Epinephrine in rat hypophysial portal blood is derived mainly from the adrenal medulla

This study was performed to determine if epinephrine (EPI) present in hypophysial portal blood has a peripheral or a central origin. Pituitary stalk and femoral arterial EPI plasma levels were simultaneously measured in rats anesthetized with thiopental or urethane. EPI was measured by two different methods: radioenzymatic assay or HPLC followed by electrochemical detection. In thiopental-anesthetized rats, levels were higher in hypophysial portal than in femoral arterial plasma with both methods. In urethane-anesthetized rats, no difference in EPI concentrations was found between peripheral and portal plasma. A rapid blood volume depletion (15 ml/kg in 3 min) evoked a marked elevation of pituitary stalk and arterial EPI plasma concentration while norepinephrine (NE) and dopamine (DA) levels were unaffected. Under both types of anesthesia, the increase of EPI levels was higher in peripheral than in portal plasma. After removal of the adrenal glands, EPI was undetectable or barely detectable in pituitary stalk and arterial plasma. The hemorrhage-induced stimulation of EPI secretion was blunted in portal and peripheral plasma of adrenalectomized rats. These findings indicate that: (1) hypophysial portal EPI plasma concentration is highly dependent on an adrenal source; (2) hypothalamic EPI is not released into portal circulation in response to acute hemorrhage, and (3) anesthesia markedly influences catecholamines plasma levels.     

Concentrations of dopamine and noradrenaline in hypophysial portal blood in the sheep and the rat

The concentrations of dopamine, noradrenaline and their respective primary neuronal metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and 3,4-dihydroxyphenylethyleneglycol (DHPG) were measured in the hypophysial portal and peripheral plasma of sheep and rats by combined gas chromatography-mass spectrometry. Hypophysial portal and jugular blood samples were taken at 5- to 10-min intervals for 3-7 h from six conscious ovariectomized ewes. Blood was also collected for 30 min under urethane anaesthesia from the cut pituitary stalk from 16 pro-oestrous female and five intact male rats. In ovariectomized ewes, noradrenaline concentrations were higher in hypophysial portal plasma than in peripheral plasma (6.6 +/- 0.8 vs 2.2 +/- 0.4 nmol/l). In contrast, dopamine was undetectable (less than 1 nmol/l) in the portal and peripheral plasma of all ewes. Plasma levels of DOPAC and DHPG in portal and jugular samples were similar. In all pro-oestrous female rats, plasma concentrations of dopamine were higher in portal blood than in jugular blood (8.0 +/- 1.4 vs 4.8 +/- 0.6 nmol/l). Detectable concentrations of dopamine were measured in the portal plasma of two out of five male rats. Noradrenaline concentrations were higher in portal plasma than in peripheral plasma of both female (8.3 +/- 1.7 vs 3.7 +/- 0.6 nmol/l) and male (14.8 +/- 2.7 vs 6.1 +/- 1.2 nmol/l) rats. These data show that noradrenaline, but not dopamine, is secreted into the long portal vessels in sheep. The results suggest that there are species differences in the secretion of hypothalamic dopamine into hypophysial portal blood.     

Intermale competition in sexually mature arctic charr: effects on brain monoamines, endocrine stress responses, sex hormone levels, and behavior

