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Endothelium‐derived vasodilator responses to sympathetic stimulation of the submandibular gland in the cat.
Author(s) -
Edwards A V,
Garrett J R
Publication year - 1992
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1992.sp019348
Subject(s) - vasodilation , stimulation , medicine , submandibular gland , endocrinology , cats , endothelium derived relaxing factor , propranolol , fissipedia , adrenergic , basal (medicine) , chemistry , receptor , insulin
1. The extent to which vasodilator responses to electrical stimulation of the sympathetic innervation, in the submandibular gland of the cat, depend upon release of endothelium‐derived relaxing factor (EDRF) within the gland has been investigated in anaesthetized cats given N‐nitro‐L‐arginine methyl ester (L‐NAME) which specifically blocks the synthesis of EDRF from arginine. 2. Close intra‐arterial infusions of L‐NAME (> or = 100 mg kg‐1) produced a steady and significant rise in mean aortic pressure together with a steady increase in basal submandibular vascular resistance over the next 20‐30 min. It also reduced, but failed to abolish, the vasodilatation which occurs during intermittent stimulation of the sympathetic innervation (20 Hz for 1 s at 10 s intervals) together with the after‐dilatation which occurs immediately after a period of continuous stimulation of these nerve fibres (2 Hz). 3. In cats pretreated with the beta‐blocker propranolol (> or = 1.0 mg kg‐1) both vasodilator responses were reduced, but persisted until L‐NAME was administered, whereupon both were abolished. 4. It is concluded that release of EDRF within the submandibular gland of the cat contributes to the basal tone of the vasculature and is responsible for the alpha‐adrenergic vasodilator responses to stimulation of the sympathetic innervation, but not for the beta‐adrenergic vasodilator responses.