Table 1.

Major noradrenergic receptor subtypes

Receptor	Subtype	Action	G-coupled mechanism
Alpha-1	A, B, D	Smooth muscle, mucosa, gastrointestinal (GI) contraction, vasoconstriction and mydriasis. Activation produces anorexia, decreases cellular excitability in the temporal cortex and decreases glutamatergic excitatory postsynaptic potential	Gq: phospholipase C (PLC) activated, inositol triphosphate (IP3), diacylglycerol (DAG), increase calcium output
Alpha-2	A, B, C	Smooth muscle contraction/relaxation, NE inhibition, platelet activation, inhibition of insulin release and induction of glucan from pancreas, negative feedback in neuronal synapses, presynaptic inhibition of NE release in the CNS	Gi: adenylate cyclase inactivation (cAMP) decrease
Beta-1	-	Increase cardiac output (positive chronotropic, dromotropic and inotropic effects,) increased amylase secretion, renin secretion from kidney and ghrelin from stomach.	Gs: adenylate cyclase activation (cAMP) increase
Beta-2	-	Smooth muscle relaxation, glycogenolysis and gluconeogenesis, stimulate insulin secretion from the pancreas, increases renin secretin from kidney. The Beta-2 receptor in the brain is involved in immune communication and in the flight-fight response	Gi and Gs: adenylate cyclase activation (cAMP) increase
Beta-3	-	Enhances lipolysis, promotes relaxation in the muscle in the bladder. Some beta-3 agonists have anti-stress properties in animal models	Gs: adenylate cyclase activation(cAMP) increase