The apocrine sweat glands, located on the palms of the hands and a few other areas, are nonthermoregulatory glands that respond to psychological stress and adrenoceptor stimulation with increased sweat production. (The diffusely distributed thermo-regulatory eccrine sweat glands are regulated by sympathetic cholinergic postganglionic nerves that activate muscarinic cholinergic receptors; see Chapter 6.)
Sympathomimetic drugs have important effects on intermediary metabolism. Activation of β adrenoceptors in fat cells leads to increased lipolysis with enhanced release of free fatty acids and glycerol into the blood. Beta3 adrenoceptors play a role in mediating this response in animals, but their role in humans is not clear. Experimentally, the β3 agonist mirabegron stimulates brown adipose tissue in humans. The potential importance of this finding is that brown fat cells (“good fat”) are thermogenic and thus have a positive metabolic function. Brown adipose tissue is present in neonates, but only remnant amounts are normally found in adult humans. Therefore, it is not clear whether β3 agonists can be used therapeutically for the treatment of obesity. Human fat cells also contain α2 receptors that inhibit lipolysis by decreasing intracellular cAMP. Sympathomimetic drugs enhance glycogenolysis in the liver, which leads to increased glucose release into the circulation. In the human liver, the effects of catecholamines are probably mediated mainly by β receptors, although α1 receptors may also play a role. Catecholamines in high concentration may also cause metabolic acidosis. Activation of β2 adrenoceptors by endogenous epinephrine or by sympathomimetic drugs promotes the uptake of potassium into cells, leading to a fall in extracellular potassium. This may result in a fall in the plasma potassium concentration during stress or protect against a rise in plasma potassium during exercise. Blockade of these receptors may accentuate the rise in plasma potassium that occurs during exercise. On the other hand, epinephrine has been used to treat hyperkalemia in certain conditions, but alternatives are more commonly used. Beta receptors and α2 receptors that are expressed in pancreatic islets tend to increase and decrease insulin secretion, respectively, although the major regulator of insulin release is the plasma concentration of glucose.
Catecholamines are important endogenous regulators of hormone secretion from a number of glands. As mentioned above, insulin secretion is stimulated by β receptors and inhibited by α2 receptors. Similarly, renin secretion is stimulated by β1 and inhibited by α2 receptors; indeed, β-receptor antagonist drugs may lower blood pressure in patients with hypertension at least in part by lowering plasma renin. Adrenoceptors also modulate the secretion of parathyroid hormone, calcitonin, thyroxine, and gastrin; however, the physiologic significance of these control mechanisms is probably limited. In high concentrations, epinephrine and related agents cause leukocytosis, in part by promoting demargination of sequestered white blood cells back into the general circulation.