ABSTRACT
The significant observation was so important that the physiologist might be forgiven for supposing that, if the salivary gland had no other function, its role in the history of noncholinergic nonadrenergic vasodilatation would almost justify its existence. J. Lundvall and J. Holmberg noted that activation of the salivary gland was accompanied by an increase in osmolarity in the blood leaving the gland. A few years later C. Bernard showed that vinegar instilled into the mouth of a dog led to both secretion of saliva and a quickening of the flow of blood draining the gland. The parasympathetic blocking effect of atropine had just been discovered when R. Heidenhain noted that although atropine completely blocked the salivation produced by chorda tympani nerve stimulation, the associated vasodilatation was largely unaffected. Salivary responses that were once described as “atropine-sensitive” and therefore wholly reliant upon activation of muscarinic receptors have, quite recently, been shown to be “atropine-resistant”, at least to some extent.
