Physiology and pharmacology of the splanchnic‐adrenal medullary junction.

Abstract

The adrenal medulla is the ancestral homologue of autonomic ganglia. The innervation of the medulla through a complex of nerves rather than a single trunk allows physiological dissection of synaptic behaviour. In previous experiments, synaptic function within the adrenal medulla of the cat has been studied by testing its response to nervous excitation and by investigating properties such as threshold, fatigue and susceptibility to ganglion-blocking drugs (Marley & Paton, 1961). New data are here presented on the threshold to nerve excitation, spatial and temporal recruitment, fatigue, the effect of drugs on these phenomena and the presence of functional units within the adrenal medulla. The preliminary findings have been communicated to the Physiological Society (Marley, 1961;Marley & Prout, 1963). METHODSCats were anaesthetized with chloralose (80 mg/kg i.v.) after induction with ethyl chloride and ether. The vagi were cut in the neck and the animal was artificially respired. Carotid arterial blood pressure was recorded with a mercury manometer on a kymograph.Usually the splanchnic nerves of one side were stimulated. They were approached retroperitoneally through a lumbar incision and the adrenolumbar vessels were divided between ligatures. As described elsewhere (Marley & Prout, 1965), there are three or four upper splanchnic nerves to the adrenal medulla. These were identified and cut through and the sympathetic chain was removed from the first to the fourth lumbar sympathetic ganglia. The abdominal viscera including the adrenal gland not under test were removed, and the renal vessels were tied. Heparin (10 mg/kg i.v.) was injected. In several recovery experiments the adrenal glands were chronically denervated under aseptic conditions, the cats being anaesthetized with halothane (Fluothane) and oxygen by a modification of the method for anaesthetizing new-born animals (Marley & Payne, 1962). These cats were re-anaesthetized with chloralose 10-14 days later and prepared as described.The splanchnic nerves were stimulated with platinum electrodes (cathode distal) using supramaximal rectangular (0-5 msec) pulses of 20 V at varying frequencies. The excitation frequency and number of stimuli were counted with a Racal digital frequency meter. For rapid excitation with up to ten stimuli, one stimulator provided the excitation frequency and the other a variable 'gate' during which a Stevens-Arnold 'millisec relay' was closed connecting the first stimulator to the electrodes; the stimuli were counted on an oscilloscope. In experiments to determine the stimulation frequency for optimal sympathin output, as well as those in which cocaine or phenoxybenzamine was injected into the cat, the excitation 31-2

The release and fate of vaso‐active hormones in the circulation

“…In endotoxin shock, for instance, Spink, Reddin, Zak, Peterson, Star-zeki & Seljeskog (1966) found only adrenaline; in haemorrhage, Glaviano, Bass & Nykiel (1960) occasionally found both catecholamines and Marley & Paton (1961) and Marley & Prout (1965) found mixtures after stimulation of the splanchnic nerve. A possible explanation of these differences arises from a study of the fate of the released catecholamine in the circulation.…”

Spatial and activity-dependent catecholamine release in rat adrenal medulla under native neuronal stimulation

“…Emotional or psychological stress, injury or environmental insult initiates the sympathetic “fight or flight” stress response, leading to a surge in serum catecholamine levels. Under this condition, NE is released from postganglionic sympathetic nerves throughout the periphery as well as from the adrenal medulla, while Epi is exclusively released from the adrenal medulla (Marley and Prout ; Goldstein et al. ; Carmichael and Winkler ; Habib et al.…”

“…Emotional or psychological stress, injury or environmental insult initiates the sympathetic "fight or flight" stress response, leading to a surge in serum catecholamine levels. Under this condition, NE is released from postganglionic sympathetic nerves throughout the periphery as well as from the adrenal medulla, while Epi is exclusively released from the adrenal medulla (Marley and Prout 1965;Goldstein et al 1983;Carmichael and Winkler 1985;Habib et al 2001). Moreover, within the spectrum of stress responses, specific stressors differentially elevate serum levels of one catecholamine relative to the other in order to evoke the appropriate physiological counterresponse (Coupland 1958;Klevans and Gebber 1970;Goldstein et al 1983;Scheurink and Ritter 1993;Vollmer 1996;Jeong et al 2000;Goldstein 2010;Kvetnansky et al 2013).…”

Reduced calcium current density in female versus male mouse adrenal chromaffin cells in situ

“…Basal catecholamine help regulate physiological parameters including shunting of blood from the periphery to viscera, increasing enteric activity and maintaining basal heart rate. Emotional or psychological stress, injury or environmental insult initiates the sympatho-adrenal ‘fight or flight’ stress response and drives adrenal chromaffin cells to greatly increase catecholamine release [1, 2]. Specific physiological consequences of stress-evoked adrenal catecholamine release include increased glucagon secretion and decreased insulin release from the pancreas, as well as increased hepatic blood flow, which all combine to elevate blood glucose levels.…”