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Biomedical subjects

W Vale

Publications and source records attributed to W Vale.

At least 451 records · Page 25Linked to original sources
PubMed1978

Chronic effects of [D-Trp6-Pro9-NEt]luteinizing hormone-releasing factor on reproductive processes in the female rat.

LRF and one of its highly potent analogs, [D-Trp6-Pro9-NEt]LRF (A), were tested for their effects on pregnancy. Daily doses of A prevented implantation and/or caused resorption of implanted blastocysts in mated female rats. This effect was dose related and was most evident when given in regimens including days 5-7 or days 9-10 or pregnancy. LRF also has antigonadal effects, but at much higher doses than A. The use of corn oil vs. 0.1% gelatin-saline improved the effectiveness of low doses of A. Termination of pregnancy in A- or LRF-treated rats is most probably due to the markedly diminished progesterone secretion, which could result from the secretion of biologically inactive gonadotropins, reduced pituitary responsiveness to endogenous LRF, or down-regulation of gonadal receptors for LH.

Animals↗
PubMed1977

beta-Endorphin and adrenocorticotropin are selected concomitantly by the pituitary gland.

The opiate-like peptide beta-endorphin and adrenocorticotropin are concomitantly secreted in increased amounts by the adenohypophysis in response to acute stress or long-term adrenalectomy as well as in vitro in response to purified corticotropin releasing factor and other secretagogues. Conversely, administration of the synthetic glucocorticoid dexamethasone inhibits the secretion of both adrenocorticotropin and beta-endorphin. Thus, both hormones possess common and identical regulatory mechanisms and there may be a functional role for circulating beta-endorphin.

Adrenocorticotropic Hormone↗
PubMed1977

Somatostatin: analogs with selected biological activities.

[D-Cys14]-Somatostatin is the first analog of somatostatin found to be more potent in inhibiting glucagon and growth hormone secretion that it is in inhibiting insulin secretion. [D-Trp8]-Somatostatin is eight to ten times more potent than somatostatin in inhibiting insulin, glucagon, and growth hormone secretion. [D-Trp8, D-Cys14]-Somatostatin is more potent than [D-Cys14]-Somatostatin, but retains its relative selectivity in being a more potent inhibitor of the secretion of glucagon and growth hormone than of insulin.

Animals↗
PubMed1977

Bombesin:potent effects on thermoregulation in the rat.

Several vasoactive peptides administered intracisternally have been assessed for the effect of lowering the core temperature of rats exposed to cold. Peptides structurally related to neurotensin lower core temperature while those related to substance P do not. The tetradecapeptide bombesin, orginally isolated from the extracts of the skin of the frog Bombina bombina, is 10(4) times more potent than neurotensin in lowering core temperature, with a minimal effective dose less than or equal to 1 nanogram per 200 grams of body weight. Thus bombesin is one of the most potent peptides reported to affect the central nervous system.

Amino Acid Sequence↗
PubMed1977

Pancreatic immunoreactive somatostatin release.

The location of the somatostatin-containing D-cells of the pancreatic islets between the A- and B-cells suggests that their function might be to inhibit insulin and/or glucagon secretion by these neighboring cells. To determine if insulin and/or glucagon, in concentrations that might be present in the extracellular space surrounding the D-cells, stimulate immunoreactive somatostatin (IRS) release, we perfused 10 microng of glucagon or 10 milliunits of insulin per ml in 11 isolated dog pancreases, for 40 min in seven experiments and for 100 min in four experiments. In eight of the nine experiments in which glucagon was perfused, a prompt and significant rise in mean IRS release, ranging from 71 to 128% above the control level, was observed. In the eight experiments in which insulin was perfused. IRS did not increase during the first 40 min; in the two 100-min insulin experiments, it did rise during the final 50 min, however. To determine the effect of an A- and B-cell secretogogue on IRS release, we perfused 20 mM arginine for 60 min in six experiments. In all, IRS rose within 3 min and reached a level 71-465% above the control, remaining significantly elevated throughout the perfusion, while glucagon and insulin rose to peak levels at 2 min and then declined somewhat despite continuing arginine perfusion. The results indicate that perfusion of the normal dog pancreas with high doses of glucagon or arginine is accompanied by a prompt increase in IRS release and are compatible with a local feedback circuit involving A- and D-cells. Insulin appears not to augment IRS release, at least not promptly, but IRS stimulated by local endogenous glucagon could inhibit the B-cell response to locally secreted glucagon and thereby influence the composition of the insulin/glucagon secretion mixture.

