Huang A, Sun D, Koller A, Kaley G
Department of Physiology, New York Medical College, Valhalla 10595, USA.
Am J Physiol. 1997 Apr;272(4 Pt 2):H1804-9. doi: 10.1152/ajpheart.1997.272.4.H1804.
The characteristics of arteriolar myogenic responses of female rats have not been investigated. Thus experiments were conducted on isolated gracilis muscle arterioles (approximately 55 microm diameter) of four groups of 12-wk-old rats: male rats, female rats, ovariectomized female rats with no estrogen replacement (OV), and ovariectomized female rats with estrogen replacement (OV + E2, 50 microg/kg s.c. injection of 17beta-estradiol benzoate every 48 h). Diameter changes in response to increases in perfusion pressure from 20 to 140 mmHg and to various concentrations of substance P (SP, 10(-9)-5 x 10(-8) M) and sodium nitroprusside (SNP, 10(-8)-10(-6) M) were measured before and after administration of N(omega)-nitro-L-arginine (L-NNA, 10(-4) M), an inhibitor of NO synthase. Arteriolar diameters of male and OV female rats were significantly less at 60-140 mmHg pressure than those of normal female and OV + E2 female rats (at 80 mmHg, 45.4 +/- 1.8 and 43.1 +/- 2.2 vs. 58.4 +/- 1.6 and 57.3 +/- 1.3%). L-NNA elicited a significantly greater downward shift of pressure-diameter curves in arterioles of normal female and OV + E2 female rats than in arterioles of male and OV female rats (28.6 +/- 4.6 and 30.6 +/- 4.7 vs. 13.2 +/- 0.9 and 10.4 +/- 2.6%). Dilations of arterioles from normal female and OV +/- E2 female rats to SP were significantly greater (by 50-60%) than those from male and OV female rats (20.8 +/- 1.8 and 22.3 +/- 1.9 vs. 13.8 +/- 1.4 and 13.8 +/- 0.6% at 10(-8) M). L-NNA did not affect dilations to SNP but significantly reduced the dilation of arterioles in all groups to SP, more so in arterioles of male and OV female rats than in arterioles of the other two groups. We conclude that pressure-induced myogenic constriction of arterioles of female rats is less pronounced than that of male rats; this is, most likely, due to the enhanced release and/or activity of NO related to the presence of estrogen.
雌性大鼠小动脉肌源性反应的特征尚未得到研究。因此,对四组12周龄大鼠的分离股薄肌小动脉(直径约55微米)进行了实验:雄性大鼠、雌性大鼠、未进行雌激素替代的去卵巢雌性大鼠(OV)以及进行雌激素替代的去卵巢雌性大鼠(OV + E2,每48小时皮下注射50微克/千克的17β-雌二醇苯甲酸酯)。在给予一氧化氮合酶抑制剂N(ω)-硝基-L-精氨酸(L-NNA,10^(-4) M)之前和之后,测量了小动脉直径对灌注压力从20毫米汞柱增加到140毫米汞柱以及对不同浓度的P物质(SP,10^(-9)-5×10^(-8) M)和硝普钠(SNP,10^(-8)-10^(-6) M)的变化。在60 - 140毫米汞柱压力下,雄性和OV雌性大鼠的小动脉直径显著小于正常雌性和OV + E2雌性大鼠(在80毫米汞柱时,分别为45.4±1.8和43.1±2.2,而正常雌性和OV + E2雌性大鼠为58.4±1.6和57.3±1.3%)。L-NNA引起正常雌性和OV + E2雌性大鼠小动脉压力-直径曲线的向下位移显著大于雄性和OV雌性大鼠(分别为28.6±4.6和30.6±4.7,而雄性和OV雌性大鼠为13.2±0.9和10.4±2.6%)。正常雌性和OV + E2雌性大鼠的小动脉对SP的舒张反应显著大于雄性和OV雌性大鼠(在10^(-8) M时,分别为20.8±1.8和22.3±1.9,而雄性和OV雌性大鼠为13.8±1.4和13.8±0.6%)。L-NNA不影响对SNP的舒张反应,但显著降低了所有组中小动脉对SP的舒张反应,雄性和OV雌性大鼠小动脉的降低幅度大于另外两组。我们得出结论:雌性大鼠小动脉压力诱导的肌源性收缩比雄性大鼠的不明显;这很可能是由于雌激素的存在导致一氧化氮释放和/或活性增强。