Sexually mature Arctic charr (Salvelinus alpinus) males were allowed to interact in pairs for 4 days in the absence of females. Agonistic behavior was quantified, and at the end of the experiment, plasma levels of glucose, cortisol, testosterone (T), 11-ketotestosterone (11-KT), and 17alpha,20beta-dihydroxy-4-pregnen-3-one (17alpha, 20beta-P) were determined alongside brain concentrations of serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA, the major 5-HT metabolite), dopamine (DA), and 3,4-dihydroxyphenylacetic acid (DOPAC, a major DA metabolite). Plasma cortisol and glucose were significantly elevated in subordinate fish, and the number of aggressive acts received showed positive correlations with plasma levels of glucose on day 1, during the development of the dominance relationship, and of cortisol on day 4, when the dominance relationship was established. In contrast, plasma concentrations of T and 11-KT were significantly higher in dominant than in subordinate males, and there was a similar tendency in plasma concentrations of 17alpha,20beta-P. Further, plasma levels of these gonadal steroids were correlated with the number of aggressive acts performed on day 4, but not with the number of aggressive acts received. The plasma cortisol concentrations did not correlate with either 5-HIAA:5-HT or DOPAC:DA ratios in any of the brain parts analyzed. Plasma glucose levels showed positive correlations with brain 5-HIAA:5-HT ratios. Negative correlations were observed between 5-HIAA:5-HT ratios in the optic tectum and between plasma levels of T, 11-KT, and 17alpha,20beta-P. Telencephalic DOPAC/DA ratios displayed a negative correlation with plasma levels of T, 11-KT, and 17alpha,20beta-P, but only in dominant males.     

Vasopressin and CRF-ACTH in adrenalectomized and dexamethasone-treated rats

Median eminence corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) and pituitary and peripheral plasma adrenocorticotropin (ACTH) and AVP were measured in male Wistar rats 1 and 2 weeks after bilateral adrenalectomy (ADX), sham operation (SHAM) or dexamethasone-treatment (DEX). Median eminence AVP content was unchanged 1 week after ADX but was significantly elevated 2 weeks after ADX, whereas CRF activity was reduced at 1 week after ADX and returned to control range at 2 weeks. Anterior pituitary ACTH content was elevated but posterior pituitary AVP content was reduced at 1 and 2 weeks after ADX. Plasma ACTH was greatly elevated in ADX rats and reduced in DEX rats, whereas plasma AVP did not differ significantly between these two groups or the control group. When ADX and SHAM rats were laparotomized under ether, plasma ACTH increased greatly, but this elevation was prevented by DEX treatment. The plasma AVP level was elevated in all three groups 2.5 min after onset of stress but returned to the basal range at 20 min. Median eminence CRF and AVP and pituitary ACTH and AVP were not significantly changed after onset of stress. These results indicate that the vasopressin and CRF-ACTH responses were not consistent in the median eminence, pituitary and peripheral plasma and suggest that vasopression is not involved in the feedback and acute stress mechanism of CRF-ACTH secretion. However, we have to measure CRF activity and AVP concentration in the hypophysial portal blood to confirm this conclusion.     

Effect of prostaglandin E1 on vasoactive intestinal polypeptide release from the hypothalamus and on prolactin secretion from the pituitary in rats

In order to elucidate the mechanisms by which prostaglandin (PG) affects PRL secretion, the effect of PGE1 on vasoactive intestinal polypeptide (VIP) release from the rat hypothalamus was examined by determining plasma VIP levels in rat hypophysial portal blood in vivo and VIP release from the perifused hypothalamus in vitro. Intraventricular injection of PGE1 (1 and 5 micrograms/rat) caused a 2- to 3-fold increase in the concentration of plasma VIP in hypophysial portal blood in anesthetized rats. The flow rate of portal blood was slightly increased after the injection of PGE1. VIP release from the perifused rat hypothalamus was stimulated by high potassium levels (56 mM). The infusion of PGE1 (10 microM) resulted in a significant increase in VIP release from the hypothalamus in vitro. Both these responses were calcium dependent. The intraventricular injection of PGE1 (1 and 5 micrograms/rat) resulted in a dose-related increase in peripheral plasma PRL levels in the rat. These findings suggest that PGE1 plays a stimulatory role in regulating VIP release from the hypothalamus into hypophysial portal blood and causes PRL secretion from the pituitary in rats.     

