通过生长抑素类似物阻断腺苷受体引起的高血压和心血管结构改变预防

C. Calhau, F. Martel, M.N.M.P. Alçada, I. Azevedo
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引用次数: 4

摘要

1长期服用腺苷受体拮抗剂1,3-二丙基-8-磺苯基黄嘌呤(DPSPX)可引起动脉高血压和心血管肥厚和增生性改变(Matias, Albino-Teixeira, Polónia &代理,1991)。由于生长抑素是细胞生长的抑制因子,而腺苷是生长抑素基因的有效诱导剂,我们研究了生长抑素在DPSPX心血管效应中的可能参与。2 DPSPX (90 μg kg−1 h−1,ig)或生理盐水与生长抑素类似物奥曲肽(75 μg kg−1 d−1,s.c),或生理盐水通过Alzet微型泵输注Wistar大鼠。采用尾袖技术测量血压。植入微型泵7天后处死大鼠,组织制备用于显微镜观察。DPSPX引起动脉高血压和心血管肥厚和增生性改变,如前所述(Matias et al., 1991)。单用奥曲肽治疗大鼠对血压和血管形态均无影响。然而,奥曲肽可以预防DPSPX的高血压和心血管形态学影响。该结果与生长抑素参与腺苷的长期心血管效应是一致的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Prevention by a somatostatin analogue of the hypertensive and cardiovascular structural changes induced by blockade of adenosine receptors

1 Long-term administration of the adenosine receptor antagonist, 1,3-dipropyl-8-sulfophenylxanthine (DPSPX), causes arterial hypertension and cardiovascular hypertrophic and hyperplastic changes (Matias, Albino-Teixeira, Polónia & Azevedo, 1991). As somatostatin is a repressor of cell growth, and adenosine is a potent inducer of the somatostatin gene, we investigated the putative involvement of somatostatin in the cardiovascular effects of DPSPX.

2 DPSPX (90 μg kg−1 h−1, i.p.) or saline and the somatostatin analogue, octreotide (75 μg kg−1 day−1, s.c.), or saline were infused through Alzet minipumps to Wistar rats. Blood pressure was measured with the tail-cuff technique. Seven days after implantation of the minipumps the rats were killed and the tissues prepared for microscopy.

3 DPSPX induced arterial hypertension and cardiovascular hypertrophic and hyperplastic changes as previously described (Matias et al., 1991). Treatment of the rats with octreotide alone had no effect either on blood pressure or in blood vessel morphology. However, octreotide prevented both the hypertensive and the cardiovascular morphologic effects of DPSPX.

4 The results are compatible with the involvement of somatostatin in the long-term cardiovascular effects of adenosine.

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