Neurons adrenergic

Neuronal Norepinephrine Depleting Agents. Reserpine (Table 6) is the most active alkaloid derived from Rauwolfia serpentina. The principal antihypertensive mechanism of action primarily results from depletion of norepinephrine from peripheral sympathetic nerves and the brain adrenergic neurons. The result is a drastic decrease in the amount of norepinephrine released from these neurons, leading to decrease in vascular tone and lowering of blood pressure. Reserpine also depletes other transmitters including epinephrine, serotonin [50-67-9] dopamine [51-61-6] ... 

PTX caused a dose-dependent release of norepinephrine (NE). The NE release induced by lower concentrations of PTX increased proportionately with increasing Na concentrations, but was not modified by tetrodotoxin. However, the NE-releasing action of higher concentrations of PTX was dependent on external Ca, but not Na . Thus our experimental results suggest that in adrenergic neurons the PTX-induced release of NE by lower concentrations of PTX is brought about by tetrodotoxin-insensitive Na permeability, whereas that induced by higher concentrations is mainly caused by a direct increase of Ca influx into smooth muscle cells. 

Palytoxin (PTX) is one of the most potent marine toxins known and the lethal dose (LD q) of the toxin in mice is 0.5 Mg/kg when injected i.v. The molecular structure of the toxin has been determined fully (1,2). PTX causes contractions in smooth muscle (i) and has a positive inotropic action in cardiac muscle (4-6). PTX also induces membrane depolarization in intestinal smooth (i), skeletal (4), and heart muscles (5-7), myelinated fibers (8), spinal cord (9), and squid axons (10). PTX has been demonstrated to cause NE release from adrenergic neurons (11,12). Biochemical studies have indicated that PTX causes a release of K from erythrocytes, which is followed by hemolysis (13-15). The PTX-induced release of K from erythrocytes is depress by ouabain and that the binding of ouabain to the membrane fragments is inhibited by PTX (15). 

Lejeune R, Millan M. (1999). Pindolol excites dopaminergic and adrenergic neurons, and inhibits serotonergic neurons, by activation of 5-HT1A receptors. Eur. J. Neurosci 12, 3265-75. 

The answers are 321-cT 322-e, 323-i. (Hardman, pp 238-239, 791.) Reserpine is an adrenergic neuronal blocking agent that causes depletion of central and peripheral stores of NE and dopamine Reserpine acts by irreversibly inhibiting the magnesium-dependent ATP transport process that functions as a carrier for biogenic amines from the cytoplasm... 

Sympathetic adrenergic neuron SIF cell Chromaffin cell... 

Adrenalin, chloroacetyl chloride in production of, 7 142 P-Adrenergic agonists as animal growth regulators, 73 14-17 genotype, gender, and nutritional interactions related to, 73 16 mechanism of action of, 73 17 Adrenergic neuronal blockers,... 

Destruction of central adrenergic neurons by intraventricular injection of 6-hydroxydopamine (6 OHDA) virtually abolished the hypotensive effect of methyl-dopa. Adrenergic neurons are probably required to con-... 

STRUCTURE-ACTIVITY RELATIONSHIPS FOR ADRENERGIC NEURONE BLOCKADE 139... 

Relationship between noradrenaline depletion and adrenergic neurone blockade 200 ADDENDUM 203... 

An excellent review of the pharmacological actions of adrenergic neurone blocking agents has been given by Boura and Green [10]. The biochemistry of guanethidine itself has been reviewed by Furst [11], with particular emphasis on tissue distribution and metabolism consequently these two topics are not discussed in detail. 

Adrenergic neurone blocking (e.g. xylocholine, guanetHidine) Blocked Blocked Normal Yes No... 

---