Aging and diurnal rhythms of pineal serotonin, 5-hydroxyindoleacetic acid, norepinephrine, dopamine and serum melatonin in the male rat

Pineal serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), norepinephrine (NE) and dopamine (DA) were measured by high-pressure liquid chromatography with electrochemical detection and serum melatonin was measured by radioimmunoassay in rats aged 3 weeks, 8 weeks and 18 months. They were killed either at mid-light or mid-dark of a 12 h light:12 h dark cycle. Diurnal rhythms were observed for 5-HT and 5-HIAA in all ages studied while those for NE and DA were not observed in the 18-month-old animals. Pineal 5-HT and 5-HIAA were higher in 3-week-old rats at mid-dark, and lower at mid-light than in older animals. The pineal content of NE was lower in the 3-week-old rats at mid-dark and mid-light compared with that in the 8-week-old while the DA content was lower at mid-dark. In addition, pineal 5-HT, 5-HIAA, NE and DA were lower in the 18-month-old than in the 8-week-old animals at mid-dark. At mid-dark serum melatonin levels showed an age-related decrease. This study shows that an age-related decrease of pineal 5-HT, 5-HIAA, NE and DA can only be demonstrated at mid-dark and that the age-related decrease of melatonin may not be due to a decrease in sympathetic activity.     

Immunoreactive somatostatin in rat hypophysial portal blood.

Somatostatin levels have been determined by RIA in hypophysial portal blood of pentobarbital-anesthetized male rats. In most animals, immunoreactive somatostatin (SRIF) levels were higher in hypophysial portal blood than in systemic blood. In euthyroid rats, the mean level was 158 +/- 27 pg/ml (n = 8); SRIF was undetectable (less than 30 pg/ml) in systemic blood of these rats. It is suggested that endogenous SRIF was not degraded during the collection of stalk blood, since synthetic SRIF is stable when incubated in rat serum during 4 min at 37 c and 2 h at 0 C, i.e. under the conditions the blood was kept during the collection. SRIF in hypophysial portal plasma had the same immunoreactivity with a specific antiserum against SRIF as did synthetic SRIF. Gel filtration of hypophysial portal plasma revealed two immunoreactive peaks, the major one corresponding to synthetic SRIF, the smaller one representing a larger molecular form. Thyroidectomy and excess of T4 did not modify the levels of SRIF in hypophysial portal blood, suggestinc SRIF is stable when incubated in rat serum during 4 min at 37 C and 2 h at 0 C, i.e. under the conditions the blood was kept during the collection. SRIF in hypophysial portal plasma had the same immunoreactivity with a specific antiserum against SRIF as did synthetic SRIF. Gel filtration of hypophysial portal plasma revealed two immunoreactive peaks, the major one corresponding to synthetic SRIF, the smaller one representing a large molecular form. Thyroidectomy and excess of T4 did not modify the levels of SRIF in hypophysial portal blood, suggesting that the feedback of thyroid hormones on TSH secretion does not involve changes in the secretion of SRIF by the hypothalamus.     

Oxytocin and vasopressin in rat hypophysial portal blood: experimental studies in normal and Brattleboro rats

