Modulatory action of potassium channel openers on field potential and histamine release from rat peritoneal mast cells.
Can J Physiol Pharmacol
; 87(8): 624-32, 2009 Aug.
Article
en En
| MEDLINE
| ID: mdl-19767887
To determine whether changes in membrane potential affect the extent of mast cell degranulation, compound 48/80 was added to rat peritoneal mast cell suspensions in the absence or presence of potassium channel openers (KCOs). Changes were compared between the field potential (FP) and the amount of histamine released. The results demonstrated that (i) the onset and duration of FP, which reflects the hyperpolarizing nature of the response, increased as the concentration of compound 48/80 increased; (ii) both FP and the amount of histamine released increased as the concentration of compound 48/80 increased; (iii) although both KCOs (SDZ PCO400, a benzopyran derivative, and P1060, a cyanoguanidine derivative) potentiated compound 48/80-induced increases in FP and histamine release, without compound 48/80, they had no effect on either parameter; (iv) both glibenclamide and charybdotoxin significantly attenuated the compound 48/80-induced increase in FP; and (v) glibenclamide was able to attenuate the KCO-induced potentiation of FP. The results show that drugs presumably causing hyperpolarization can affect histamine release from rat peritoneal mast cells. The effect of KCOs on compound 48/80-induced response appears to be potentiation in nature rather than synergism. It is possible that KCO hyperpolarizes the cell membrane, enhances Ca2+ influx, and thus increases histamine release. As such, selective blockers of K+ channels may be useful for the treatment of immunological disorders.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Peritoneo
/
Benzopiranos
/
P-Metoxi-N-metilfenetilamina
/
Ciclopentanos
/
Canales de Potasio de Gran Conductancia Activados por el Calcio
/
Canales KATP
/
Guanidinas
/
Liberación de Histamina
/
Mastocitos
Límite:
Animals
Idioma:
En
Revista:
Can J Physiol Pharmacol
Año:
2009
Tipo del documento:
Article
País de afiliación:
Hong Kong
Pais de publicación:
Canadá