Abstract
Responses of the dog submaxillary gland and its vascular bed to various compounds administered into the glandular branch of the facial artery were investigated under the constant perfusion pressure. Cholinergic drugs such as acetylcholine, bethaneehol, methacholine, carbachol, pilocarpine, physostigmine and neostigmine; ganglionic stimulants such as nicotine, DMPP, lobeline, TMA and McN-A-343; β-adrenergic stimulant such as isoproterenol; and biogenic amines such as histamine and 5-hydroxytryptamine, produced a salivary secretion and dilation of the glandular vascular bed. Adrenergic drugs catehcholamine releaser such as epinephrine, norepinephrine, dopamine, phenylephrine, tyramine and methoxamine, caused a salivary secretion and vasoconstriction. Although either vasoconstrictors such as angiotensin II, lys-vaso-pressin, oxytocin, TEA, cocaine and ergotamine, or vasodilators such as bradykinin, kallikrein, secretin, panereozymin, gastrin, adenosine, AMP, ADP, ATP, uridine, UMP, UDP, UTP, DPN, TPN, nitroglycerin, papaverine, dipyridamole, verapamil, hydralazine, caffeine, theophilline, theobromine, morphine, procaine and tolazoline, produced prominent vascular effects, they exerted no effect on the salivary secretion. There is no evidence on the direct relation between secretagogue and vasodilating effects of drugs which are administered selectively into the submaxillary glandular artery.
