Adrenergic nerve fibres

Mercuric chloride may induce catecholamine release from adrenals. The initial phase may be due to amine displacement by the mercury ion but the secondary phase probably involves alteration of membrane structures [95]. Mercury compounds have also been shown to increase the efflux of monoamines from mouse striated slices [96] and from adrenergic nerve fibre terminals [97], the effect being attributed to inhibition of Na /K+-ATPase activity and(or) disruption of intracellular Ca2+ regulatory mechanisms [96]. 

Von Euler, U. S. A specific sympathomimetic ergone in adrenergic nerve fibres (sympathin) and its relations to adrenaline and nor-adren-aline. Acfa. Physiol. Scand. 1946,12, 73-97. 

The "False Neurotransmitter" concept as a basis for explaining the mechanism of the hypotensive action of MAO-I s is presented in greater detail by Gohen et al.61. The delayed action of the MAO-I s with respect to their clinical antidepressant and hypotensive activities is presumably due to an indirect effect dependent on the gradual accumulation of monoamines at the adrenergic nerve fibres. According to the... 

Adrenergic Nerve Effects. Catecholamines -adrenergic effects. It is well known that insulin secretion is modified by j8-receptor agonists which cause release via stimulation of adenylate cyclase, as well as by a2-receptor agonists which cause inhibition of insulin secretion (for a review see Holst, 1992). Since noradrenaline is the predominating hormone of sympathetic nerve fibres it must be assumed that, since catecholamines act via nerve stimulation but not via the circulation, stimulation of sympathic nerves will inhibit insulin secretion. This has in fact been shown by several authors in in vivo studies stimulating splanchnic nerves (for a review see Holst, 1992). Whether or not this holds also for catecholamines that come from the circulation is not clear, but such an effect should be markedly concentration-dependent. A-cells but not B-cells are equipped with /3-... 

---