Oxytocin (OT) and vasopressin (VP) were measured by radioimmunoassay in hypophysial portal and peripheral blood from male Wistar rats and heterozygous and homozygous Brattleboro rats anaesthetized with urethane. In Wistar rats the concentrations of OT and VP were about 50 times greater than the concentrations in peripheral blood, whether or not the pituitary gland was left in situ during collection, and also considerably greater than the reported concentrations of the peptides in the cerebrospinal fluid. The release of both peptides was increased significantly by a lesion of the supraoptico-hypophysial tract that led to diabetes insipidus, but which left intact the external layer of the median eminence (ME). Concentrations of VP were undetectable in plasma from homozygous Brattleboro rats, but the portal plasma concentrations of VP in heterozygous Brattleboro rats were not significantly lower than in Wistar rats. The concentrations of OT in portal plasma from both types of Brattleboro rat were significantly higher than in Wistar rats. The output of VP and OT into hypophysial portal blood of Wistar rats was not significantly affected by electrical stimulation of the suprachiasmatic, supraoptic or paraventricular nuclei or the ME using two types of stimuli, one of which produced an increase in peripheral plasma concentrations of VP and OT in intact rats and a significant increase in the release of LH-releasing hormone into hypophysial portal blood. The output of VP and OT into portal blood was also not significantly affected by either adrenalectomy with or without injection of dexamethasone or the injection of either the 5-hydroxytryptamine (5-HT) synthesis blocker, parachlorophenylalanine, or the 5-HT uptake blockers, alaproclate or zimelidine. These results show that large amounts of OT as well as VP are released into hypophysial portal blood from fibres of the hypothalamo-neurohypophysial system that terminate in the external layer of the ME. Although distinct from the fibres that terminate in the pars nervosa (PN), the findings in Brattleboro rats show that the VP fibres of the ME system originate in neurones with a genomic mechanism for VP synthesis similar to that of the VP neurones that project to the PN. The lack of effect of adrenalectomy and the administration of 5-HT synthesis and uptake blockers must be interpreted with caution since the results obtained with electrical stimulation suggest that when the pituitary stalk is cut the release of OT and VP into portal blood approaches a maximum and may therefore be difficult to alter by experimental manipulation.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effects of intracerebroventricular administration of growth hormone-releasing factor and corticotropin-releasing factor on somatostatin secretion into rat hypophysial portal blood

To clarify the regulatory mechanisms for the secretion of somatostatin (SRIF) from the hypothalamus, the effects of intracerebroventricular (i.c.v.) administration of growth hormone-releasing factor (GRF) and corticotropin-releasing factor (CRF) on SRIF secretion into hypophysial portal blood were examined in pentobarbital-anesthetized male rats. Neither the concentration of SRIF in portal plasma nor the secretion rate of SRIF was changed after i.c.v. administration of 0.9% saline. Administration of 10 ng or 5 micrograms human GRF i.c.v. produced a significant increase in the portal plasma concentration and secretion rate of SRIF. Likewise, 5 micrograms CRF significantly increased the portal plasma concentration and secretion rate of SRIF. These results suggest that the neuropeptides GRF and CRF centrally influence SRIF secretion into hypophysial portal blood.     

The concentration of arginine vasopressin in pituitary stalk plasma of the rat after adrenalectomy or morphine

We have investigated the role of adrenal steroids and the opiates in regulating arginine vasopressin (AVP) secretion into the pituitary stalk blood of the rat. The portal plasma concentration of AVP in urethane-anesthetized male rats was 532 +/- 68 pg/ml (mean +/- SEM), while the peripheral plasma AVP concentration in intact urethane-anesthetized rats was 20.7 +/- 5.7 pg/ml. Column chromatography on Sephadex G-25 of an extract of a pool of portal plasma revealed that the material being assayed comigrated with synthetic AVP. Bilateral adrenalectomy (ADX) 5 days before the collection of portal blood elevated portal plasma AVP concentrations approximately 6-fold (655 +/- 124 pg/ml in controls vs. 4090 +/- 504 pg/ml in adrenalectomized animals). Dexamethasone administration (15 micrograms/kg X day) for 5 days prevented the ADX-induced increase in portal plasma AVP concentrations without significantly changing portal plasma AVP concentrations in intact rats. Portal plasma concentrations of beta-endorphin were not changed by ADX or dexamethasone treatment. The iv infusion of morphine sulfate (3 mg/kg) dramatically decreased the concentration of AVP in the portal plasma of the rat (501 +/- 101 pg/ml before morphine vs. 185 +/- 50 pg/ml after morphine). The inhibitory effect of morphine was reversed by naltrexone (1.0 mg/kg), whereas naltrexone alone did not alter AVP secretion. Morphine administration also decreased systemic plasma AVP concentrations in urethane-anesthetized rats (27.1 +/- 6.6 pg/ml in controls vs. 3.3 +/- 1.3 pg/ml in morphine-treated rats). Naltrexone treatment reversed this effect. These results suggest that AVP secretion into pituitary stalk blood is under the inhibitory influence of the adrenal steroids, and the increased concentration of AVP found in portal blood may be partially responsible for the elevated levels of ACTH after ADX. Furthermore, morphine-induced activation of the pituitary-adrenal axis is apparently independent of hypothalamic AVP secretion.     

