Pharmacological investigation into the effects of histamine and histamine analogues on guinea‐pig and rat colon <i>in vitro</i>

Aguilar, María-José; Morales‐Olivas, Francisco J.; Rubio, E.

doi:10.1111/j.1476-5381.1986.tb10229.x

Cited by 17 publications

(6 citation statements)

References 21 publications

(22 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Drugs and chemicals utilized in the present study were from Sigma-Aldrich (St. Louis, MO) or Tocris Bioscience (Bristol, UK). The solutions of histamine (100 μM; [ 26 – 28 ]), 2-pyridylethylamine (100 μM; [ 29 – 33 ]) and amthamine (20 μM; [ 34 – 36 ]) were prepared in ACSF or HEPES-buffered saline. The solutions of bumetanide (10 μM; [ 16 , 37 , 38 ]), CFTR inh -172 (50 μM; [ 39 – 41 ]), gallein (100 μM; [ 42 – 44 ]), H89 (10 μM; [ 45 – 47 ]), KT5720 (1 μM; [ 48 – 50 ]), bicuculline (30 μM; [ 51 – 53 ]) and strychnine (1 μM; [ 54 – 56 ]) were prepared by diluting the stock solutions with ACSF or HEPES-buffered saline; the solvent of stock solutions was dimethyl sulphoxide and its final concentration was 0.01–0.003 %.…”

Section: Methodsmentioning

confidence: 99%

Histamine 1 receptor-Gβγ-cAMP/PKA-CFTR pathway mediates the histamine-induced resetting of the suprachiasmatic circadian clock

Kim

et al. 2016

Mol Brain

View full text Add to dashboard Cite

BackgroundRecent evidence indicates that histamine, acting on histamine 1 receptor (H1R), resets the circadian clock in the mouse suprachiasmatic nucleus (SCN) by increasing intracellular Ca2+ concentration ([Ca2+]i) through the activation of CaV1.3 L-type Ca2+ channels and Ca2+-induced Ca2+ release from ryanodine receptor-mediated internal stores.ResultsIn the current study, we explored the underlying mechanisms with various techniques including Ca2+- and Cl−-imaging and extracellular single-unit recording. Our hypothesis was that histamine causes Cl− efflux through cystic fibrosis transmembrane conductance regulator (CFTR) to elicit membrane depolarization needed for the activation of CaV1.3 Ca2+ channels in SCN neurons. We found that histamine elicited Cl− efflux and increased [Ca2+]i in dissociated mouse SCN cells. Both of these events were suppressed by bumetanide [Na+-K+-2Cl− cotransporter isotype 1 (NKCC1) blocker], CFTRinh-172 (CFTR inhibitor), gallein (Gβγ protein inhibitor) and H89 [protein kinase A (PKA) inhibitor]. By itself, H1R activation with 2-pyridylethylamine increased the level of cAMP in the SCN and this regulation was prevented by gallein. Finally, histamine-evoked phase shifts of the circadian neural activity rhythm in the mouse SCN slice were blocked by bumetanide, CFTRinh-172, gallein or H89 and were not observed in NKCC1 or CFTR KO mice.ConclusionsTaken together, these results indicate that histamine recruits the H1R-Gβγ-cAMP/PKA pathway in the SCN neurons to activate CaV1.3 channels through CFTR-mediated Cl− efflux and ultimately to phase-shift the circadian clock. This pathway and NKCC1 may well be potential targets for agents designed to treat problems resulting from the disturbance of the circadian system.

show abstract

Section: Methodsmentioning

confidence: 99%

Histamine 1 receptor-Gβγ-cAMP/PKA-CFTR pathway mediates the histamine-induced resetting of the suprachiasmatic circadian clock

