Different tissues have different receptor types. For example, both α and β receptors are found in pancreatic islet beta cells, but the primary response to sympathetic discharge is mediated by α2 receptors.

The adrenal medulla receives direct innervation from the autonomic nervous system, leading to rapid adrenomedullary responses. These responses can occur before the actual stress begins due to involvement from various centers in the central nervous system, particularly the cerebral cortex.

Adrenomedullary output, primarily consisting of epinephrine, is often coordinated with sympathetic nervous activity, which involves the release of norepinephrine from postganglionic sympathetic neurons. However, some stimuli, such as hypoglycemia, evoke a stronger adrenomedullary response compared to sympathetic nervous response, and vice versa.

A sympathoadrenal response affects many organs and tissues. During exercise, the sympathoadrenal system plays a significant role. Exercise triggers a greater adrenomedullary response (endocrine role of epinephrine) compared to sympathetic nervous response (neurotransmitter role of norepinephrine). The overall aim of the sympathoadrenal system during exercise is to meet the increased energy demands of skeletal and cardiac muscle while ensuring sufficient oxygen and glucose supply to the brain.

Epinephrine and norepinephrine work together to increase blood flow to muscles. They affect the heart, veins, lymphatics, and arteriolar beds in nonmuscular (e.g., splanchnic) and muscular tissues.

Epinephrine promotes glycogenolysis in muscle and stimulates lipolysis in adipose tissue. It also increases blood glucose levels by enhancing hepatic glycogenolysis and gluconeogenesis. Lipolysis in adipose tissue is coordinated with an increase in hepatic ketogenesis induced by epinephrine. Catecholamines stimulate glucagon secretion (β2 receptors) and inhibit insulin secretion (α2 receptors), further impacting metabolism during exercise.

Catecholamines also promote the relaxation of bronchiolar smooth muscle, facilitating efficient exchange of gases and adequate oxygen supply to exercising muscle during normal exercise.

Additionally, a sympathoadrenal response decreases overall motility of smooth muscle in the gastrointestinal and urinary tracts, conserving energy where immediate need is not present.

Metabolism of catecholamines plays a crucial role in these physiological actions.
Location and relative density of receptors. Importantly, different receptor types predominate in different tissues. For example, although both α and β receptors are expressed by pancreatic islet beta cells, the predominant response to a sympathetic discharge is mediated by α2 receptors.
Physiological Actions  of Adrenomedullary Catecholamines
Because the adrenal medulla is directly innervated by the autonomic nervous system, adrenomedullary responses are very rapid. Furthermore, because of the involvement of several centers in the central nervous system (CNS), most notably the cerebral cortex, adrenomedullary responses can precede onset of the actual stress (i.e., they can be anticipated) (see
Fig. 43.5 ). In many cases the adrenomedullary output, which is primarily epinephrine, is coordinated with sympathetic nervous activity as determined by the release of norepinephrine from postganglionic sympathetic neurons. However, some stimuli (e.g., hypoglycemia) evoke a stronger adrenomedullary than sympathetic nervous response and vice versa.
Many organs and tissues are affected by a sympathoadrenal response (
Table 43.2). An informative example of the major physiological roles of catecholamines is the sympathoadrenal response to exercise. Exercise is similar to the “fight-or-flight” response but without the subjective element of fear, and it involves a greater adrenomedullary response (i.e., endocrine role of epinephrine) than a sympathetic nervous response (i.e., neurotransmitter role of norepinephrine). The overall goal of the sympathoadrenal system during exercise is to meet the increased energy demands of skeletal and cardiac muscle while maintaining sufficient oxygen and glucose supply to the brain. The response to exercise includes the following major physiological actions of epinephrine (
Fig. 43.6): 1. Increased blood flow to muscles is achieved by the integrated action of norepinephrine and epinephrine on the heart, veins and lymphatics, and nonmuscular (e.g., splanchnic) and muscular arteriolar beds.
•Fig. 43.4 Stepsinsynthesisandsecretionofcatecholaminesfromadrenalmedullarychromaffincells.
2. Epinephrine promotes glycogenolysis in muscle. Exercising muscle can also utilize free fatty acids (FFAs), and epinephrine and norepinephrine promote lipolysis in adipose tissue. Epinephrine increases blood glucose by increasing hepatic glycogenolysis and gluconeogenesis. The promotion of lipolysis in adipose tissue is also coordinated with an epinephrine-induced increase in hepatic ketogenesis. Finally, the effects of catecholamines on metabolism are reinforced by the fact that they stimulate glucagon secretion (β2 receptors) and inhibit insulin secretion (α2 receptors). Efficient production of adenosine triphosphate (ATP) during normal exercise •Fig. 43.5 Stimulithatenhancecatecholaminesecretion.
cAMP,cyclicadenosinemonophosphate;DAG,diacylglycerol.
Arteriolardilation:↓ BP↑ Arteriolarvasoconstriction; (β2)(muscle)↑ BP(α1)(splanchnic,renal,cutaneous,genital)
BP,bloodpressure.
(i.e., a 1-hour workout) also requires efficient exchange of gases with an adequate supply of oxygen to exercising muscle. Catecholamines promote this by relaxation of bronchiolar smooth muscle.
3. Catecholamines decrease energy demand by visceral smooth muscle. In general a sympathoadrenal response decreases overall motility of the smooth muscle in the gastrointestinal (GI) and urinary tracts, thereby conserving energy where it is not immediately needed.
Metabolism of Catecholamines