Part of “CHAPTER 85 – PHYSIOLOGY OF THE ADRENAL MEDULLA AND THE SYMPATHETIC NERVOUS SYSTEM“

Sympathoneural and adrenomedullary activation in response to physiologic or pharmacologic manipulations can be generalized or patterned. Consideration of the appropriateness of adjustments to a particular challenge can help to explain the observed patterns of responses.

Sympathetic neural outflow to most vascular beds increases in response to orthostasis, isometric exercise, exposure to cold, and extracellular volume depletion; thus, plasma NE increases.76 Pharmacologic agents such as amphetamine, tyramine, clonidine, and isoproterenol also affect plasma NE levels preferentially. The pharmacologic findings imply that mechanisms of modulation of catecholamine release may differ between sympathetic nerve endings and adrenomedullary cells. The physiologic stimuli have in common a relatively minor influence on compensatory mechanisms for fuel production or utilization and seem mainly to elicit sympathetic neural responses leading to appropriate shifts in blood flow distribution or glandular secretion.Stimulation of arterial “high-pressure” baroreceptors appears to inhibit sympathetic outflow diffusely, although with quantitative differences among regional beds.77

Adrenomedullary activity increases markedly in response to hypoglycemia, hemorrhage, asphyxiation, circulatory collapse, and emotional distress; therefore, plasma EPI increases to a greater extent than does plasma NE in these situations.77,78 and 79 Because of the potential threat to the organism’s existence, even small decreases in levels of glucose trigger circulatory, metabolic, and visceral responses to maximize delivery of this vital fuel; adrenomedullary activation contributes importantly to these responses.