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Histamine-induced ion secretion across rat distal colon: involvement of histamine H1 and H2 receptors.
Eur J Pharmacol. 2006 Sep 28; 546(1-3):161-70.EJ

Abstract

The aim of the present study was to investigate the effect of histamine, a product of e.g. mast cells, on short-circuit current (I(sc)) across rat distal colon. Histamine concentration-dependently stimulated an increase in I(sc), which often was preceded by a transient negative current. Neither a release of neurotransmitters nor a release of prostaglandins contributed to the histamine response. The histamine-induced increase in I(sc) was blocked by the histamine H(1) antagonist, pyrilamine, but was resistant against the histamine H(2) antagonist, cimetidine. Conversely, the histamine H(1) agonist, TMPH (2-(3-trifluoromethylphenyl)histamine), exclusively evoked an increase in I(sc), whereas the histamine H(2) agonist, amthamine, evoked only a decrease in I(sc) suggesting that stimulation of different types of histamine receptors is responsible for the two phases of the response evoked by native histamine. Histamine induces the opening of glibenclamide-sensitive Cl(-) channels and of charybdotoxin-sensitive K(+) channels in the apical membrane as demonstrated by experiments at basolaterally depolarized epithelia. A further action site is the basolateral membrane, because histamine stimulates a charybdotoxin- and tetrapentylammonium-sensitive K(+) conductance in this membrane as observed in tissues, in which the apical membrane was permeabilized with an ionophore, nystatin. The increase in I(sc) evoked by histamine was blocked after depletion of intracellular Ca(2+) stores with cyclopiazonic acid and after blockade of inositol 1,4,5-trisphosphate (IP(3)) receptors, suggesting a release of stored Ca(2+). This was confirmed by the observation that the histamine H(1) agonist TMPH induced an increase in the fura-2 ratio signal of epithelial cells within isolated colonic crypts. Consequently, the mediator histamine seems to stimulate both histamine H(1) and H(2) receptors, from which the former seems to be prominently involved in the induction of epithelial chloride secretion.

Authors+Show Affiliations

Institut für Veterinär-Physiologie, Justus-Liebig-Universität Giessen, Frankfurter Str. 100, D-35392 Giessen, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16919622

Citation

Schultheiss, Gerhard, et al. "Histamine-induced Ion Secretion Across Rat Distal Colon: Involvement of Histamine H1 and H2 Receptors." European Journal of Pharmacology, vol. 546, no. 1-3, 2006, pp. 161-70.
Schultheiss G, Hennig B, Schunack W, et al. Histamine-induced ion secretion across rat distal colon: involvement of histamine H1 and H2 receptors. Eur J Pharmacol. 2006;546(1-3):161-70.
Schultheiss, G., Hennig, B., Schunack, W., Prinz, G., & Diener, M. (2006). Histamine-induced ion secretion across rat distal colon: involvement of histamine H1 and H2 receptors. European Journal of Pharmacology, 546(1-3), 161-70.
Schultheiss G, et al. Histamine-induced Ion Secretion Across Rat Distal Colon: Involvement of Histamine H1 and H2 Receptors. Eur J Pharmacol. 2006 Sep 28;546(1-3):161-70. PubMed PMID: 16919622.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Histamine-induced ion secretion across rat distal colon: involvement of histamine H1 and H2 receptors. AU - Schultheiss,Gerhard, AU - Hennig,Britta, AU - Schunack,Walter, AU - Prinz,Gundula, AU - Diener,Martin, Y1 - 2006/08/01/ PY - 2006/03/23/received PY - 2006/07/05/revised PY - 2006/07/13/accepted PY - 2006/8/22/pubmed PY - 2007/1/12/medline PY - 2006/8/22/entrez SP - 161 EP - 70 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 546 IS - 1-3 N2 - The aim of the present study was to investigate the effect of histamine, a product of e.g. mast cells, on short-circuit current (I(sc)) across rat distal colon. Histamine concentration-dependently stimulated an increase in I(sc), which often was preceded by a transient negative current. Neither a release of neurotransmitters nor a release of prostaglandins contributed to the histamine response. The histamine-induced increase in I(sc) was blocked by the histamine H(1) antagonist, pyrilamine, but was resistant against the histamine H(2) antagonist, cimetidine. Conversely, the histamine H(1) agonist, TMPH (2-(3-trifluoromethylphenyl)histamine), exclusively evoked an increase in I(sc), whereas the histamine H(2) agonist, amthamine, evoked only a decrease in I(sc) suggesting that stimulation of different types of histamine receptors is responsible for the two phases of the response evoked by native histamine. Histamine induces the opening of glibenclamide-sensitive Cl(-) channels and of charybdotoxin-sensitive K(+) channels in the apical membrane as demonstrated by experiments at basolaterally depolarized epithelia. A further action site is the basolateral membrane, because histamine stimulates a charybdotoxin- and tetrapentylammonium-sensitive K(+) conductance in this membrane as observed in tissues, in which the apical membrane was permeabilized with an ionophore, nystatin. The increase in I(sc) evoked by histamine was blocked after depletion of intracellular Ca(2+) stores with cyclopiazonic acid and after blockade of inositol 1,4,5-trisphosphate (IP(3)) receptors, suggesting a release of stored Ca(2+). This was confirmed by the observation that the histamine H(1) agonist TMPH induced an increase in the fura-2 ratio signal of epithelial cells within isolated colonic crypts. Consequently, the mediator histamine seems to stimulate both histamine H(1) and H(2) receptors, from which the former seems to be prominently involved in the induction of epithelial chloride secretion. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/16919622/Histamine_induced_ion_secretion_across_rat_distal_colon:_involvement_of_histamine_H1_and_H2_receptors_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(06)00750-3 DB - PRIME DP - Unbound Medicine ER -