Levels of LH-releasing hormone in hypophysial stalk plasma during an oestrogen-stimulated surge of LH in ovariectomized rats

Treatment of ovariectomized rats with 50 micrograms oestradiol benzoate, followed by 20 micrograms oestradiol benzoate 3 days later, induced surges of LH and FSH on the day following the second injection with oestradiol benzoate. During this surge of gonadotrophins, which was not blocked by the anaesthetic required to collect hypophysial stalk blood, increased hypophysial stalk plasma levels of immunoreactive LHRH were noted. Furthermore, the levels of LHRH in hypophysial portal blood were found to fluctuate. Measurement of LHRH in a pool of portal plasma revealed similar results when determined by radioimmunoassay and by a sensitive in-vitro bioassay. To mimic the observed release of LHRH during the surge of gonadotrophins, LHRH was infused, either systemically or directly into a long portal vessel, into oestrogen-treated, ovariectomized rats which had their endogenous release of LHRH blocked by pentobarbitone. An infusion of LHRH into the jugular vein, resulting in peripheral levels of LHRH which were somewhat lower than those measured in hypophysial stalk plasma, caused a surge of FSH similar to that found in rats used for collection of hypophysial stalk blood. When compared with the values in the latter animals, however, the levels of LH became two to four times higher by this infusion of LHRH. When LHRH was infused directly into a long portal vessel to mimic the observed secretion rate of LHRH during the oestrogen-stimulated surge of gonadotrophins, then the surges of LH and FSH were lower than those observed in the rats used for collection of stalk blood.     

Effect of intraventricular injection of neurotensin and other various bioactive peptides on plasma immunoreactive somatostatin levels in rat hypophysial portal blood

The role of various bioactive peptides in the control of secretion of hypothalamic somatostatin into the hypophysial portal blood was examined in anesthetized rats. Hypophysial portal blood was withdrawn at a rate of 5.0 microliter/min into a chilled tube through a cannula placed over the stump of the pituitary stalk and segmented every 20 min by air bubbles. Immunoreactive somatostatin (IRS) in the plasma was extracted with acetic acid and acetone and quantified by RIA. Basal levels (mean +/- SE) of plasma IRS in the hypophysial portal blood were 646 +/- 36 and 317 +/- 44 pg/ml in urethane- and pentobarbital-anesthetized rats, respectively. Under urethane anesthesia, injection of synthetic neurotensin into the lateral ventricle at various doses in the range of 0.016--2 microgram/rat caused a significant and dose-related increase of plasma IRS levels in the hypophysial portal blood, and this effect of neurotensin was significantly (P less than 0.05) suppressed by pretreatment with diphenhydramine (1 mg/100 g BW, iv), a histamine receptor blocker. Enhancement of IRS release by neurotensin was also observed in pentobarbital-anesthetized rats. Intraventricular injection of substance P (10 microgram/rat), beta-endorphin (1 and 5 microgram/rat), or [Met5]enkephalin had no effect on the level of somatostatin in the hypophysial portal blood of urethane-anesthetized rats. These results suggest a release of hypothalamic somatostatin into the hypophysial portal blood in response to intraventricular administration of neurotensin, probably by a histaminergic mechanism.     

