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VASCULAR EFFECTS OF SELECTED ANTIHYPERTENSIVE DRUGS DERIVED FROM TRADITIONAL MEDICINAL HERBS
Author(s) -
Kwan ChiuYin
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02925.x
Subject(s) - panax notoginseng , pharmacology , phenylephrine , tetrandrine , vasodilation , chemistry , antagonist , vascular smooth muscle , ginseng , contraction (grammar) , receptor , medicine , biochemistry , smooth muscle , blood pressure , alternative medicine , pathology
Summary 1. The pharmacological actions of the active ingredients extracted or purified from two selected traditional Chinese medicinal plants on vascular smooth muscles are briefly reviewed. The active ingredients of these herbal drugs include tetrandrine (TET) and total ginseng saponins (TGS). These natural products have been clinically used in China for the treatment of cardiovascular diseases due to their vasodilatory and antihypertensive actions. 2. Studies from this laboratory have confirmed previously reported characteristics of these drugs as Ca 2+ antagonists in vascular tissues. On the other hand, they also elicited inhibitory effects in response to a wide variety of receptor stimulations as indicated by contractility studies using isolated vascular tissues and radioligand binding studies using isolated subcellular membranes. 3. TET has been demonstrated as an effective but not very selective Ca 2+ antagonist. Other than the vasodilatory action on arteries and veins, TET also shows a vasoconstrictive effect in veins. 4. TGS from panax notoginseng may be acting as a novel and selective Ca 2+ antagonist that does not interact with the L‐type Ca 2+ channel (e.g. in KCl‐induced contraction) but may interact with the putative receptor operated Ca 2+ channel (e.g. in phenylephrine‐induced contraction). TGS from panax quin‐quefolium, on the other hand, enhanced the vasoconstrictor effect produced by phenylephrine, but not KCI.

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