Animals↗
PubMed1977

Release of immunoreactive somatostatin from the pancreas in response to glucose, amino acids, pancreozymin-cholecystokinin, and tolbutamide.

The effects of glucose, amino acids, pancreozymin-cholecystokinin, and tolbutamide upon the release of immunoreactive somatostatin (IRS) from the isolated perfused pancreas were studied. In seven experiments in which glucose was perfused either at a concentration of 100 or 350 mg/dl or at 25 mg/dl, IRS levels were significantly greater at the higher glucose concentrations. In three dose-response experiments in which the perfusing glucose concentration was increased at 30-min intervals from an initial concentration of 25 mg/dl to a final concentration of 300 mg/dl, progressive increases in IRS release were noted at glucose concentrations of 100 mg/dl and above. Perfusion of a 20 mM mixture of 10 amino acids also elicited a prompt and significant biphasic IRS rise in each of six experiments. In five experiments, 20 mM leucine evoked a similar response in mean IRS. Perfusion with 0.075 Ivy U/ml of pancreozymin-cholecystokinin, with or without the presence of a 1 mM 10-amino acid mixture, elicited a prompt rise in IRS with a pattern resembling that of insulin in a total of six experiments. Tolbutamide (0.75 mg/min) also stimulated IRS release in five of six challenges. The IRS responses to nutrients and to pancreozymin and their similarity to the insulin responses raise the possibility that, like insulin, pancreatic somatostatin may have an endocrine role related to nutrient homeostasis.

Amino Acids↗
PubMed1977

The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of cholecystokinin upon immunoreactive somatostatin release by the perfused canine pancreas.

The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of pancreozymin-cholecystokinin on immunoreactive somatostatin release were studied in the isolated perfused dog pancreas. Gastrin at a concentration of 65 ng/ml and the octapeptide of pancreozymin-cholecystokinin at a concentration of 25 ng/ml produced a prompt, but transient statistically significant, twofold rise in mean somatostatin concentration. Secretion at a concentration of 0.3 U/ml and gastric inhibitory polypeptide concentration of 58 ng/ml produced a prompt two- to threefold rise in mean somatostatin release, which persisted throughout the perfusion period. With all four polypeptides the pattern of the somatostatin response resembled that of insulin. It appears that pancreatic somatostatin release is stimulated by gastrointestinal hormones that influence the secretion of insulin and glucagon.

Animals↗
PubMed1977

Stimulation in vivo of the secretion of prolactin and growth hormone by beta-endorphin.

Morphine sulfate (MS) and the opioid peptide beta-endorphin beta-LPH-(61-91) stimulate prolactin and growth hormone release in steroid-primed and non-treated male rats when injected intravenously or intracisternally. On a molar basis beta-endorphin is at least 20 times more potent than MS, whereas Met5-enkephalin (beta-LPH-(61-65)) and alpha-endorphin (beta-LPH-(61-76)) are devoid of activity at the dose injected (300 mug). The in vivo stimulatory effects of beta-endorphin on prolactin secretion are reversed by the opiate antagonist naloxone. The absence of in vitro effect of MS and beta-endorphin on prolactin and growth hormone secretion by cultured rat pituitary cells suggest that they have a central nervous system site of action.

Animals↗
PubMed1977

Effect of neurotensin, substance P and morphine sulfate on the secretion of prolactin and growth hormone in the rat.

Neurotensin (NT), substance P (SP) and morphine sulfate (MS) elevate plasma prolactin and growth hormone levels in both normal or estrogen-progesterone pretreated male rats. By contrast, steroid priming is required for TRF to exhibit PRL-releasing activity. Naloxone, an opiate receptor blocker, reverses the stimulatory effect of MS only. Diphenhydramine, a histamine antagonist, inhibits the response to NT, SP and MS without affecting the response to TRF. These results suggest the involvement of a histaminic step in the action of NT, SP and MS. TRF, NT and SP do not appear to stimulate PRL and GH through activation of an opiate receptor.

Animals↗
PubMed1977

Effects of gamma-aminobutyric acid and histamine on prolactin secretion in the rat.

Histamine releases prolactin (PRL) in estrogen-progesterone primed male rats after both iv and intracisternal (ic) injection, but does not affect in vitro PRL secretion. This stimulatory effect is reversed by the alpha-adrenergic antagonist phenoxybenzamine and the histamine antagonist diphenhydramine, gamma-Amino butyric acid (GABA), which has little in vivo effect of its own, interferes with the activity of histamine and a variety of other stimulators of PRL secretion. These results suggest the involvement of the naturally-occurring substances histamine and GABA in the central regulation of PRL secretion.

Aminobutyrates↗