Jones D R, Penner S B, Smyth D D
Br J Pharmacol. 1985 Dec;86(4):889-97. doi: 10.1111/j.1476-5381.1985.tb11111.x.
Rats were placed on either a low sodium intake (low sodium diet 0.025% dry weight, tap water for drinking) or a high sodium intake (normal sodium diet 0.45% dry weight, 0.9% saline for drinking) for 10 days. The pressor-response curve to angiotensin II in rats previously on a high sodium intake was shifted to the left of that found in rats previously on a low sodium intake. Suppression of endogenous angiotensin II formation with captopril (0.3 mg kg-1) or acute volume repletion (3% body wt per 30 min) resulted in a significant parallel shift of the pressor-response curve for angiotensin II to the left in the low salt group. In the high salt group captopril produced a similar but smaller parallel shift of the dose-response curve to the left. Similar manipulation of endogenous angiotensin II concentrations with high and low salt intake plus captopril treatment or acute volume repletion, produced no alterations in the pressor response for noradrenaline. The attenuated in vivo response to angiotensin II in the low salt intake group may be explained in part by the suppressed vascular sensitivity to angiotensin II in this group, as measured in the isolated perfused kidney of the rat. In kidneys from rats previously on a low sodium intake, an enhanced maximal vasoconstrictor response to noradrenaline was observed as compared to kidneys from high sodium intake rats. These results indicate that, whereas alterations in endogenous angiotensin II concentrations within physiological limits affects the response to exogenous angiotensin, there is little if any effect on the pressor response to noradrenaline.
将大鼠分为两组，分别给予低钠摄入（低钠饮食，干重0.025%，饮用自来水）或高钠摄入（正常钠饮食，干重0.45%，饮用0.9%盐水），持续10天。先前高钠摄入的大鼠对血管紧张素II的升压反应曲线，相较于先前低钠摄入的大鼠，向左偏移。用卡托普利（0.3mg/kg）抑制内源性血管紧张素II的形成，或急性扩容（每30分钟补充3%体重），导致低盐组中血管紧张素II的升压反应曲线显著平行左移。在高盐组中，卡托普利使剂量反应曲线产生类似但较小的平行左移。通过高盐和低盐摄入加卡托普利治疗或急性扩容对内源性血管紧张素II浓度进行类似操作，去甲肾上腺素的升压反应未发生改变。低盐摄入组中对血管紧张素II的体内反应减弱，部分原因可能是该组中血管对血管紧张素II的敏感性降低，这在大鼠离体灌注肾中得到了测量。与高钠摄入大鼠的肾脏相比，先前低钠摄入大鼠的肾脏对去甲肾上腺素的最大血管收缩反应增强。这些结果表明，尽管生理范围内内源性血管紧张素II浓度改变会影响对外源性血管紧张素的反应，但对去甲肾上腺素的升压反应几乎没有影响。
