO animals, with calculated half-lives of 1.1 and 2.0 days, respectively. In HO, chronic administration of VP reduced receptor concentration by about 80%, while the same dose of oxytocin (OT) produced only a 20–30% reduction. Whereas dexamethasone injections did reverse the depressing effect of adrenalectomy on pituitary AVP receptors, they failed to enhance binding in sham-operated controls, treated or not with VP; thereby suggesting a central site of action of the steroid. In contrast, in rats with hypothalamic ALCs (i.e. with the pituitary lacking central control), corticosterone implants did antagonize the reduction in receptor density caused by adrenalectomy. We conclude that the pituitary AVP receptor system lies mainly under control of the central nervous system, through a mechanism of action that not only seems to imply AVP and OT, but probably also some other hypothalamic factor(s). Glucocorticoids appear to exert a dual effect, acting indirectly through negative feedback control of neuropeptide release and, possibly, also directly on the pituitary to regulate binding site

ISSN:0028-3835    

DOI:10.1159/000124590

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Intraventricular perfusion with a hypertonic sodium chloride solution elicits increases in cerebrospinal fluid vasopressin and blood pressure and a decrease in heart rate. The central peptide response was greatly reduced in the hypertensive rat. Central pretreatment with the vasopressin (V1) antagonist completely abolished the pressor response to hypertonic sodium chloride in the normotensive animal. Results suggest that a central vasopressin receptor may play a role in the control of blood pressure.

ISSN:0028-3835    

DOI:10.1159/000124591

出版商:S. Karger AG    

年代:1986

数据来源: Karger