Is yohimbine-induced increase in salivary secretion a kinin-dependent mechanism?
We have previously reported that the alpha 2-adrenoceptor antagonist yohimbine induced a significant increase in both salivary flow rate and kallikrein output. In order to assess the possible role of the kinin-kallikrein system in the increase in salivary secretion elicited by yohimbine, the effects of aprotinin, an inhibitor of kallikrein activity, were investigated in yohimbine-treated conscious dogs. Aprotinin (at a dose, 5000 IU/kg iv, which reduced both resting and yohimbine-induced increase in kininogenase and amidolytic activities of saliva) which remained inactive alone, failed to modify the increase in salivary volume elicited by yohimbine (0.5 mg/kg iv). These results show that the rise in salivary flow rate observed under alpha 2-adrenoceptor antagonist is not induced by the kinin-kallikrein system. The release of kallikrein into saliva observed after yohimbine is rather the consequence than the cause of the increase in salivary secretion.
Laboratoire de Pharmacologie Médicale et clinique, INSERM U317, Faculté de Médecine, Toulouse, France.
H
H
Bagheri
G
G
Bompart
J P
JP
Girolami
J L
JL
Montastruc
P
P
Montastruc
D000818:Animals; D007611:Aprotinin / Q000494:pharmacology; D004285:Dogs; D005260:Female; D007610:Kallikreins / Q000032:analysis; D007705:Kinins / Q000502:physiology*; D008297:Male; D012463:Saliva / Q000737:chemistry; D012472:Salivation / Q000187:drug effects*; D015016:Yohimbine / Q000494:pharmacology*
D007705:Kinins; D015016:Yohimbine; D007611:Aprotinin; D007610:Kallikreins