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a pharmacological substance that opposes the effects of the stimulation of sympathetic nerves, that is, the transmission of excitation from sympathetic nerves to effectors.

The action of sympatholytics corresponds to the physiological phenomena that arise with the relaxation of the tonus of the sympathetic nerves: the blood vessels dilate, systoles decelerate and arterial pressure decreases. Blockage of the transmission of excitation from sympathetic nerves to effectors is produced by the intervention of sympatholytics into the basic processes that occur in the presynaptic parts of adrenergic neurons. Sympatholytics are divided into groups according to the predominant effect they have on one of these processes, although as a rule several mechanisms can be distinguished in the action of every sympatholytic.

The first group of sympatholytics includes agents that cause the emptying of the depots of adrenergic mediators (norepinephrine and adrenaline) in the endings of sympathetic nerves. This group includes reserpine and oktadin, also called guaneth-idine, isobarin, or Ismelin. Initially, these sympatholytics may cause a short-term increase in arterial pressure resulting from the ejection of the mediators from the depots.

The second group of sympatholytics obstruct the release of mediators from depots located in the endings of sympathetic nerves. This group includes ornid, which is also called brety-lium tosylate. Many scientists also distinguish a group of sympatholytics that disrupt the biosynthesis of mediators (forming a false mediator) in the endings of sympathetic nerves. These agents include alpha-methyldopa, also called Aldomet.

In their influence on the functions of effectors innervated by sympathetic nerves, sympatholytics are similar to adrenolytic agents, including such adrenal blocking agents as phentola-mine, propionic acid, dihydroergotamine, and propanolol. These agents block adrenergic receptors and obstruct the action of mediators on them. Sympatholytics are used to lower arterial pressure in the treatment of hypertension.


Zakusov, V. V. Farmakologiia, 2nd ed. Moscow, 1966.
Kaverina, N. V., and G. G. Chichkanov. “Simpatoliticheskie veshchestva.” In Itogi nauki: Seriia Biologiia, vol. 3. Moscow, 1972.
Anichkov, S. V. Izbiratel’noe deistvie mediatornykh sredstv. Leningrad, 1974.


References in periodicals archive ?
The improved specificity of dexmedetomidine for the a-2 receptor causes it to be with much more effective sedative, anxiolytic, analgesic, antihypertensive, and sympatholytic properties with much less unwanted cardiovascular effects from a-1 receptor activation.[6] It improves the quality of perioperative anesthesia and analgesia.[7]
Mysliwiec said some who suffer from TSD have benefited from being treated with prazosin, a sympatholytic drug also used to treat post-traumatic stress disorder.
Medication for cardiovascular disease and hypertension comprised the following: ace inhibitor (n = 2), angiotensin receptor blocker (n = 6), calcium channel blocker (n = 7), beta blocker (n = 3), thiazide diuretic (n = 3), aldosterone inhibitor (n = 1), alpha adrenergic blocker (n = 4), centrally acting sympatholytic agent (n =1), acetylsalicylic acid (n = 5), and lipid-lowering treatment (n = 2).
Though the antidiabetic efficacy is modest with a 0.5% reduction of glycosylated haemoglobin, the drug has a great potential in its central sympatholytic action.
[sup][46] In vivo , it functions through its sympatholytic effect that leads to the activation of the vagus nerve, which then stimulates cholinergic anti-inflammatory pathway.
Immune: anti-inflammatory (inhibits synthesis of prostaglandins and chemotaxis of leukocytes), antiallergic (reduces histamine release from mast cells); ANS: sympatholytic, parasympathomimetic;
The pre-synaptic release of noradrenalin is interrupted, which inhibits the adrenergic neurons answer, leading to a depression of the central nervous system by a sympatholytic effect with loss of warning and surveillance functions.
General anesthesia is the most commonly used especially in patients with prolonged surgical time and spinal anesthesia is usually avoided due to its rapid onset and profound sympatholytic effect.
Clonidine might reduce the HR and BP mediated by a decreased release of peripheral norepinephrine and a central sympatholytic effect [10].
Except for sympatholytic action of clonidine and profound analgesia which also reduces sympathetic activity, no other clear explanation is available.