A Novel α-Conotoxin Identified by Gene Sequencing Is Active in Suppressing the Vascular Response to Selective Stimulation of Sensory Nerves in Vivo†

SUMMARY The output of oestrogens, testosterone and their precursors was compared with that of glucocorticosteroids under standardized conditions, in a suspension of isolated human adrenal cells. Cortisol, corticosterone, androstenedione, dehydroepiandrosterone and its sulphate all increased in the same proportions after ACTH stimulation. The response to the logarithm of ACTH concentrations had a sigmoid shape but was fairly linear between 5 and 100 to 1000 μu./ml. The output of dehydroepiandrosterone plus that of its sulphate was of the same order of magnitude as the production of cortisol; the output of free dehydroepiandrosterone averaged half that of the sulphate indicating that the adrenal cortex is capable, under certain conditions, of producing large amounts of the free steroid. The output of androstenedione was very low, on average 35 times lower than that of cortisol, suggesting by extrapolation that the adrenal secretion may not be the main source of androstenedione in vivo or that ACTH is not the unique stimulus to adrenal androstenedione secretion. The output of testosterone was small to negligible and that of oestrogens was practically absent. In three additional experiments the influence of prolactin, prostaglandins, FSH and HCG was explored: no selective stimulation of androgen or oestrogen output was observed except in one experiment in which HCG stimulated adrenal testosterone production.

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Selective stimulation of mast cells with a TLR2 agonist inhibits tumor growth in vivo

The FASEB Journal ◽

10.1096/fasebj.22.1_supplement.1076.14 ◽

2008 ◽

Vol 22 (S1) ◽

Author(s):

Sharon Ann Oldford ◽

Carlos A. Leiva ◽

Brent Johnston ◽

Jean S. Marshall

Keyword(s):

Mast Cells ◽

Tumor Growth ◽

Tlr2 Agonist ◽

Selective Stimulation ◽

Stimulation Of

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Interaction of endogenous nitric oxide and CGRP in sensory neuron-induced gastric vasodilation

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1995.268.5.g791 ◽

1995 ◽

Vol 268 (5) ◽

pp. G791-G796 ◽

Cited By ~ 5

Author(s):

R. Y. Chen ◽

P. H. Guth

Keyword(s):

Nitric Oxide ◽

Sensory Nerves ◽

Cgrp Receptor ◽

Synthesis Inhibitor ◽

Calcitonin Gene ◽

Endogenous Nitric Oxide ◽

Cgrp Receptor Antagonist ◽

Dose Dependent ◽

Stimulation Of

Stimulation of capsaicin-sensitive sensory nerves induces gastric mucosal hyperemia, which is mediated in part by both calcitonin gene-related peptide (CGRP) and nitric oxide (NO). In the present study, we used in vivo microscopy in anesthetized rats to determine 1) whether these agents were released locally at the submucosal level and, if so, 2) whether CGRP dilates arterioles via release of endothelium-derived NO. Intragastric capsaicin (160 microM) dilated submucosal arterioles from 25 +/- 3 to 67 +/- 8 microns. The intragastric capsaicin-induced vasodilation was markedly reversed not only by intravenous administration of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) but also by submucosal suffusion of either L-NAME or the CGRP receptor antagonist human CGRP-(8-37). The latter findings indicate that both NO and CGRP are released locally at the submucosal level. Submucosal application of CGRP induced dose-dependent dilation of gastric submucosal arterioles, which was significantly attenuated by L-NAME. However, at the same degree of vasodilation (42 microns), the dilation induced with submucosal CGRP was much less attenuated by NO synthesis inhibition (-28%) compared with that induced with intragastric capsaicin (-79%). This indicates that endothelium-derived NO released by CGRP was not the only source of submucosal NO in the latter response. There must be another as yet undetermined source of submucosal NO, e.g., possibly nitroxidergic nerves.

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Potent and Selective Stimulation of Memory-Phenotype CD8+ T Cells In Vivo by IL-15

Immunity ◽

10.1016/s1074-7613(00)80564-6 ◽

1998 ◽

Vol 8 (5) ◽

pp. 591-599 ◽

Cited By ~ 910

Author(s):

Xiaohong Zhang ◽

Siquan Sun ◽

Inkyu Hwang ◽

David F Tough ◽

Jonathan Sprent

Keyword(s):

T Cells ◽

Cd8 T Cells ◽

Memory Phenotype ◽

Selective Stimulation ◽

Stimulation Of

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Intraluminal capsaicin does not affect fluid and electrolyte absorption in the human jejunum but does cause pain

Gut ◽

10.1136/gut.43.2.252 ◽

1998 ◽

Vol 43 (2) ◽

pp. 252-255 ◽

Cited By ~ 31

Author(s):

J Hammer ◽

H F Hammer ◽

A J Eherer ◽

W Petritsch ◽

P Holzer ◽

...

Keyword(s):

Abdominal Pain ◽

Control Period ◽

Animal Experiments ◽

Sensory Nerves ◽

Jejunal Mucosa ◽

Occlusion Balloon ◽

Electrolyte Absorption ◽

Perfusion Studies ◽

Stimulation Of

Background—Stimulation of sensory nerves with capsaicin regulates ion transport in the small intestine in animal experiments.Aim—To investigate whether sensory nerves that are stimulated by capsaicin administration influence fluid and electrolyte absorption in the human jejunum in vivo.Method—Intestinal perfusion studies were performed in 12 healthy subjects using a four lumen tube with a proximal occlusion balloon and a plasma-like electrolyte solution. After an initial control period, 5 (n = 3), 10 (n = 8), or 50 (n = 1) μg/ml capsaicin was added to the perfusate, and this was followed by a final control period. Rates of absorption of water, sodium, potassium, chloride, and bicarbonate were determined in a 30 cm segment of jejunum using a non-absorbable volume marker.Results—At all three concentrations of capsaicin there were no significant changes in water and electrolyte absorption as compared with control periods. Two subjects who received 10 μg/ml and the subject receiving 50 μg/ml experienced crampy abdominal pain.Conclusion—The results do not support the hypothesis that capsaicin sensitive afferent nerves are involved in the physiological regulation of net absorption or secretion across the human jejunal mucosa. Chemical stimulation of these nerves, however, gives rise to abdominal pain.

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