Hayashi K, Loutzenhiser R, Epstein M
Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
J Am Soc Nephrol. 1997 Jan;8(1):25-31. doi: 10.1681/ASN.V8125.
The thromboxane A2 (TXA2) mimetic U44069 has been demonstrated to reduce the GFR and filtration fraction of the normal isolated perfused rat kidney markedly, suggesting a predominant constriction of preglomerular vessels. To assess this possibility directly, effects of U44069 on the renal microvessels of the isolated perfused hydronephrotic kidney were examined. At 10(-6) mol/L, U44069 elicited a 27 +/- 2% decrease in afferent arteriolar (AA) diameter (from 18.8 +/- 0.3 to 13.7 +/- 0.3 micron, P < 0.001). In contrast, efferent arteriolar (EA) diameter decreased by only 9 +/- 1% (from 16.4 +/- 0.5 to 15.0 +/- 0.5 micron, P < 0.001). These effects on both AA and EA were completely reversed by the TXA2 receptor antagonist SQ29548. The calcium antagonist diltiazem reversed U44069-induced AA constriction by 83 +/- 5%. The U44069-induced EA constriction was insensitive to the vasodilator action of diltiazem at concentrations from 10(-8) to 10(-6) mol/L, but at 10(-5) mol/L, diltiazem increased the EA diameter significantly, albeit modestly. Nifedipine also reversed the U44069-induced AA constriction (81 +/- 7%), but failed to inhibit the EA constriction at concentrations from 10(-9) to 10(-6) mol/L. These findings constitute the first direct evidence that a TXA2 agonist preferentially constricts the afferent arteriole. Furthermore, the ability of both the calcium antagonist and SQ29548 to reverse the renal microvascular actions of TXA2 agonists suggests a potential utility of these agents in ameliorating TXA2-induced renal hemodynamic abnormalities.
血栓素A2(TXA2)模拟物U44069已被证明能显著降低正常离体灌注大鼠肾脏的肾小球滤过率(GFR)和滤过分数,提示肾小体前血管主要发生收缩。为了直接评估这种可能性,研究了U44069对离体灌注肾积水肾脏肾微血管的影响。在10^(-6) mol/L时,U44069使入球小动脉(AA)直径减小27±2%(从18.8±0.3微米降至13.7±0.3微米,P<0.001)。相比之下,出球小动脉(EA)直径仅减小9±1%(从16.4±0.5微米降至15.0±0.5微米,P<0.001)。TXA2受体拮抗剂SQ29548可完全逆转U44069对AA和EA的这些作用。钙拮抗剂地尔硫䓬可使U44069诱导的AA收缩逆转83±5%。U44069诱导的EA收缩在10^(-8)至10^(-6) mol/L浓度范围内对地尔硫䓬的血管舒张作用不敏感,但在10^(-5) mol/L时,地尔硫䓬可使EA直径显著增加,尽管增加幅度不大。硝苯地平也可逆转U44069诱导的AA收缩(81±7%),但在10^(-9)至10^(-6) mol/L浓度范围内未能抑制EA收缩。这些发现构成了TXA2激动剂优先收缩入球小动脉的首个直接证据。此外,钙拮抗剂和SQ29548均可逆转TXA2激动剂的肾微血管作用,提示这些药物在改善TXA2诱导的肾血流动力学异常方面具有潜在应用价值。