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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been shown that chronic lung diseases which increase the concentration of pulmonary carbon dioxide (CO2) at the expense of oxygen stimulate the secretion of biogenic amines and neuropeptides by pulmonary neuroendocrine cells (PNE cells) in man and laboratory animals. This increase in secretory activity is always accompanied by hyperplasia of PNE cells, and smokers with chronic obstructive lung disease are at high risk for the development of neuroendocrine lung cancer. We have previously shown that nicotine and the structurally related nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), stimulate the proliferation of neuroendocrine cell lines derived from lung carcinoid tumors via interaction with nicotinic acetylcholine receptors (nAChR). In our current experiment, we have addressed the mechanisms of cell proliferation in response to nicotine and NNK in normal PNE cells derived from fetal hamster lungs, and two cell lines derived from human neuroendocrine lung cancers. Our data show that in these systems the mitogenic effects of nicotine and NNK are potentiated in a concentration-dependent manner by elevated levels of CO2, an effect blocked by inhibitors of protein kinase C(PKC) and reduced by antagonists of receptors for 5-hydroxytryptamine (5-HT, serotonin) and mammalian bombesin. The observed effects of CO2 were saturable and independent of changes in the acidity of the tissue culture media. Our data suggest that increases in CO2 concentration at the expense of oxygen may stimulate signal transduction pathways in normal and neoplastic neuroendocrine lung cells thus enhancing their susceptibility to the mitogenic effects of tobacco-specific toxicants.
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PMID:Carbon dioxide potentiates the mitogenic effects of nicotine and its carcinogenic derivative, NNK, in normal and neoplastic neuroendocrine lung cells via stimulation of autocrine and protein kinase C-dependent mitogenic pathways. 771 58

The rat stress model of restraint and cold water immersion was used to investigate the effect of stimulating the paraventricular nucleus (PVN) of hypothalamus on the development of stress-induced gastric ulceration. The results were (1) electric stimulation of the PVN increased the stress ulceration, while electrolytic lesion of the PVN decreased it; (2) intracerebroventricular injection (i.c.v.) of acetylcholine (Ach) enhanced the effect of PVN stimulation on stress ulcers, and the M-receptor was involved; (3) i.c.v. norepinephrine (NE) attenuated the effect of PVN stimulation on stress ulcers in a dose-dependent manner, and the beta-receptor was involved; (4) i.c.v. 5-hydroxytryptamine (5-HT) enhanced the effect of PVN stimulation on stress ulcers; (5) electrolytic lesions of dorsal raphe nucleus (DR) attenuated the effect of PVN stimulation on stress ulcers, while electrolytic lesions of the locus ceruleus (LC) aggravated the effect; (6) thyroidectomy, adrenalectomy, ovariectomy, vagotomy and sympathectomy all attenuated the effect of PVN stimulation on stress ulcers; (7) electric stimulation of the PVN produced no effect on gastric juice volume, acidity, total acid output, pepsin activity or the gastric barrier mucus; but greatly reduced gastric mucosal blood flow. These results indicate that the PVN is an important brain site regulating the development of stress-induced gastric ulcers, that the classical neurotransmitters Ach, NE and 5-HT are involved, and that in the periphery, both the parasympathetic and sympathetic nervous systems and the three endocrine glands (thyroid, adrenal and gonad) take part in the effect.
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PMID:The role of paraventricular nucleus of hypothalamus in stress-ulcer formation in rats. 925 17