Supporting effects of myoepithelial cells in submandibular glands of dogs when acting against increased intraluminal pressure

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Abstract
In dogs under chloralose-urethane anesthesia secretion from the submandibular gland was recorded with the outflow at gland level and at heights of up to 50 cm above the gland. With the outflow level increased, secretion elicited by sympathetic nerve stimulation was far better maintained before than after injection of the .alpha.-adrenoceptor blocking agent dihydroergotamine. When the outflow level was raised while no secretion occurred, fluid flowed into the gland. Part of this amount was returned on lowering the outflow to gland level. This volume was assumed to have been accommodated in the distended luminal system; some fluid was obviously lost into the gland tissues. Both these fractions of the fluid flowing into the gland when the outflow level was high could be reduced by injecting the .alpha.-receptor agonist phenylephrine. Bradykinin, which like phenylephrine is known to contract salivary myoepithelial cells, had the same effect on the 2 inflow volumes. Myoepithelial contraction reduced the distensibility of the luminal system and supported the acini, thereby diminishing backflow into the glandular tissues and enabling the gland to discharge saliva against a high pressure. In resting glands PAS[periodic acid-Schiff]-positive saliva was displaced from the ductal system when the outflow cannula was raised, but it was preserved in the lumina under similar conditions when the myoepithelial cells were being stimulated by phenylephrine or bradykinin. Although sympathetic secretion could be maintained against a head of pressure, so long as it was accompanied by myoepithelial contraction, the increased force caused by the secretion led to disruptive damage of striated ducts which are the 1st part of the luminal system not supported by myoepithelial cells. Contraction of myoepithelial cells gives active support to the underlying parenchyma.