去氧皮质酮盐（DOCA-盐）大鼠后肢阻力动脉肌膜钠钾泵的改变

Yamamoto K, Takeshita A, Ashihara T, Imaizumi T, Nakamura M

Research Institute of Angiocardiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

Clin Exp Hypertens A. 1990;12(7):1237-54. doi: 10.3109/10641969009074751.

It has been suggested that a circulating inhibitor of the Na(+)-K+ pump contributes to the development and maintenance of DOCA-salt hypertension. However, the discordant results have been reported as to whether the sarcolemmal Na(+)-K+ pump in DOCA-salt hypertension is inhibited. Furthermore, no study has examined alteration in the sarcolemmal Na(+)-K+ pump of the true resistance arteries. We examined hindquarters vasoconstriction induced by ouabain (10(-3) M) in the vascularly isolated hindquarters of the DOCA-salt treated or control rats, which were perfused with Krebs-Henseleit solution. Hindquarters vasoconstriction induced by ouabain (10(-3) M) was greater in the prehypertensive and hypertensive DOCA-salt rats than in the corresponding control rats (p less than 0.01). We also examined hindquarters vasoconstriction induced by ouabain (10(-3) M) in the vascularly isolated hindquarters of the normal assay rats which were perfused by the plasma obtained from the DOCA-salt or control rats. The plasma of the prehypertensive and hypertensive DOCA-salt rats attenuated ouabain-induced hindquarters vasoconstriction in the assay rats (p less than 0.01). The plasma of the DOCA-salt rats did not alter nonspecific vasoconstriction caused by barium chloride. These results suggest that the plasma of the prehypertensive and hypertensive DOCA-salt rats had an inhibitor of the sarcolemmal Na(+)-K+ pump of the resistance arteries, but the sarcolemmal Na(+)-K+ pump molecules of the resistance arteries of those rats were increased. The in vivo activity of the sarcolemmal pump of the resistance arteries of the DOCA-salt rats would be determined by the relative influence of increased pump molecules and a circulating pump inhibitor.

有人提出，钠钾泵的循环抑制剂有助于去氧皮质酮盐性高血压的发生和维持。然而，关于去氧皮质酮盐性高血压时肌膜钠钾泵是否受到抑制，已有不一致的报道。此外，尚无研究检测真正阻力动脉肌膜钠钾泵的变化。我们在血管隔离的后肢灌注Krebs-Henseleit溶液的去氧皮质酮盐处理大鼠或对照大鼠中，检测了哇巴因（10⁻³ M）诱导的后肢血管收缩。哇巴因（10⁻³ M）诱导的后肢血管收缩在高血压前期和高血压去氧皮质酮盐大鼠中比相应的对照大鼠更大（p < 0.01）。我们还在正常测定大鼠的血管隔离后肢中检测了哇巴因（10⁻³ M）诱导的后肢血管收缩，这些后肢用从去氧皮质酮盐大鼠或对照大鼠获得的血浆灌注。高血压前期和高血压去氧皮质酮盐大鼠的血浆减弱了测定大鼠中哇巴因诱导的后肢血管收缩（p < 0.01）。去氧皮质酮盐大鼠的血浆未改变由氯化钡引起的非特异性血管收缩。这些结果表明，高血压前期和高血压去氧皮质酮盐大鼠的血浆中存在阻力动脉肌膜钠钾泵的抑制剂，但这些大鼠阻力动脉的肌膜钠钾泵分子增加。去氧皮质酮盐大鼠阻力动脉肌膜泵的体内活性将由泵分子增加和循环泵抑制剂的相对影响决定。