Kim

et al. 2016

Mol Brain

View full text Add to dashboard Cite

show abstract

“…Effective concentration 50% (EC 50 ) was calculated graphically from a plot of log concentration vs. the maximum response (E max ) produced by each agonist in individual experiments. The pA 2 value for antagonism was calculated according to the method of Arunlakshana & Schild (1959), as previously described (Aguilar, Morales-Olivas & Rubio, 1986). For optimum fitting of pA 2 , the maximum response (E max ) and halfmaximal effective concentrations (EC 50 ) of agonists were calculated from concentration-response curves by fitting the experimental data to a logistic-equation by non-linear regression analysis.…”

Section: Methodsmentioning

confidence: 99%

The effects of histamine on the isolated mouse uterus

Rubio

Navarro-Badenes

Palop³

et al. 1999

Journal of Autonomic Pharmacology

View full text Add to dashboard Cite

1. A study is made of the contractile and relaxant effects, and mechanism of action, of histamine on isolated uterus from mice treated with diethylstilboestrol, employing acetylcholine and adrenaline as contractile and relaxant standard agents. 2. Concentration-response curves for histamine agonists were obtained in the absence and presence of selective histaminergic blocking drugs (clemizole, ranitidine and thioperamide) and indomethacin. A number of experiments were carried out in uterus from reserpinised mice. Concentration-response curves for acetylcholine and adrenaline were also obtained in the absence and presence of their selective antagonist (atropine and propranolol). 3. In isolated oestrogenised mouse uterus, histamine and acetylcholine produced a concentration-related contractile response. When the uterus was precontracted with KCl, histamine at lower doses produced a slight contraction, though in the presence of clemizole it induced concentration-related relaxation, reminiscent of that produced by adrenaline. Atropine and propranolol antagonised the contractile and relaxant effects of acetylcholine and adrenaline, respectively. 4. In isolated uterus from reserpinised mice, histamine and 2-pyridylethylamine, but not 4-methylhistamine, produced a concentration-related contractile response. Ranitidine potentiated the contractile effect of histamine, though clemizole--in the presence of ranitidine--competitively antagonised the contractile effect of histamine (pA2 = 10.50 +/- 0.81). The concentration-relaxant curve of histamine in the presence of clemizole was not modified by ranitidine or indomethacin, but shifted to the right with thioperamide. The same displacement was also observed in the presence of clemizole plus ranitidine. 5. In mouse isolated uterus, histamine mainly produced contraction mediated by histamine H1-receptors, though the existence of histamine H2- or H3-receptors mediating relaxation could not be excluded.

show abstract

“…The calculation of the pA2 values was according to Arunlakshana & Schild (1959) as described previously (Aguilar et al 1986). All data are shown as mean standard error of the mean.…”

Section: Methodsmentioning

confidence: 99%

Antihistaminic and anticholinergic activities of mequitazine in comparison with clemizole

Martínez-Mir

Estañ

Rubio

et al. 1988

Journal of Pharmacy and Pharmacology

View full text Add to dashboard Cite

The antihistamine and anticholinergic properties of mequitazine have been investigated and compared with those of clemizole. Both mequitazine and clemizole antagonized the effect of histamine in guinea-pig ileum competitively, the pA2 values calculated by Schild plot were 9.95 +/- 0.44 for mequitazine and 10.54 +/- 0.44 for clemizole. Mequitazine at 10(-7) M produced a parallel shift of the dose-response curve to acetylcholine in the rat duodenum, clemizole and the lower doses of mequitazine failed to modify the effect of acetylcholine. The potency of mequitazine and clemizole as H1-histamine blockers is similar, but only mequitazine at highest concentration used showed anticholinergic activity.

show abstract

Pharmacological investigation into the effects of histamine and histamine analogues on guinea‐pig and rat colon in vitro

Cited by 17 publications

References 21 publications

Histamine 1 receptor-Gβγ-cAMP/PKA-CFTR pathway mediates the histamine-induced resetting of the suprachiasmatic circadian clock

Histamine 1 receptor-Gβγ-cAMP/PKA-CFTR pathway mediates the histamine-induced resetting of the suprachiasmatic circadian clock

The effects of histamine on the isolated mouse uterus

Antihistaminic and anticholinergic activities of mequitazine in comparison with clemizole

Contact Info

Product

Resources

About