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Drugs Affecting Autonomic Ganglia (Including the Adrenal Medulla)
Published in Kenneth J. Broadley, Autonomic Pharmacology, 2017
The bisquatemary ammonium compounds do not produce initial stimulation of the receptor but cause competitive antagonism. The dose-response curves for contractile responses of guinea-pig ileum to nicotine or DMPP are displaced in a parallel manner with no depression of maximum by hexamethonium, pentamethonium, trimethaphan and TEA. In contrast, chlorisondamine produces non-competitive blockade, depressing the maximum with little or no rightwards displacement. Mecamylamine and pempidine produce both shift and depression of the maximum (Figure 11.5). The competitive antagonists shifted both the ascending and descending limbs of the dose-response curve in parallel manner, implying that the bell-shaped curve arises from autoinhibition of the response to receptor activation rather than autoinhibition at the receptors.
Enzymes
Published in Stephen W. Carmichael, Susan L. Stoddard, The Adrenal Medulla 1986 - 1988, 2017
Stephen W. Carmichael, Susan L. Stoddard
The role of nicotinic cholinergic transmission in cold stress-induced alterations in rat adrenal medullary TH mRNA was investigated by Stachowiak, Strieker, Zigmond et al. (1988) by using RNA dot-blot hybridization and a cloned TH cDNA probe. Chlorisondamine, a ganglionic blocker, greatly attenuated the induction of TH mRNA levels caused by cold exposure, whereas carbachol and nicotine, cholinergic agonists, increased TH mRNA levels. These results suggest that cholinergic nicotinic receptors play a key role in the transsynaptic induction of adrenal TH gene expression.
Hindbrain Neuroactive Substances Controlling Gastrointestinal Function
Published in T. S. Gaginella, Regulatory Mechanisms — in — Gastrointestinal Function, 2017
Zbigniew K. Krowicki, Pamela J. Hornby
Neurotensin (NT) is a known antisecretory agent when given parenterally. Administered icv, nanomolar doses of NT inhibited basal181, 182 and pentagastrin-, carbachol-, and 2-deoxy-D-glucose-stimulated gastric acid secretion in pentobarbital-anesthetized rats182 and pentagastrin-stimulated gastric acid secretion in conscious dogs.133 Blockade of the autonomic nervous system with chlorisondamine abolished the gastric inhibitory action induced by NT.133
Hypothesis: Fever control, a niche for alpha-2 agonists in the setting of septic shock and severe acute respiratory distress syndrome?
Published in Temperature, 2018
F. Petitjeans, S. Leroy, C. Pichot, A. Geloen, M. Ghignone, L. Quintin
In the setting of experimental sepsis, depletion (reserpine, 6-0HDA) of noradrenaline neurons [230,231] and normalization toward baseline activity of sympathetic activity with an alpha-2 agonist, dexmedetomidine [232], improve survival24. In healthy resting volunteers, inhibition of sympathetic activity with clonidine increases the density of beta-receptors on mononuclear cells and lowers the affinity of those beta receptors [76]: upregulation of adrenergic receptors [62,63,71,217] may occur on immunocompetent cells not only for beta receptors but for alpha-2 receptors as well. In addition, radiation increases the bacteria-induced inflammatory cytokines of the innate immune system; a ganglionic blocker, chlorisondamine, suppresses the phenomenon25 [233]: the implication is that the sympathetic system modifies the activity of the innate immune system, explaining, partially, the immuno-paralysis observed in the acute setting (septic shock). Clinically, administration of alpha-2 agonists lowers mortality in various subsets of CCU patients [40,64,234,235]. In the setting of septic shock or major surgery, normalization of sympathetic hyperactivity toward baseline levels by alpha-2 agonists has anti-inflammatory effects [195,217] including in the setting of septic shock ((233), Quintin, unpublished data)). Apparently, in our hands, the net overall effect of alpha-2 agonists is anti-inflammatory26. Thus, the possibility of normalizing the sympathetic hyperactivity back towards baseline levels to optimize a dysfunctional innate immune system, inflammation, immuno-paralysis and outcome in the acute setting of septic shock or ARDS should be studied.