Adrenergic fibres

Although neuronal uptake appears to be the dominant inactivation process in tissues with a dense sympathetic innervation (Para. 5.2.8), this may not be true for all tissues. In some, such as the aorta, adrenergic fibres are only sparsely distributed, often at some distance from the effector cells. Here the enzymatic catabolism of catecholamines may play a more important rdle in inactivation. Similarly catabolism is an important factor in terminating the actions of circulating catecholamines, following their release from the adrenal medulla, or the injection of exogenous amines. 

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]. 

The antiarrhythmic action is due to cardiac adrenergic blockade. It decreases the slope of phase 4 depolarization and automaticity in SA node, Purkinje fibres and other ectopic foci. It also prolongs the effective refractory period of AV node and impedes AV conduction. ECG shows prolonged PR interval. It is useful in sinus tachycardia, atrial and nodal extrasystoles. It is also useful in sympathetically mediated arrhythmias in pheochromocytoma and halothane anaesthesia. 

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-... 

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... 

Shah S, Page CP, Spina D (1998) Nociceptin inhibits non-adrenergic non-choUnergjc contraction in guinea-pig airway. Br J Pharmacol 125 510-516 Shams H, Daffonchio L, Scheid P (1996) Effects of levodropropizine on vagal afferent C-fibres in the cat. Br J Pharmacol 117 853-858... 

Martin, W., S. Murphree and J. Saffitz, 1989. Beta-adrenergic receptor distribution among muscle fibre types and resistance arterioles of white, red, and intermediate skeletal muscle. Circul. Res. 64, 1096-1105. 

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