Beta-endorphin-induced increases in plasma epinephrine, norepinephrine and dopamine in rats: inhibition of adrenomedullary response by intracerebral somatostatin.

Synthetic human beta-endorphin, 7.25 nmol intracisternally, in unanesthetized, freely moving, chronically cannulated, adult male rats increased plasma concentrations of all 3 catecholamines: epinephrine, norepinephrine and dopamine, for the 2 h period studied. Blockade of these endorphin effects by the prior systemic administration of naloxone supports mediation of the effects at opioid receptors.

Decreased plasma and urinary dopamine during dietary sodium depletion in man.

This study was designed to investigate the influence of dietary sodium restriction on plasma and urine dopamine levels. Five normal white male volunteer subjects wee studied in metabolic balance at constant 150 meq sodium, 60 meq potassium intake and then daily for 7 days on an isocaloric constant diet of 10 meq sodium and 60 meq potassium/day. With dietary sodium restriction, urinary sodium excretion decreased from 152 +/- 13 meq/day in stepwise fashion to 7 +/- 1 meq/day (P less than 0.

D2- but not D3-dopamine receptors detected in the anterior pituitary.

Using conditions which revealed high affinity binding sites for [3H]ADTN (KD of 1.6 nM), [3H]apomorphine (DK of 3.5 nM) and [3H]dopamine (KD of 1,5 nM) in the calf caudate nucleus, no such high affinity sites could be detected in the calf anterior pituitary gland.

Decreased brain serotonin turnover after short term (two-hour) adrenalectomy in rats: a comparison of four turnover methods.

Within the first 2 h after adrenalectomy in rats there is a marked decrease in hypothalamic, brain stem, and hippocampal serotonin (5HT) turnover. This adrenalectomy-induced decrease in brain 5HT turnover was demonstrated in this study using four different methods. These include 1) accumulation of 5HT after monoamine oxidase inhibition with pargyline, 2) decline of 5-hydroxyindoleacetic acid after pargyline, 3) accumulation of 5-hydroxytryptophan after aromatic L-amino acid decarboxylase inhibition with m-hydroxybenzylhydrazine, and 4) accumulation of 5-hydroxyindoleacetic acid after probenecid.

beta-Endorphin-induced hyperglycemia is mediated by increased central sympathetic outflow to adrenal medulla.

Synthetic human beta-endorphin increased plasma glucose concentration when administered intracisternally in chronically cannulated, conscious, unrestrained, adult male rats. This hyperglycemic effect of beta-endorphin was blocked by prior systemic administration of naloxone, supporting mediation of the effect at opioid receptors in brain. Adrenal denervation blocked the beta-endorphin-induced increase in plasma glucose, supporting a thesis that this effect is mediated at least in part by increased epinephrine secretion.

Abnormal catecholamine mechanisms in hypothalamic-pituitary disorders.

Patients with growth hormone or prolactin-secreting pituitary tumors failed to show normal plasma catecholamine (especially norepinephrine) responses to oral bromocriptine. These patients had normal basal plasma catecholamine concentrations. Patients with anorexia nervosa had low basal levels of dopamine, norepinephrine, and epinephrine.

Plasma dopamine: source, regulation, and significance.

Plasma dopamine is present in free form in a concentration approximately equivalent to that of epinephrine and about 25% that of norepinephrine. It originates in a variety of tissues including sympathetic nerves and adrenal, and the percentage originating from the various sources remains unknown. Events that are associated with increases in sympathetic activity such as stress, exercise, standing, or hypovolemia are associated with increases in plasma dopamine concentration, although the responses may be of considerably smaller magnitude than those for plasma norepinephrine and epinephrine.

Dopaminergic mediation of beta-endorphin-induced prolactin secretion.

Intracisternal administration of synthetic human beta-endorphin increases plasma praolactin concentration, and this effect is blocked by naloxone. Drugs which stimulate dopamine receptors (apomorphine or bromocriptine) or increase availability of dopamine (pargyline) inhibited the effect of beta-endorphin on plasma prolactin. Drugs which antagonize dopamine receptors (haloperidol) or decrease availability of dopamine (alpha-methyltyrosine) potentiated the effect of beta-endorphin on plasma prolactin.

Lesions of the thymus. A study of 53 cases.

This is a retrospective study of 53 cases of thymic lesions diagnosed in a pathology department in Israel over the 18-year period 1960-78. The lesions encountered included 8 cysts, 28 thymomas, 4 thymic carcinomas, 10 lymphomas, 2 carcinoid tumors of the thymus, and one unclassifiable tumor. The range of histological appearances of thymomas is described and the possible association of the epithelial type (absent lymphocyte population) with aggressiveness is raised.

beta-Endorphin-induced increases in plasma dopamine, norepinephrine and epinephrine.

