Sympathetic postganglionic neurons generally release nor-epinephrine, which can stimulate some effector cells and inhibit others. The target cells possess α or β-adrenergic receptors, which can be further classified into α1, α2, β1, β2, and β3 receptor types based on their pharmacological and genetic characteristics. Table 11.1 provides the distribution of these receptors and the corresponding actions when activated by sympathetic postganglionic neurons in various target organs. α1 receptors are found postsynaptically, while α2 receptors can be either presynaptic or postsynaptic. Presynaptic α2 receptors, also known as autoreceptors, typically suppress transmitter release. The effects of agents stimulating α1 or α2 receptors can be distinguished using specific receptor blockers, such as prazosin for α1-adrenergic receptors and yohimbine for α2-adrenergic receptors. The activation of α1 receptors triggers the inositol triphosphate/diacylglycerol second messenger system. Conversely, α2 receptors decrease cyclic adenosine monophosphate (cAMP) synthesis through the influence of a G protein.

Originally, β receptors were classified based on their susceptibility to blockade by antagonists. However, this classification has been complemented by genetic research. The β1 and β2 proteins have been extensively studied compared to β3, but it is believed that all three types of β receptors consist of similar proteins with seven membrane-spanning regions linked by intracellular and extracellular domains. Agonist drugs acting on β receptors activate a G protein that stimulates adenylyl cyclase, leading to an increase in cAMP levels. The action of these drugs is terminated by the accumulation of guanosine diphosphate.

Effector Organ          Receptor Type     Adrenergic Impulses     Responses     Cholinergic Impulses     Responses
Radial muscle, iris    α                     Contraction (mydriasis)  ++                      —                                     Sphincter muscle, iris  α                     —                                     Contraction (miosis)   +++                                    Ciliary muscle           β                     Relaxation for far vision   +                                   Contraction for near vision   ++

Sinoatrial node          β1                   Increase in heart rate     ++                      Decrease in heart rate; vagal arrest  +++                      Atria                         β1                   Increase in contractility and conduction  Decrease in contractility and (usually) velocity  ++                        Increase in conduction velocity  ++
Atrioventricular (AV) node  β1             Increase in automaticity and conduction velocity  Decrease in conduction velocity; AV block  ++                            +++
His-Purkinje system   β1                   Increase in automaticity and little effect on conduction velocity  +++                    Ventricles                β1                   Increase in contractility, conduction velocity, automaticity, and rate of idioventricular pacemakers  ++

Coronary                 α, β2               Constriction+; dilation                                          Skeletal muscle          α, β2               Constriction++; dilation c, e                           Pulmonary                α, β2               Constriction+; dilation                                         Abdominal viscera, renal  α, β2               Constriction+++; dilation                                    —
Salivary glands          α                    Constriction+++                                                     Dilation++                                                          Veins (Systemic)         α, β2               Constriction++; dilation++                                      —

Responses of Effector Organs to Autonomic Nerve Impulses—cont’d 11.1
Effector Organs               Receptor Type     Adrenergic Impulses       Responsesb      Cholinergic Impulses   Responsesb
Bronchial muscle            β2                 Relaxation+                       Contraction++                               Bronchial glands           ?                  Inhibition(?)                    Stimulation+++                        Motility and tone          α2, β2          Decrease (usually)             Increase+++                                Sphincters                   α                  Contraction (usually)          Relaxation (usually)                    Secretion                   ?                  Inhibition(?)                    Stimulation+++
Sympathetic postganglionic neurons typically release nor-epinephrine, which excites some effector cells but inhibits others. The receptors on target cells may be either α-or β-adrenergic receptors. These receptors are further subdivided into α1, α2, β1, β2, and β3 receptor types on the basis of pharmacological and genetic features. The distribution of these types of receptors and the actions that they mediate when activated by sympathetic postganglionic neurons are listed for various target organs in
Table 11.1 α1 receptors are located postsynaptically, but α2 receptors may be either presynaptic or postsynaptic. Receptors located presynaptically are generally called autoreceptors; they usually inhibit release of transmitter. The effects of agents that excite α1 or α2 receptors can be distinguished through the use of antagonists to block these receptors specifically. For example, prazosin is a selective α1-adrenergic antagonist, and yohimbine is a selective α2-adrenergic antagonist. The effects of α1 receptors are mediated by activation of the inositol triphosphate/diacylglycerol second messenger system (see
Chapter 3).
In contrast, α2 receptors decrease the rate of synthesis of cyclic adenosine monophosphate (cAMP) through action on a G protein.
β receptors were originally classified on the basis of the ability of antagonists to block them, but this has been supplemented by genetic studies. The β1 and β2 proteins have been much more extensively studied than has β3, but it is thought that the proteins that make up all three types of β receptors are similar, with seven membrane-spanning regions connected by intracellular and extracellular domains (see ). Agonist drugs that work on β receptors activate a G protein that stimulates adenylyl cyclase to increase the cAMP concentration. This action is terminated by the buildup of guanosine diphosphate.
Radialmuscle,irisα Contraction(mydriasis)++ —Sphinctermuscle,irisα —Contraction(miosis)+++ Ciliarymuscleβ Relaxationforfarvision+ Contractionfornearvision+++
Sinoatrialnodeβ1Increaseinheartrate++ Decreaseinheartrate;vagalarrest+++ Atriaβ1IncreaseincontractilityandconductionDecreaseincontractilityand(usually)velocity++ increaseinconductionvelocity++ Atrioventricular(AV)nodeβ1IncreaseinautomaticityandDecreaseinconductionvelocity;AVblockconductionvelocity++ +++ His-Purkinjesystemβ1IncreaseinautomaticityandLittleeffectconductionvelocity+++ Ventriclesβ1Increaseincontractility,conductionSlightdecreaseincontractilityvelocity,automaticity,andrateofidioventricularpacemakers+++
Coronaryα,β2Constriction+;dilation
Skeletalmuscleα,β2Constriction++;dilation c,e
Pulmonaryα,β2Constriction+;dilation
Abdominalviscera,renalα,β2Constriction+++;dilation + —Salivaryglandsα Constriction+++ Dilation++ Veins (Systemic) α,β2Constriction++;dilation++ —
Responses of Effector Organs to Autonomic Nerve Impulses—cont’d 11.1
Effector Organs Receptor Type Adrenergic Impulses,a Responsesb Cholinergic Impulses,a Responsesb
Bronchialmuscleβ2Relaxation+ Contraction++ Bronchialglands?Inhibition(?)Stimulation+++
Motilityandtoneα2,β2Decrease(usually) + Increase+++ Sphinctersα Contraction(usually)+ Relaxation(usually)+ SecretionInhibition(?)Stimulation+++