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Downregulation of beta-adrenergic receptors and signal transduction response in salivary glands of NOD mice
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1994
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Stimulus ResponseImmunologyDiabetic Nod MiceSalivary GlandMetabolic SyndromeAdrenal GlandNeuroendocrine MechanismCell SignalingHealth SciencesSignal Transduction ResponseEndocrine MechanismHormonal ReceptorInsulin ManagementSalivary GlandsNod MiceNervous SystemEndocrinologyPharmacologySignal TransductionPhysiologyDiabetesMedicine
The nonobese diabetic (NOD) mouse is subject to autoimmune disease-associated lymphocytic attack on the salivary glands with a corresponding loss of exocrine function. Downregulation of stimulus response to the beta-adrenoceptor agonist, isoproterenol, appears to be related to a decline in beta-adrenergic receptor density, changes in the level of intracellular second messenger signaling component adenosine 3',5'-cyclic monophosphate, and protein kinase A activity. An autoantibody to the beta 1-adrenergic receptor present in the sera of diabetic NOD mice may be involved in the reduced agonist response by virtue of its ability to retard dihydroalprenolol radioligand binding to receptors in the membranes of salivary glands from control mice and recognition of purified beta 1-adrenergic receptor by immunoblotting techniques.