Regulation by monovalent cations of histamine H2 receptor-coupled adenylate cyclase from guinea pig fundic gastric mucosa

Life Sciences ◽  
1983 ◽  
Vol 33 (9) ◽  
pp. 895-902 ◽  
Author(s):  
Bie Shung Tsai ◽  
T.O. Yellin
1976 ◽  
Vol 6 (6) ◽  
pp. 677-682 ◽  
Author(s):  
P. Scholes ◽  
Ann Cooper ◽  
D. Jones ◽  
J. Major ◽  
M. Walters ◽  
...  

1996 ◽  
Vol 320 (1) ◽  
pp. 27-32 ◽  
Author(s):  
Yasushi FUKUSHIMA ◽  
Tomoichiro ASANO ◽  
Hideki KATAGIRI ◽  
Makoto AIHARA ◽  
Toshihito SAITOH ◽  
...  

The histamine H2 receptor is a member of the family of G-protein-coupled receptors and is linked to the activation of adenylate cyclase phospholipase C (PLC). In this study we examined the effects of protein kinase C (PKC) activation in Chinese hamster ovary (CHO) cells stably expressing canine histamine H2 receptors. Pretreatment with 100 nM phorbol 12-myristate 13-acetate at 37 °C for 15 min led to significant potentiation of histamine-dependent and forskolin-dependent cAMP production, whereas the biologically inactive phorbol ester, 4α-phorbol 12,13-didecanoate, was without effect. These potentiating effects were abolished by preincubation with 0.5 µM bisindolylmaleimide, a PKC inhibitor. Thus the activation of PKCs seems to be involved in the potentiation of cAMP production by acting on a post-receptor mechanism. Preincubation of a CHO cell line, CHO-H2R, with 10 µM histamine for 30 min had two effects. Maximal histamine-dependent cAMP production and forskolin-dependent cAMP production were potentiated by 36% and 105.2% respectively. The other effect was a desensitization of the histamine-dependent adenylate cyclase response as demonstrated by a three-fold increase in EC50. Administration of 0.5 µM bisindolylmaleimide before preincubation of CHO-H2R with 10 µM histamine did not alter the desensitizing effect on cAMP production, but did abolish the sensitizing effect. Preincubation of CHO-H2R cells with 10 nM histamine resulted in moderate potentiation, which was also abolished by bisindolylmaleimide, but not in desensitization of the histamine-dependent cAMP production. Thus these results suggest that preincubation with histamine had a sensitizing effect on cAMP production mediated by PLC and PKC activation, as well as a desensitizing effect on the H2 receptor. The former effect is dependent on the intensity of PLC and PKC signals delivered by H2 receptors. The latter effect requires a higher concentration of histamine.


2001 ◽  
Vol 60 (6) ◽  
pp. 1210-1225 ◽  
Author(s):  
Melissa T. Kelley ◽  
Tilmann Bürckstümmer ◽  
Katharina Wenzel-Seifert ◽  
Stefan Dove ◽  
Armin Buschauer ◽  
...  

1995 ◽  
Vol 268 (3) ◽  
pp. G465-G470 ◽  
Author(s):  
H. J. Cooke ◽  
Y. Z. Wang ◽  
R. Reddix ◽  
N. Javed

Previous studies demonstrated neurally mediated recurrent increases in short-circuit current (Isc) suggestive of anion secretion in guinea pig distal colon. To determine the neural pathways involved, segments of distal colon from guinea pigs were mounted in flux chambers. In muscle-stripped or whole thickness preparations, serosal addition of the histamine H2 receptor agonist, dimaprit, caused cyclical increases in Isc, which were reduced by the chloride channel blocker, N-phenylanthranilic acid, but not by the sodium channel blocker amiloride. Dimaprit stimulated release of [3H]acetylcholine and vasoactive intestinal polypeptide (VIP) from submucosal/mucosal sheets. Dimaprit caused recurrent increases in Isc, which were significantly decreased by mecamylamine, a nicotinic receptor antagonist, and nearly abolished by the muscarinic antagonist, atropine (M3 > M1 = M2). The muscarinic antagonist, 4-diphenylacetoxy-N-methyl-piperidine methiodide (4-DAMP, M3 > M1), was more potent than pirenzepine (M1 > M3) in reducing recurrent increases in Isc. Dimaprit- and electrically evoked secretion were inhibited by the VIP antagonists [4Cl-D-Phe6, Leu17]VIP and VIP hybrid. The results suggest the involvement of VIP-ergic and cholinergic neurons utilizing nicotinic and muscarinic synapses in mediating secretion.


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