Hemorrhage-induced secretion of corticotropin-releasing factor-like immunoreactivity into the rat hypophysial portal circulation and its inhibition by glucocorticoids

A paradigm for reliably stimulating ACTH secretion in urethane-anesthetized male rats has been used to examine hypothalamic secretion of corticotropin-releasing factor-like immunoreactivity (CRF-LI) into the hypophysial portal circulation. Hemorrhage of 15% estimated blood volume evoked a maximal 4.6-fold elevation in circulating ACTH levels from an initial level of 178.4 +/- 51.2 (+/-se) to 814.7 +/- 184.6 pg ml-1. The cumulative amount of ACTH secreted in response to hemorrhage was 10-fold greater than the cumulative amount of ACTH secreted by nonhemorrhaged rats (unweighted cumulative effect over all time points). In another experiment from a similarly hemorrhaged group, the hypophysial portal plasma CRF-LI concentration rose 2-fold from an initial level of 429.7 +/- 34.2 to 839.3 +/- 170.4 pg ml-1. Pretreatment with dexamethasone (100 microgram/kg BW, im) had no effect on initial levels of either CRF-LI or ACTH. The hemorrhage-induced elevations of both CRF-LI and ACTH were abolished in dexamethasone-treated rats. The secretory rate of CRF-LI was calculated to be 1.61 +/- 0.7 pg min-1 in nonhemorrhaged animals. Reversible pharmacological hyperpolarization of the paraventricular nuclei by stereotaxically microinjected procaine (15 micrograms/100 nl) reduced portal plasma CRF-LI and peripheral plasma ACTH to undetectable levels. These observations led to the following conclusions: 1) CRF-LI is an important hypothalamic regulator of adenohypophysial ACTH secretion, 2) CRF-LI in the hypophysial portal circulation is derived from CRF-LI-containing neurons within the paraventricular nuclei, and 3) glucocorticoid negative feedback effects can be exerted at the central level.     

The secretory activity of the tuberoinfundibular dopaminergic neurons is modulated by the thyroid status in the adult rat: consequence on prolactin secretion

An influence of thyroid status on the secretory activity of hypothalamic dopaminergic neurons was observed in adult rats and its involvement in the regulation of prolactin (PRL) secretion was examined. The secretory activity of the tuberoinfundibular dopaminergic (TIDA) neurons was evaluated by measurement of dopamine (DA) biosynthesis in the neurons and DA release into hypophysial portal blood. The accumulation of DA and PRL in the adenohypophysis as well as PRL concentration in plasma were also estimated, and the various parameters were studied in thyroidectomized (TX), sham TX, TX rats treated for 7 days with thyroxine (T4; 20 micrograms/kg body weight daily) as well as in intact rats treated similarly with T4. An enhanced secretory activity of the TIDA neurons was observed in TX compared to sham TX rats, as attested by an increased synthesis of DA in the neurons, a greater concentration of DA in hypophysial portal plasma as well as an augmented accumulation of DA in the adenohypophysis. In the same animals, PRL was reduced in the adenohypophysis and in plasma, reflecting a blunted secretion of PRL in severe hypothyroidism. Treatment of TX rats with T4 for 7 days abolished all effects observed in TX rats, DA synthesis in TIDA neurons of TX rats treated with T4 being even less than in neurons of sham TX animals. A similar treatment with T4 administered to intact rats did not affect the secretory activity of the TIDA neurons nor the secretion of PRL.(ABSTRACT TRUNCATED AT 250 WORDS)     

Duration of streptozotocin diabetes influences the response of hypothalamic serotonin metabolism to immobilization stress

