摘要:

Specific binding sites for vasopressin (AVP) were compared in the kidney and posterior pituitary gland from normal and homozygous Brattleboro rats using autoradiography with [3H]-AVP. The specificity of ligand binding was assessed by displacement with AVP analogues differing in specificity and potency. In the kidney, specific [3H]-AVP binding was found in the medulla, with much less in the cortex, in both normal and Brattleboro rats. Binding of [Η]-AVP was displaced most effectively by dDAVP and least by AVP-OH, in line with their relative antidiuretic potencies. In the pituitary gland, specific AVP binding was much higher in the posterior lobe than in the intermediate or anterior lobes. This posterior lobe AVP binding was greatly reduced in Brattleboro rats, even in animals given exogenous AVP to restore their water balance. It was unlikely that neurophysin binding was responsible since there was no correlation between [3H]-AVP displacement and neurophysin binding in a series of analogues slightly modified at the N or C terminus to affect selectively neurophysin or receptor binding. We suggest that specific AVP receptors may be present in the posterior pituitary gland, possibly on or in the AVP terminals themselves, associated with the normal synthesis, packaging and/or transport of AVP granules to the neural lobe

ISSN:0028-3835    

DOI:10.1159/000125013

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Male rats were treated acutely with nicotine (4 × 2 mg/kg, 30-min time intervals, total treatment time 2 h) or exposed to cigarette smoke from 4 × 1 cigarette (30-min time intervals, total treatment time 2 h). Some rats were pretreated with the Dl dopamine (DA) receptor antagonist SCH 23390 (0.1–3.0 mg/kg, i.p.), or with the D2 DA receptor antagonists remoxipride and raclopride (1 mg/kg, i.p.), or with the 5-hydroxytryptamine 2 (5-HT2) receptor antagonist ketanserin (0.3 mg/kg, i.p.) 5 min before nicotine treatment or the acute intermittent exposure to cigarette smoke. Some rats were treated with the Dl DA receptor agonist SK&F 38393 (1–10 mg/kg, i.p.) 15 min, 30 min or 2 h before decapitation. Hypo-thalamic and pre-optic catecholamine (CA) levels were measured by quantitative histofluorimetry in discrete DA and noradrenaline (NA) nerve terminal systems. Serum thyroid-stimulating hormone (TSH), prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), vasopressin, corticosterone and testosterone levels were determined by radio-immunoassay procedures. Nicotine treatment and to a minor degree also acute intermittent exposure to cigarette smoke produced a reduction in serum prolactin, LH and TSH but not in serum FSH, vasopressin and testosterone levels. Nicotine treatment also increased serum corticosterone levels. Pretreatment with the Dl DA receptor antagonist SCH 23390 (1–3 mg/kg) counteracted the lowering of serum LH, but not of prolactin and TSH levels induced by nicotine or exposure to cigarette smoke. SCH 23390 alone (1–3 mg/kg) increased serum TSH levels. Remoxipride, raclopride or ketanserin did not counteract any of the neuro-endocrine actions induced by nicotine treatment. However, ketanserin alone lowered serum prolactin levels. SK&F 38393 increased serum TSH, prolactin and LH levels. It was found that nicotine treatment and exposure to cigarette smoke with few exceptions produced a depletion of CA stores in NA and DA nerve terminals of the hypothalamus, pre-optic area and median eminence which was counteracted by SCH 23390 (1 mg/kg) but not by remoxipride, raclopride (1 mg/kg) or ketanserin (0.3 mg/kg). The results indicate that Dl but not D2 DA or 5-HT2 receptors may modulate the NA and DA release in the median eminence, the hypothalamus and the pre-optic area induced by nicotinic cholinoceptor activation. Furthermore, Dl DA receptors in the median eminence may at least in part mediate the inhibitory effects of nicotine on LH but not on TSH and prolactin secretion, although there appears to exist a Dl DA receptor in the median eminence which inhibits TSH secretion. The results are in line with our hypothesis that activation of the tubero-infundibular DA neurons via Dl DA receptors mediates the inhibition of LH secretion caused by nicotine treatment or exposure to cigarette smoke. Finally, the facilitatory serotonergic mechanism on prolactin secretion is probably mediated via 5-HT2

