STUDIES ON THE ANTAGONISM BETWEEN THE OPTICAL ISOMERS OF <i>N</i>‐(1‐PHENYLETHYL)GUANIDINE

Fielden, R.; Green, A. L.

doi:10.1111/j.1476-5381.1966.tb01829.x

Cited by 1 publication

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“…However, additional actions must also be present. Besides having a weak anti-reserpine activity, which we have attributed elsewhere to monoamine oxidase inhibition (Fielden & Green, 1966), some of the guanidines can also partly relieve the ptosis caused by ganglion blocking agents. (+)-N-( 1-Phenylethy1)guanidine (Vb) has been shown to produce a short-lasting antagonism of the relaxation of the nictitating membranes produced by pempidine in conscious cats.…”

Section: Ox)mentioning

confidence: 82%

“…We have shown (Fielden, Green & Willey, 1965 ; that adrenergic neurone blockade could also be prevented, and in some circumstances reversed, by certain aralkylguanidines. The mechanism of this reversing action for one particular compound, (+)-N-( l-phenylethyl) guanidine, has been discussed in detail elsewhere (Fielden & Green, 1966). In the present paper we have compared a variety of aralkylamines and aralkylguanidines as antagonists to different types of adrenergic neurone blocking agent in cats and mice in an attempt to obtain further insight into the mechanism of adrenergic neurone blockade.…”

Section: Mphetamine and Some Other Sympathomimetic Amines Arementioning

confidence: 97%

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A comparison of aralkylamines and aralkylguanidines as antagonists of adrenergic neurone blockade

Fielden¹,

Green²

1966

Journal of Pharmacy and Pharmacology

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Structure‐activity relationships have been studied for aralkylamines and aralkylguanidines which restore the responses of the nictitating membranes to nerve stimulation in anaesthetised cats given sympathetic blocking drugs. This reversing action was largely specific for adrenergic neurone blockade; blockade of sympathetic ganglia or of α‐adrenergic receptors was unaffected. (+)‐Amphetamine was the most active amine and N‐benzyl‐N‐methylguanidine was the most active guanidine. In mice, ptosis resulting from adrenergic neurone blockade was much more readily prevented or abolished by the aralkylamines and aralkylguanidines than was ptosis caused by other types of sympathetic blocking agent. The most potent antagonist of ptosis was N‐(2‐phenylcyclopropyl)guanidine which was about ten times as active as amphetamine. The relative antagonistic potencies of 2 amines and 8 guanidines were virtually identical for all types of adrenergic neurone blocking drug, regardless of whether or not they cause noradrenaline depletion. The prevention of guanethidine‐induced ptosis was always accompanied by some reduction in the extent of heart‐noradrenaline depletion, but the minimum dose of antagonist required to prevent ptosis completely was always lower than that required to eliminate depletion.

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Section: Ox)mentioning

confidence: 82%

Section: Mphetamine and Some Other Sympathomimetic Amines Arementioning

confidence: 97%