Human beta-endorphin administered intracisternally in conscious, freely moving, adult male rats increased plasma concentrations of dopamine, norepinephrine and epinephrine. These data suggest that endorphins increase central sympathetic outflow.

Plasma ACTH, cortisol, LH, FSH, testosterone, and dihydrotestosterone responses to bromocriptine in normal men.

The effects of an initial oral 2.5 mg dose of bromocriptine and of a similar dose after treatment with 2.5--5 mg daily for one week on plasma concentrations of ACTH, cortisol, LH, FSH, testosterone, and dihydrotestosterone were studied in normal men.

Beta-endorphin-induced decrease in hypothalamic dopamine turnover.

The effect of beta-endorphin on hypothalamic dopamine metabolism was examined in male rats. Intracisternal administration of synthetic human beta-endorphin (15 microgram blunted the alpha-methyltyrosine-induced decline in the concentration of hypothalamic dopamine. Also, beta-endorphin blunted the pargyline-induced accumulation of hypothalamic dopamine.

Mechanism of propranolol withdrawal phenomena.

Nine patients on chronic treatment with propranolol for essential hypertension for 3 months or longer were studied after abrupt discontinuation of the drug. Each patient demonstrated transient supersensitivity to the chronotropic effects of isoproterenol, beginning 2--6 days (median 4 days) after propranolol withdrawal, lasting for 3--13 days (median 6 days), with the maximum sensitivity on day 6. A significantly lower dose of isoproterenol was necessary to increase heart rate 25 beats/min on day 6 (median dose 1.

Abnormal plasma catecholamine responses in acromegalics.

Plasma dopamine, norepinephrine, and epinephrine responses to bromocriptine (2.5 mg orally) or to LRH (100 microgram iv) were studied in seven acromegalic patients. In contrast to normal men, in whom plasma concentrations of catecholamines decrease markedly, acromegalic subjects fail to show decreases in plasma dopamine, norepinephrine, or epinephrine in response to bromocriptine (four of four studied) or LRH (three of four studied).

Legionnaires's disease.

The fist case of legionnaires' disease in Israel is described. In a previously healthy woman, the disease was manifested by a rapidly progressive pneumonia, which was unresponsive to conventional therapy. The diagnosis was confirmed by positive serologic tests and the demonstration of the responsbile microorganism in the patient's lung tissue.

Effects of bromocriptine on plasma catecholamines in normal men.

Administration of a single oral 2.5 mg dose of bromocriptine (Brc), a dopamine (DA) receptor agonist, to normal male volunteers results in comparable marked decreases in resting supine plasma concentrations of DA (decrement 2 h after drug administration was 67 +/- 5%; mean +/- SE), norepinephrine (NE; 63 +/- 3%) and epinephrine (E; 65 +/- 5%); decreases in all three plasma catecholamine (CA) concentrations were significant at p less than 0.001.

Alterations in brain dopamine and serotonin metabolism during the development of tolerance to human beta-endorphin in rats.

Repeated intracisternal injections of human beta-endorphin lead to development of tolerance with respect to the catalepsy, analgesia, and hypothermia which are seen following a single injection. The initial injection of beta-endorphin results in increases in the dopamine metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in neostriatum, as well as increases in the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in hypothalamus and brainstem and a decrease in 5-HIAA in hippocampus. In the present study, we report changes in metabolism of dopamine and serotonin in specific brain areas during the development of tolerance to beta-endorphin.

A defect in catecholamine neurons in patients with prolactin-secreting pituitary adenoma.

Although basal plasma concentrations of dopamine, noradrenaline, and adrenaline in patients with prolactin-secreting pituitary adenoma are normal, responses to oral bromocriptine are not. 1 and 2 h after bromocriptine, plasma concentrations of these three catecholamines are decreased in normal men but not in patients with hyperprolactinaemia secondary to prolactin-secreting pituitary adenoma or in normoprolactinaemic patients in whom a pituitary adenoma has been removed. Patients with prolactin-secreting pituitary adenoma probably have a defect in the regulation of brain catecholamine metabolism.

Development of tolerance to the ACTH-releasing effects of beta-endorphin.

Acute intracisternal injection of human beta-endorphin results in increased plasma concentration of adrenocorticotropic hormone (ACTH). Repeated injections of beta-endorphin are associated with the development of tolerance with regard to this ACTH-stimulating effect.