Role of Tissue Hyperosmolality in Functional Vasodilatation in the Submandibular Gland

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Abstract
Parasympathetic activation of the submandibular gland in the cat was found to cause considerable regional tissue hyperosmolality concomitant with the functional hyperemia response. The hyperosmolality, as traced in the venous effluent, was present at all rates of chorda nerve stimulation (0.25‐20 Hz). Osmolality was clearly raised already during the initial phase of the dilator response and reached plateau values during the later, steady state hyperemia response. In the latter phase it could exceed the resting control level by as much as 50 mOsm/kg H2O. There was a direct relation between the degree of venous hyperosmolality and the dilator response during low and moderate rates of chorda stimulation. Experimental hyperosmolality in die resting gland, produced by intra‐arterial infusion of hypertonic solutions, evoked a pattern of dilator response resembling that observed during chorda stimulation. Graded experimental hyperosmolality of magnitudes similar to those seen during chorda stimulation evoked progressively increasing dilatations of the resistance vessels. Comparison of the dilator effects during chorda stimulation and during hypertonic infusion at comparable levels of venous hyperosmolality indicated that tissue hyperosmolality contributed significantly to both the initial and maintained functional hyperemia response in the gland. The factor seemed to be of special importance at low and moderate rates of chorda excitation. This conclusion was supported by a separate series of experiments in which the effects of atropine on the functional hyperemia response and on the hyperosmolality were studied.