Potentiation histamine

Burdyga In the guinea-pig ureter force is exclusively controlled by action potential. Agonists just modulate it by increasing the duration of the plateau component of the action potential. Histamine for example can increase plateau component duration up to 10 times. 

Effects on inflammation and pain E- and F-series PGs are known to be released in the inflammation and increase capillary permeability, producing edema and painful erythema. PGE, can produce this in quantities as low as 1 (ig PGFla requires about 1 jig. Erythema produced by an intradermal application may persist for 10 h. There is evidence that PGs Ej, E2, A2, and F2ot stimulate (potentiate ) histamine and bradykinin. Low concentrations of PGs induce hyperalgesia. This appears to be a sensitization of pain receptors. It was also demonstrated that subdermal infusion of PGE only pro-... 

An acetone extract of the bark and carscarillin potentiated histamine-stimulated gastric acid secretion in a mouse stomach preparation. The essential oil has shown antimicrobial activities. 

After the identification of the effects of histamine in the early twentieth century, screening for potential histamine antagonists was carried out. The first effective antihistamine compound to be found was cyclizine, which was discovered in the 1940s (Fig. 17.4). It was effective both in treating allergy and as an antiemetic. Investigations of the phenothiazine class of compounds led to the discovery of promethazine (Fig. 17.4) which is a very effective... 

Cuss FM, Dixon CMS, Barnes PJ. Effects of inhaled platelet activating factor on pulmonary function and bronchial responsiveness in man. Lancet 1986 ii 189-192. Johnson PR, Ammit AJ, Carlin SM, Armour CL, Caughey GH, Black JL. Mast cell tryptase potentiates histamine-induced contraction in human sensitized bronchus. Eur Respir J 1997 10 38-43. 

Melatonin [73-31-4] C 2H N202 (31) has marked effects on circadian rhythm (11). Novel ligands for melatonin receptors such as (32) (12), C2yH2gN202, have affinities in the range of 10 Af, and have potential use as therapeutic agents in the treatment of the sleep disorders associated with jet lag. Such agents may also be usehil in the treatment of seasonal affective disorder (SAD), the depression associated with the winter months. Histamine (see Histamine and histamine antagonists), adenosine (see Nucleic acids), and neuropeptides such as corticotropin-like intermediate lobe peptide (CLIP) and vasoactive intestinal polypeptide (VIP) have also been reported to have sedative—hypnotic activities (7). 

UV spectroscopy and. 500 Histamine, structure of, 965 Histidine, electrostatic potential map of, 1021... 

Few prospective studies of induced anaphylaxis have been performed in human subjects to imderstand the molecular basis of systemic anaphylaxis, because of the potentially rapid, Ufe-threatening outcome. Accordingly, various models of anaphylaxis have been estabUshed in laboratory animals, particularly mice, and extensively studied to clarify the underlying mechanisms. Such studies revealed that the classical pathway utilizing mast cells, IgE and histamine cannot explain all cases of anaphylaxis. 

With regard to epinephrines potential adverse cardiac effects, it is important to remember that in anaphylaxis, the heart is a target organ. Mast cells located between myocardial fibers, in perivascular tissue, and in the arterial intima are activated through IgE and other mechanisms to release chemical mediators of inflammation, including histamine, leukotriene C4, and prostaglandin D2. Coronary artery spasm, myocardial injury, and cardiac dysrhythmias have been documented in some patients before epinephrine has been injected for treatment of anaphylaxis, as well as in patients with anaphylaxis who have not been treated with epinephrine [11, 12]. 

Sea urchin toxins extracted from spines or pedicellariae have a variety of pharmacological actions, including electrophysiological ones (75). Dialyzable toxins from Diadema caused a dose-dependent increase in the miniature end-plate potential frequency of frog sartorius muscle without influencing membrane potential (76). A toxin from the sea urchin Toxopneustes pUeolus causes a dose-dependent release of histamine (67). Toxic proteins from the same species also cause smooth muscle contracture in guinea pig ileum and uterus, and are cardiotoxic (77). 

Leurs, R, Blandina, P, Tedford, C and Timmerman, H (1998) Therapeutic potential of histamine H3 receptor agonists and antagonists. Trends Pharmacol. Sci. 19 177-183. 

Daum, P. R., Hill, S. J. Young, J. M. (1982). Histamine Hl-agonist potentiation of adenosine-stimulated cyclic AMP accumulation in slices of guinea-pig cerebral cortex comparison of response and binding parameters. Br. J. Pharmacol. 77, 347-57. 

Haas, H. L. (1984). Histamine potentiates neuronal excitation by blocking a calcium-dependent potassium conductance. Agents Actions 14, 534-7. 

Munzar, R, Tanda, G., Justinova, Z., Goldberg, S.R. Histamine h3 receptor antagonists potentiate methamphetamine self-administration and methamphetamine-induced accumbal dopamine release. Neuropsychopharmacology. 29 705, 2004. 

Histaminergic activation of ion channels may also occur through NMDA receptors [ 1 ]. This action occurs at the polyamine binding site on NR1/NR2B subunits and is sensitive to pH. Endogenous histamine may act at this site to facilitate the induction of long term potentiation, but this has not been established. Additional histamine receptors may still be discovered. 

---