Pipili E, Poyser N L
Prostaglandins. 1982 Apr;23(4):543-9. doi: 10.1016/0090-6980(82)90114-9.
The spontaneous output of prostaglandin (PG) I2 from the perfused mesenteric arterial bed in vitro was significantly higher in hypertensive rats than in normotensive rats. Sympathetic nerve stimulation (at 1OHz) of the mesenteric arterial bed from normotensive rats caused a rapid and short-lived (less than 4 min) two-fold increase in PGI2 output and a smaller increase in PGE2 output. Sympathetic nerve stimulation (at 1OHz) of the mesenteric arterial bed from hypertensive rats failed to increase PGI2 and PGE2 output. It is not possible to conclude whether this lack of response is a cause or a result of hypertension. Surprisingly, norepinephrine administration stimulated PGI2 and PGE2 release from the mesenteric arterial bed of both normotensive and hypertensive rats. Obviously, differences exist in the responsiveness of rat mesenteric arteries to endogenous and exogenous norepinephrine concerning PG release between the normotensive and hypertensive states.
在体外,高血压大鼠灌注肠系膜动脉床中前列腺素(PG)I2的自发输出量显著高于正常血压大鼠。对正常血压大鼠的肠系膜动脉床进行交感神经刺激(频率为10Hz)会导致PGI2输出迅速且短暂(少于4分钟)地增加两倍,PGE2输出量增加幅度较小。对高血压大鼠的肠系膜动脉床进行交感神经刺激(频率为10Hz)未能增加PGI2和PGE2的输出。无法确定这种无反应是高血压的原因还是结果。令人惊讶的是,给予去甲肾上腺素会刺激正常血压和高血压大鼠肠系膜动脉床释放PGI2和PGE2。显然,在正常血压和高血压状态下,大鼠肠系膜动脉对内源性和外源性去甲肾上腺素在PG释放方面的反应性存在差异。