DIFFERENTIAL SECRETION OF PROTEINS BY RAT SUBMANDIBULAR ACINI AND GRANULAR DUCTS ON GRADED AUTONOMIC NERVE STIMULATIONS

The influence of graded parasympathetic and sympathetic nerve stimulations on the secretion of protein from rat submandibular gland was studied. Peroxidase was used as a marker for the acini and rat tissue kallikrein (official nomenclature rK1) as the marker for granular ducts. Tonin (rK2) was also measured, and the ratio of rK2 : rK1 was calculated as an indication of the cellular route of secretion. 2. Continuous parasympathetic nerve stimulation caused a copious flow of saliva that had a low protein content. The secretion of peroxidase (acini) showed a gradual moderate increase as the frequency increased. However, the concentrations of rK1. and rK2 (granular ducts) showed little change throughout, and the ratio of rK2 : rK1 remained relatively constant. 3. Graded sympathetic stimulation was applied against a background of parasympathetic stimulation. Secretion of peroxidase was increased by the addition of 0.1 Hz continuous sympathetic stimulation. The amount increased thereafter up to 2 Hz, but showed no further increase if the stimulation was applied as bursts of 10 or 20 Hz. In comparison, the secretion of proteinase activity showed little change with superimposed continuous sympathetic stimulation, and the rK2 : rK1 ratio was similar to that in saliva produced by parasympathetic stimulation alone. Sympathetic stimulation applied in bursts, however, caused a large increase in the secretion of proteinase activity, and with 20 Hz burst stimulation the rK2 : rK1 ratio was indistinguishable from that of sympathetic saliva per se. There was an augmented secretion of both peroxidase and kallikrein when 20 Hz burst stimulation was combined with parasympathetic stimulation. The effects of sympathetic stimulation were abolished by alpha- and beta-adrenoceptor blockade. 4. It is concluded that parasympathetic stimulation causes a moderate increase in the concentration and output of acinar peroxidase with increasing stimulation rates. On the other hand, the concentration of kallikreins secreted from the granular ducts did not change significantly. Since the rK2:rK1 ratio remained significantly different from that in saliva produced by sympathetic stimulation alone, which is attributable to exocytotic release of secretory granules, it is likely that parasympathetic secretion of kallikreins was by vesicular (constitutive) transport. Sympathetic impulses provide a much greater drive for protein secretion by both acini and granular ducts, but increased secretion from the latter required a much higher frequency of impulse formation. These data imply that complex central integration is required to induce granule secretion from these ducts.