Matsumura Y, Ozawa Y, Suzuki H, Saruta T
Am J Physiol. 1986 May;250(5 Pt 2):F811-6. doi: 10.1152/ajprenal.1986.250.5.F811.
The effects of vasoactive substances on the release of prostaglandin (PG) and thromboxane (TX) from isolated rat glomeruli were investigated. The PGE2, PGF2 alpha, 6-keto-PGF1 alpha, and TXB2 release during 60 min into Krebs-Henseleit medium was assessed by radioimmunoassay following extraction. Norepinephrine (NE) stimulated PGE2 (from 2,117 +/- 117 to 3,968 +/- 182 pg X mg protein-1 X 60 min-1, P less than 0.01) at a concentration of 10(-4)M and PGF2 alpha (from 2,748 +/- 285 to 8,535 +/- 495 pg X mg protein-1 X 60 min-1, P less than 0.01) at a concentration of 10(-5)M. However, neither angiotensin II (ANG II) nor arginine vasopressin (AVP) affected the release of PG and TXB2 at concentrations up to 10(-5)M. In the presence of 10(-5) M NE, ANG II enhanced the release of PGE2 (from 3,307 +/- 207 to 6,865 +/- 469 pg X mg protein-1 X 60 min-1., P less than 0.01) and PGF2 alpha (from 3,652 +/- 252 to 6,612 +/- 388 pg X mg protein-1 X 60 min-1, P less than 0.01) at a concentration of 10(-8)M, whereas AVP lacked any similar effect. These results indicate that catecholamine acts as a major stimulant for the release of PG from isolated glomeruli via alpha-receptors. ANG II may work in cooperation with catecholamine, but AVP appears to play little role.
研究了血管活性物质对离体大鼠肾小球前列腺素（PG）和血栓素（TX）释放的影响。提取后，通过放射免疫分析法评估60分钟内PGE2、PGF2α、6-酮-PGF1α和TXB2向Krebs-Henseleit培养基中的释放量。去甲肾上腺素（NE）在浓度为10⁻⁴M时刺激PGE2释放（从2,117±117增加到3,968±182 pg·mg蛋白⁻¹·60分钟⁻¹，P<0.01），在浓度为10⁻⁵M时刺激PGF2α释放（从2,748±285增加到8,535±495 pg·mg蛋白⁻¹·60分钟⁻¹，P<0.01）。然而，血管紧张素II（ANG II）和精氨酸加压素（AVP）在浓度高达10⁻⁵M时均不影响PG和TXB2的释放。在存在10⁻⁵M NE的情况下，ANG II在浓度为10⁻⁸M时增强了PGE2（从3,307±207增加到6,865±469 pg·mg蛋白⁻¹·60分钟⁻¹，P<0.01）和PGF2α（从3,652±252增加到6,612±388 pg·mg蛋白⁻¹·60分钟⁻¹，P<0.01）的释放，而AVP没有任何类似作用。这些结果表明，儿茶酚胺通过α受体作为离体肾小球PG释放的主要刺激物。ANG II可能与儿茶酚胺协同作用，但AVP似乎作用不大。
