Osol G, Halpern W
Department of Physiology and Biophysics, University of Vermont College of Medicine, Burlington 05405.
Am J Physiol. 1988 Jan;254(1 Pt 2):H28-33. doi: 10.1152/ajpheart.1988.254.1.H28.
Resistance-sized branches of posterior cerebral arteries from Wistar-Kyoto (WKY), spontaneously hypertensive (SHR), spontaneously hypertensive stroke-prone (SHRSP), and antihypertensive-treated SHRSP (SHRSP-TRT) rats were studied in vitro. After the rats were killed, arterial segments were excised, mounted on microcannulas, and pressurized. After equilibration, intravascular pressure was increased in a stepwise fashion from 30 to 150-200 mmHg. All vessels developed a myogenic tone, which resulted in diameter reductions of 31-37% at 100 mmHg when compared with fully relaxed diameters [approximately 200 micron in 1 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid]. Differences in the extent of tone were not significant between animal groups (P greater than 0.05). Rhythmic vasomotion was present in 94% SHRSP and 100% SHRSP-TRT, 83% SHR, and only 6% of the WKY arteries. At higher pressures, the amplitude of the diameter oscillations decreased and frequency increased. Vasomotion was unaltered by tetrodotoxin or indomethacin, but could be abolished by cooling to 34 degrees C, ouabain (a depolarizing solution containing 125 mM K+), potassium-free physiological saline solution, or by calcium entry blockade with diltiazem or MnCl2. In normally quiescent WKY arteries, vasomotion, which was qualitatively similar to that observed in the hypertensive strains, could be induced by the addition of 5 mM tetraethylammonium chloride. Thus intrinsic oscillations in membrane calcium and potassium conductance may underlie the rhythmic contractile activity of rat cerebral arteries. This property appears to have a major genetic component, the expression of which is relatively independent of blood pressure history and is not related to the myogenic properties of the preparation.
对来自Wistar-Kyoto（WKY）大鼠、自发性高血压（SHR）大鼠、自发性高血压易中风（SHRSP）大鼠以及接受抗高血压治疗的SHRSP（SHRSP-TRT）大鼠的大脑后动脉阻力大小的分支进行了体外研究。处死大鼠后，切下动脉段，安装在微插管上并加压。平衡后，血管内压力从30 mmHg逐步升高至150 - 200 mmHg。所有血管都产生了肌源性张力，与完全松弛直径（在1 mM乙二醇双（β-氨基乙基醚）-N，N，N'，N'-四乙酸中约为200微米）相比，在100 mmHg时直径减少了31 - 37%。动物组之间张力程度的差异不显著（P大于0.05）。94%的SHRSP和100%的SHRSP-TRT、83%的SHR以及仅6%的WKY动脉存在节律性血管运动。在较高压力下，直径振荡的幅度减小而频率增加。血管运动不受河豚毒素或吲哚美辛影响，但可通过冷却至34℃、哇巴因（含125 mM K +的去极化溶液）、无钾生理盐溶液或用维拉帕米或MnCl2阻断钙内流而消除。在正常静止的WKY动脉中，加入5 mM四乙铵氯化物可诱导出与高血压品系中观察到的性质相似的血管运动。因此，膜钙和钾电导的内在振荡可能是大鼠脑动脉节律性收缩活动的基础。这种特性似乎有一个主要的遗传成分，其表达相对独立于血压病史，且与制剂的肌源性特性无关。
