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Kinins, beta‐adrenergic receptors and functional vasodilatation in the submaxillary gland of the cat
Author(s) -
Skinner N. Sheldon,
Webster Marion E.
Publication year - 1968
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.1968.sp008471
Subject(s) - hyperaemia , endocrinology , medicine , vasodilation , stimulation , chemistry , atropine , bradykinin , adrenergic , receptor , blood flow
1. The close arterial infusion of bradykinin into the submaxillary gland of the cat produced a pronounced hyperaemia that could be blocked by simultaneous perfusion of the gland with blood containing carboxypeptidase B. Carboxypeptidase B, however, failed to reduce the vasodilatation of chorda tympani nerve stimulation suggesting that the kinins are not involved in the regulation of submaxillary gland blood flow. 2. Isoproterenol injections produced pronounced salivary gland vasodilatation. Beta‐adrenergic blocking drugs reduced or abolished the hyperaemia of isoproterenol and reduced that of chorda tympani nerve stimulation. The combination of beta‐blocking drugs and atropine could abolish or reduce further this nerve induced hyperaemia. 3. The above results suggest that stimulation of cholinergic and beta‐adrenergic receptors could account for the chorda tympani induced hyperaemia. Conclusive proof of this possibility remains to be determined.