Nigro D, Sannomiya P, de Carvalho M H, Scivoletto R, Fortes Z B
Department of Pharmacology, University of São Paulo, Brazil.
Hypertension. 1994 Dec;24(6):728-33. doi: 10.1161/01.hyp.24.6.728.
We designed experiments to study the interaction of activated rat peritoneal neutrophils with aortas from spontaneously hypertensive rats (SHR) compared with those from normotensive rats. In aortic rings precontracted with phenylephrine, neutrophils obtained from normotensive rats caused a cell number-dependent relaxation of normotensive rat aorta with or without endothelium, whereas relaxation (at lower concentrations) followed by contraction (at higher concentrations) was observed in SHR aorta with endothelium. In SHR aortic rings denuded of endothelium, neutrophils did not induce contraction. The relaxation might be due to a factor indistinguishable from nitric oxide. The contraction might be due to prostaglandin H2 because it was blocked by indomethacin, a cyclooxygenase inhibitor, and ridogrel, a thromboxane A2 synthetase inhibitor/thromboxane A2-prostaglandin H2 antagonist, but not by superoxide dismutase, a superoxide anion scavenger, or dazoxiben, a thromboxane A2 synthetase inhibitor. SHR neutrophils caused a cell number-dependent relaxation of normotensive rat aorta with or without endothelium, whereas relaxation followed by contraction was observed in SHR aorta with endothelium. In SHR aortic rings denuded of endothelium, neutrophils did not induce contraction. The relaxation might be due to a factor indistinguishable from nitric oxide. The contraction seems to be due to superoxide anion because it was inhibitable by indomethacin and superoxide dismutase but not by dazoxiben and ridogrel. Equivalent amounts of superoxide anion were produced by unstimulated and phorbol myristate acetate-stimulated neutrophils obtained from either SHR or normotensive rats. Therefore, increased production of this anion could not explain the contraction observed in hypertensive aortas.(ABSTRACT TRUNCATED AT 250 WORDS)
我们设计了实验，以研究活化的大鼠腹膜中性粒细胞与自发性高血压大鼠（SHR）的主动脉之间的相互作用，并与正常血压大鼠的主动脉进行比较。在用去氧肾上腺素预收缩的主动脉环中，从正常血压大鼠获得的中性粒细胞会导致有或无内皮的正常血压大鼠主动脉出现细胞数量依赖性舒张，而在有内皮的SHR主动脉中观察到先舒张（较低浓度时）后收缩（较高浓度时）。在去除内皮的SHR主动脉环中，中性粒细胞不会诱导收缩。这种舒张可能归因于一种与一氧化氮难以区分的因子。收缩可能归因于前列腺素H2，因为它被环氧化酶抑制剂吲哚美辛和血栓素A2合成酶抑制剂/血栓素A2 - 前列腺素H2拮抗剂利托格雷阻断，但不被超氧化物阴离子清除剂超氧化物歧化酶或血栓素A2合成酶抑制剂达唑氧苯阻断。SHR中性粒细胞会导致有或无内皮的正常血压大鼠主动脉出现细胞数量依赖性舒张，而在有内皮的SHR主动脉中观察到先舒张后收缩。在去除内皮的SHR主动脉环中，中性粒细胞不会诱导收缩。这种舒张可能归因于一种与一氧化氮难以区分的因子。收缩似乎归因于超氧化物阴离子，因为它可被吲哚美辛和超氧化物歧化酶抑制，但不被达唑氧苯和利托格雷抑制。从SHR或正常血压大鼠获得的未刺激和佛波酯刺激的中性粒细胞产生的超氧化物阴离子量相等。因此，这种阴离子产生的增加无法解释在高血压主动脉中观察到的收缩。（摘要截短于250字）