ISSN:0028-3835    

DOI:10.1159/000125007

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The development of melatonin receptors in the rat pituitary and median eminence was studied using [125I]melatonin as a ligand. The specific binding was detected in pituitaries of 20-day-old fetuses already. The affinity of the receptor to the ligand (Kd) was in the range 63–133 pM and it did not change significantly during development. The pituitary concentration of [125I]melatonin binding sites was highest in 20-day-old fetuses (Bmax = 31 fmol/mg protein) and then it gradually decreased in the course of postnatal development, until it reached 10% of that value in 29-day-old males. In contrast, the concentration of melatonin receptors in median eminence did not change markedly in the course of development and it was about 15 fmol/mg protein. The marked decrease in the number of the pituitary receptors may be the cause of the reported developmental loss of the melatonin inhibitory effect on LHRH-induced LH release from anterior pituitar

ISSN:0028-3835    

DOI:10.1159/000125008

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

In previous studies we demonstrated that exogenous oxytocin induces a decrease of basal and stimulated cortisol and ACTH plasma levels in the normal male. To rule out the possibility that oxytocin could also act at the adrenal level, we tested, in the present work, the influence of exogenous oxytocin on the cortisol increase secondary to the intravenous injection of a supraphysiological dose (0.25 mg) of synthetic ACTH1–24 (Synachten) in 9 normal male volunteers. We demonstrate that oxytocin infusion does not modify the ACTH plasma levels but, however, induces a decreased cortisol response to ACTH1–24. These results support the hypothesis that, beside its hypophysial inhibitory action on ACTH release, oxytocin acts also at the adrenal gland level to decrease cortisol release and/or synthesis in normal human subje

ISSN:0028-3835    

DOI:10.1159/000125009

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

We studied neuropeptide Y (NPY) binding sites in the bovine adrenal gland by incubating tissue sections with [125I]-Bolton Hunter NPY, and then by measuring the number and affinity of binding sites in the tissue with quantitative autoradiography. Specific NPY binding sites were localized exclusively in the zona glomerulosa. These binding sites have an apparent dissociation constant (Kd) of 0.45 ± 0.06 nM and a binding capacity (Bmax of 134 ± 15 fmol mg–1 protein. Our results suggest that NPY may directly affect the release of aldosterone in the zona glomerulosa of the adrenal gl

ISSN:0028-3835    

DOI:10.1159/000125010

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Among the enzymes capable of degrading thyrotropin-releasing hormone (TRH) in vitro, two pyroglutamate aminopeptidases (PGA) are specific for TRH: thyroliberinase, a seric enzyme and PGAII, a membrane-bound peptidase. The effect of thyroid hormone status on the activity of these enzymes was evaluated in serum and various tissues. Only in adenohypophysis, triiodothyronine treatment increased PGAII to 376% of control; hypothyroidism produced the reverse effect (decrease to 23% of control). As previously reported, similar changes were observed for thyroliberinase. TRH degradation at the adenohypophysis level may participate in the negative feedback control of thyroid hormones.

ISSN:0028-3835    

DOI:10.1159/000125011

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Recent studies have demonstrated that oxytocin (OT) stimulates prolactin (PRL) release from the anterior pituitary gland and that the secretion of OT into pituitary portal blood changes during the rat estrous cycle. To better define the role of OT on PRL release during the reproductive cycle, the effect of administration of antiserum specific for OT on preovulatory PRL secretion in female rats was studied. Intravenous injection of OT antiserum into cyclic female rats between 13.30 and 14.00 h of proestrus neutralized the elevated levels of OT in pituitary portal blood and significantly reduced the subsequent PRL surge. The characteristic proestrous surge of luteinizing hormone (LH) was not affected by the OT antiserum treatment. These data support a physiological role for OT in the regulation of PRL release during the reproductive cycle.

ISSN:0028-3835    

DOI:10.1159/000125012

出版商:S. Karger AG    

年代:1988

数据来源: Karger