Zanchetti A, Stella A, Golin R
J Cardiovasc Pharmacol. 1985;7 Suppl 6:S194-8. doi: 10.1097/00005344-198500076-00034.
Stimulation and denervation experiments have provided evidence that adrenergic mechanisms can enhance sodium and water reabsorption from the renal tubule, and that this influence is probably exerted on the entire tubular extent. Reflexes originating from cardiopulmonary and renal receptors can control adrenergic renal sodium handling, and evidence has recently been presented that a reno-renal reflex tonically inhibits the contralateral sympathetic control of tubular reabsorption of sodium and water. Other investigations indicate that adrenergic renal sodium handling is mediated through alpha-rather than beta-receptors, and that the alpha-receptors are of the alpha 1-subtype. The question of whether the natriuretic action of calcium antagonists is, at least in part, mediated by interference with adrenergic control of tubular reabsorption cannot yet be definitely answered. Although available data are only preliminary, they do not support an important action of calcium antagonists on adrenergic renal sodium handling, but a separate contribution of impaired adrenergic control and of a direct tubular effect of calcium antagonists cannot be excluded.
刺激和去神经实验已提供证据表明，肾上腺素能机制可增强肾小管对钠和水的重吸收，且这种影响可能作用于整个肾小管。源自心肺和肾感受器的反射可控制肾上腺素能对肾钠的处理，最近有证据表明，肾-肾反射可紧张性抑制对侧交感神经对肾小管钠和水重吸收的控制。其他研究表明，肾上腺素能对肾钠的处理是通过α受体而非β受体介导的，且α受体为α1亚型。钙拮抗剂的利钠作用是否至少部分是通过干扰肾上腺素能对肾小管重吸收的控制来介导的，这一问题尚无法明确回答。尽管现有数据只是初步的，但它们不支持钙拮抗剂对肾上腺素能肾钠处理有重要作用，但不能排除肾上腺素能控制受损和钙拮抗剂直接肾小管效应的单独作用。
