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Am J Physiol Endocrinol Metab 277: E56-E62, 1999;
0193-1849/99 $5.00
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Vol. 277, Issue 1, E56-E62, July 1999

Characterization of receptors mediating AVP- and OT-induced glucagon release from the rat pancreas

Sirintorn Yibchok-Anun, Henrique Cheng, Patricia A. Heine, and Walter H. Hsu

Department of Biomedical Sciences, Iowa State University, Ames, Iowa 50011

We characterized the receptors that mediate arginine vasopressin (AVP)- and oxytocin (OT)-induced glucagon release by use of a number of antagonists in the perfused rat pancreas and the fluorescence imaging of the receptors. AVP and OT (3 pM-3 nM) increased glucagon release in a concentration-dependent manner. The antagonist with potent V1b receptor-blocking activity, CL-4-84 (10 nM), abolished AVP (30 pM)-induced glucagon release but did not alter OT (30 pM)-induced glucagon release. d(CH2)5[Tyr(Me)2]AVP (10 nM), a V1a receptor antagonist, and L-366,948 (10 nM), a highly specific OT-receptor antagonist, failed to inhibit AVP-induced glucagon release. In contrast, L-366,948 (10 nM) abolished OT (30 pM)-induced glucagon release but did not change the effect of AVP. Fluorescent microscopy of rat pancreatic sections showed that fluorescence-labeled AVP and OT bound to their receptors in the islets of Langerhans and that the bindings were inhibited by 1 µM of Cl-4-84 and L-366,948, respectively. Because AVP and OT at physiological concentrations (3-30 pM) increased glucagon release, we conclude that AVP and OT increase glucagon release under the physiological condition through the activation of V1b and OT receptors, respectively.

L-366,948; V1b receptor; oxytocin receptor; perfusion; fluorescence


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