Role of the autonomic nervous system in the release of rat submandibular gland kallikrein into the circulation.
We have previously demonstrated that the rat submandibular gland releases immunoreactive kallikrein into the circulation. To study the role of the autonomic nervous system in this release, submandibular gland blood flow and kallikrein concentration in peripheral arterial and venous blood from the gland were measured and secretion rates calculated before and after parasympathetic and sympathetic nerve stimulation (8V, 2 msec, 10 Hz) for 1 minute. Immunoreactive kallikrein in plasma was measured by radioimmunoassay, and timed collections of venous outflow were used to measure blood flow. During basal conditions, the unstimulated submandibular gland of the rat released immunoreactive kallikrein into blood at the rate of 0.92 +/- 0.07 ng/min. Parasympathetic stimulation increased blood flow 4-fold (before, 68.5 +/- 8.3 microliters/min; after, 253.5 +/- 76.2; P less than 0.05) without significantly changing immunoreactive kallikrein secretion rate. Sympathetic stimulation produced an 11-fold increase in blood flow (before, 64.9 +/- 9.3 microliters/min; after, 709.6 +/- 97.5; P less than 0.05) and a 57-fold increase in immunoreactive kallikrein secretion rate from the gland (before, 1.05 +/- 0.25 ng/min; after, 59.8 +/- 18.6; P less than 0.05). Sympathetic stimulation also produced a 4-fold increase in the concentration of immunoreactive glandular kallikrein in arterial plasma (before, 15.2 +/- 1.1 ng/ml; after, 56.2 +/- 12.9; P less than 0.05). Pretreatment with phentolamine (1 mg/kg) or prazosin (0.2 mg/kg) blocked the increase in kallikrein secretion rate produced by sympathetic stimulation. These results indicate that the sympathetic nervous system, through activation of alpha 1-adrenoreceptors, controls kallikrein secretion from the submandibular gland into the circulation. Released kallikrein may be responsible for the reactive vasodilation observed in the rat submandibular gland after sympathetic stimulation.
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000150:complications; D001341:Autonomic Nervous System / Q000502:physiology*; D002340:Carotid Artery Diseases / Q000150:complications; D003000:Clonidine / Q000494:pharmacology; D004558:Electric Stimulation; D007610:Kallikreins / Q000097:blood*; D008297:Male; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013363:Submandibular Gland / Q000098:blood supply / Q000201:enzymology*; D015016:Yohimbine / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D015016:Yohimbine; D007610:Kallikreins; D003000:Clonidine; D011224:Prazosin