Tissue hyperosmolality as a causal factor in vasodilatation following sympathetic stimulation of the submandibular gland.

In a previous investigation, parasympathetic activation of the submandibular gland in the cat was found to cause a considerable increase of regional tissue osmolality, the degree of which was related to the evoked functional hyperemia; intra-arterial hypertonic infusion to the resting gland producing tissue hyperosmolality of similar magnitudes caused graded and marked dilatations (Lundvall and Holmberg 1974). It was concluded that hyperosmolality contributes significantly to the functional hyperemia response. In the present study evidence is presented to indicate that tissue hyperosmolality is a mediator of the dilatation associated with sympathetic activation as well. An increase of tissue hyperosmolality, as traced in the venous effluent, was found at all frequencies of sympathetic stimulation (2-16 Hz). At high stimulation rates it sometimes exceeded the resting control level by more than 20 mOsm/kg H2O. There was a direct relation between the degree of venous hyperosmolality and the hyperemia response observed immediately after cessation of stimulation. Comparison of the dilator effects evoked by sympathetic stimulation and by hypertonic infusion to the resting gland indicated that tissue hyperosmolality is an important causal factor for the nerve induced dilatation, especially at low and moderate stimulation rates.