Rabito S F, Orstavik T B, Scicli A G, Schork A, Carretero O A
Circ Res. 1983 Jun;52(6):635-41. doi: 10.1161/01.res.52.6.635.
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.
我们之前已证明，大鼠下颌下腺会将免疫反应性激肽释放到循环系统中。为研究自主神经系统在此释放过程中的作用，我们测量了下颌下腺的血流量以及该腺体外周动脉血和静脉血中的激肽浓度，并计算了副交感神经和交感神经刺激（8伏，2毫秒，10赫兹）1分钟前后的分泌率。通过放射免疫分析法测定血浆中的免疫反应性激肽，通过定时收集静脉流出液来测量血流量。在基础条件下，未受刺激的大鼠下颌下腺以0.92±0.07纳克/分钟的速率将免疫反应性激肽释放到血液中。副交感神经刺激使血流量增加了4倍（刺激前，68.5±8.3微升/分钟；刺激后，253.5±76.2；P<0.05），但免疫反应性激肽的分泌率没有显著变化。交感神经刺激使血流量增加了11倍（刺激前，64.9±9.3微升/分钟；刺激后，709.6±97.5；P<0.05），该腺体免疫反应性激肽的分泌率增加了57倍（刺激前，1.05±0.25纳克/分钟；刺激后，59.8±18.6；P<0.05）。交感神经刺激还使动脉血浆中免疫反应性腺体激肽的浓度增加了4倍（刺激前，15.2±1.1纳克/毫升；刺激后，56.2±12.9；P<0.05）。用酚妥拉明（1毫克/千克）或哌唑嗪（0.2毫克/千克）预处理可阻断交感神经刺激所引起的激肽分泌率增加。这些结果表明，交感神经系统通过激活α1 - 肾上腺素能受体，控制下颌下腺向循环系统中分泌激肽。释放的激肽可能是交感神经刺激后大鼠下颌下腺中观察到的反应性血管舒张的原因。