Neurochemical and metabolic effects of acute (immobilization for 2 h) and chronic (immobilization for 2 h/day for 4 consecutive days) stress were investigated in diabetic female rats either pretreated 1 week or 5 weeks earlier with streptozotocin (STZ). Hypothalamic serotonin (5-hydroxytryptamine, 5-HT) metabolism was estimated by measuring the respective levels of 5-HT precursor, the amino acid tryptophan (TRP), 5-HT and the 5-HT metabolite, namely 5-hydroxyindoleacetic acid (5-HIAA). To assess the respective metabolic effects of stress and diabetes, plasma total TRP, insulin, glucose and corticosterone levels were measured. Short- and long-term STZ treatment triggered marked decreases in plasma total TRP and hypothalamus TRP levels but the diabetogenic agent diminished 5-HT metabolism in the 1-week ST-treated rats only. Acute stress promoted a marked decrease in plasma total TRP in the vehicle-treated rats and in the 1-week-diabetic rats, which was associated with significant increases in hypothalamic TRP and 5-HIAA levels. In the 5-week-diabetic rats, a single restraint affected neither peripheral and central TRP levels nor hypothalamus 5-HT metabolism. Acute stress triggered hypercorticosteronemia in all groups of rats but it promoted hyperglycemia and hypoinsulinemia in the vehicle-injected rats only. Twenty-four hours after the fourth immobilization, plasma total TRP was reduced in the vehicle-injected rats only with no effect on hypothalamic levels of TRP. On the other hand, chronic restraint was found to reduce exclusively hypothalamus 5-HT and 5-HIAA levels in the 5-week-diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of adrenocorticotropin control in Brattleboro, Long-Evans, and Wistar rats. Measurement of corticotropin-releasing factor, arginine vasopressin, and oxytocin in hypophysial portal blood

The purpose of this study was to compare the control of adrenocorticotropin (ACTH) and corticosterone secretion in homozygous Brattleboro rats with their syngeneic controls, Long-Evans rats, and with rats of the Wistar strain. Plasma concentrations of ACTH and corticosterone were measured by radioimmunoassay in trunk blood, and corticotropin-releasing factor 41 (CRF-41), arginine vasopressin (AVP), and oxytocin were assayed in hypophysial portal vessel blood. Portal plasma was extracted with methanol for CRF-41 determination, and four different antisera and several different high-performance liquid chromatography (HPLC) systems were used to investigate AVP release. The peripheral plasma concentrations of ACTH and corticosterone were significantly higher in Long-Evans and homozygous Brattleboro than in Wistar rats. This difference was due, at least in part, to an approximately twofold greater release of CRF-41 into hypophysial portal blood of the Long-Evans and Brattleboro compared with Wistar rats. There was no significant difference between the strains in the output of oxytocin into portal blood. While no AVP could be detected in the neural lobe of homozygous Brattleboro rats, a small amount of AVP-like immunoreactivity was detected in unextracted hypophysial portal blood from homozygous Brattleboro rats. However, this AVP-like immunoreactivity was clearly distinct from authentic AVP in several HPLC systems, had no antidiuretic activity, and on gel filtration had a relative molecular mass greater than 5 kD. In contrast, the AVP-like immunoreactivity in hypophysial portal blood from Long-Evans rats co-eluted with authentic AVP in all HPLC systems tested.(ABSTRACT TRUNCATED AT 250 WORDS)     

Stimulation by bombesin of immunoreactive somatostatin release into rat hypophysial portal blood

Bombesin was injected into the cerebral ventricle of male rats anesthetized with urethane to study its effect on plasma levels of immunoreactive somatostatin (IRS) in hypophysial portal and jugular blood. An intraventricular injection of bombesin (0.2 and 2 micrograms/rat) caused a significant and dose-related increase in plasma IRS in hypophysial portal blood but not in jugular blood. Although bombesin placed into the cerebral ventricle is known to stimulate glucagon and epinephrine release, an iv injection of glucagon (100 micrograms/100 g BW) or epinephrine (2.5 micrograms/100 g BW) did not cause any significant changes in plasma IRS levels in hypophysial portal and jugular blood, suggesting that these substances do not mediate bombesin stimulation of portal IRS release. Pretreatment with naloxone (75 micrograms/100 g BW, iv) failed to affect the portal IRS release induced by bombesin (2 micrograms/rat), indicating that the opiate receptor is not likely to be involved in this reaction. To ascertain whether IRS released by bombesin into hypophysial portal blood is biologically active, the effect of bombesin on the plasma GH level was then examined. Bombesin (2 micrograms/rat) injected intraventricularly completely suppressed the rise of plasma GH after the intraventricular injection of beta-endorphin (1 microgram/rat) or the iv injection of prostaglandin E1 (5 micrograms/100 g BW). Bombesin thus appears to stimulate the secretion of IRS, and probably biologically active somatostatin as well, from the hypothalamus into hypophysial portal blood, thereby inhibiting GH release from the anterior pituitary.     

