Moore A F, Khairallah P A
Blood Vessels. 1979;16(4):169-76. doi: 10.1159/000158204.
The role of sodium and potassium ions, and the possible involvement of the membrane sodium pump has been studied in the development of a contractile response to, and the development of tachyphylaxis to, angiotensin II. It is suggested that a membrane depolarization may have a role in the mechanism of the contractile response to angiotensin II, as responses of the rabbit aorta to angiotensin II were selectively inhibited in K-free medium. Acute or chronic increases in medium sodium, however, did not influence the response of the rabbit aorta to angiotensin II. On the rat aorta increased medium sodium concentrations potentiated the response to angiotensin II and inhibited the development of tachyphylaxis. Membrane depolarization or hyperpolarization does not appear to be part of the mechanism of development of tachyphylaxis to angiotensin II on the rat aorta, as response to both NE and angiotensin II were inhibited equally by exposure of the rat aorta to K-free medium, i.e., nonspecific desensitization occurred, as opposed to the specific desensitization which defines tachyphylaxis.
已经研究了钠离子和钾离子的作用以及膜钠泵可能的参与情况,涉及对血管紧张素II的收缩反应的发展以及对血管紧张素II快速耐受性的发展。有人提出,膜去极化可能在对血管紧张素II的收缩反应机制中起作用,因为在无钾培养基中兔主动脉对血管紧张素II的反应被选择性抑制。然而,培养基中钠的急性或慢性增加并未影响兔主动脉对血管紧张素II的反应。在大鼠主动脉上,培养基中钠浓度的增加增强了对血管紧张素II的反应并抑制了快速耐受性的发展。膜去极化或超极化似乎不是大鼠主动脉对血管紧张素II快速耐受性发展机制的一部分,因为将大鼠主动脉暴露于无钾培养基中时,对去甲肾上腺素(NE)和血管紧张素II的反应均受到同等程度的抑制,即发生了非特异性脱敏,这与定义快速耐受性的特异性脱敏相反。