A型性格、冠心病与血浆5－羟色胺的关系

Ａ型性格者的５－羟色胺（５－ＨＴ）、５－羟吲哚乙酸（５－ＨＩＡＡ）值显著高于Ｂ型性格者；Ａ、Ｂ型性格冠心病发作患者５－ＨＴ、５－ＨＩＡＡ值分别较Ａ和Ｂ型性格对照组升高，其中以Ａ型性格冠心病者升高最为显著；Ａ和Ｂ型性格冠心病发作缓解后５－ＨＴ值均显著下降，但前者仍显著高于Ａ型性格对照组，提示５－ＨＴ与Ａ型性格及冠心病发病关系密切。     

Effects of tyrosine and tryptophan ingestion on plasma catecholamine and 3,4-dihydroxyphenylacetic acid concentrations

The effect of oral tyrosine or tryptophan ingestion on plasma concentrations of norepinephrine (NE), dopamine (DA), epinephrine (EPI), and 3,4-dihydroxyphenylacetic acid (DOPAC) was investigated in a double blind, placebo-controlled study in fasted men. Tyrosine ingestion induced within 45 min a significant but short-lasting (approximately 30 min) increase in plasma concentrations of NE, EPI, and DA and a coincident decrease in plasma DOPAC levels. Ingestion of tryptophan or lactose placebo did not after plasma DA, EPI, NE, or DOPAC levels. Since plasma catecholamines derive from peripheral sources, while circulating DOPAC may reflect both brain and peripheral DA turnover, these results suggest that the oral ingestion of tyrosine can exert acute effects on catecholamine systems within and outside the brain.     

Estrogen inhibition of dopamine release into hypophysial portal blood

The hypothesis that 17 beta-estradiol suppresses dopamine secretion into hypophysial portal blood was tested. Portal plasma concentrations of dopamine were significantly lower in proestrous rats (1.0 +/- 0.1 ng/ml; mean +/- SE) than in estrous rats (1.9 +/- 0.38 ng/ml). To deplete the animal of endogenous steroid hormones, proestrous rats were adrenalectomized (Adx) and ovariectomized (Ovx). Twenty-four hours later, hypophysial portal blood was collected for 60 min, and the plasma from this blood was analyzed for dopamine. Arterial plasma from these rats was assayed for 17 beta-estradiol and progesterone. The concentrations of dopamine in the portal plasma of sham-operated rats and bilaterally Adx-Ovx rats were similar to those in estrous animals. The concentration of dopamine in portal plasma of Adx-Ovs rats injected 24 h earlier with 50 micrograms 17 beta-estradiol was 1.0 +/- 0.31 ng/ml, which was comparable to that in proestrous animals but less than that in the estrous rats. The concentrations of 17 beta-estradiol in arterial plasma were as follows: 24 +/- 8.3 pg/ml in proestrous rats, 40 +/- 2.9 pg/ml in estrous rats, 10 +/- 1.3 pg/ml in Adx-ovx rats, and 96 +/- 17.3 pg/ml in Adx-Ovx rats injected with 50 micrograms 17 beta-estradiol. Twenty-four hours after injection of 25 micrograms 17beta-extradiol into Adx-Ovx rats, the plasma 17beta-estradiol levels were 51 +/- 7.4 pg/ml, and the dopamine concentrations in portal plasma were 1.9 +/- 0.57 ng/ml. It is concluded that an acute effect of 17 beta-estradiol is suppression of hypothalamic secretion of dopamine into hypophysial portal blood.