Wisgerhof M, Brown R D
J Clin Invest. 1978 Jun;61(6):1456-62. doi: 10.1172/JCI109065.
Studies were undertaken to determine if the dissociation of aldosterone and plasma renin activity in low-renin essential hypertension is due to altered adrenal responsiveness to angiotensin II. The responsiveness of the adrenal glands to angiotensin II was determined by infusing graded doses of angiotensin II into normal subjects and into patients with essential hypertension and measuring changes in levels of plasma aldosterone in response to the infusion. To minimize the influence of endogenous angiotensin II and ACTH, supplemental sodium and dexamethasone were given before the infusions. Levels of plasma aldosterone and plasma renin activity were determined in normal subjects and in the same patients after the combined stimuli of furosemide and upright posture, a maneuver used to increase the level of endogenous angiotensin II. To determine if the changes in levels of plasma aldosterone during infusion of angiotensin II were due to alteration of the metabolic clearance of aldosterone, the metabolic clearance of aldosterone was measured before and during the infusion of angiotensin II. After sodium loading, dexamethasone treatment, and supine posture, levels of plasma aldosterone of normal subjects and patients with essential hypertension were suppressed equally. In response to the infusion of angiotensin II, the levels of plasma aldosterone of patients with low-renin essential hypertension were significantly higher than those of normal subjects or of patients with normal-renin essential hypertension. After furosemide and upright posture, levels of plasma aldosterone of patients with low-renin essential hypertension were significantly higher than those of patients with normal-renin essential hypertension, despite a blunted response in plasma renin activity of the patients with low-renin essential hypertension. Decreases in metabolic clearance of aldosterone during infusion of angiotensin II were similar in patients with normal-renin essential hypertension and in patients with low-renin essential hypertension and accounted for only a small fraction of the marked increase in levels of plasma aldosterone of patients with low-renin essential hypertension. It is concluded that patients with low-renin essential hypertension have increased adrenal sensitivity to angiotensin II. This increased sensitivity may explain the dissociation of aldosterone and plasma renin activity in low-renin essential hypertension.
开展了多项研究，以确定低肾素性原发性高血压中醛固酮与血浆肾素活性的分离是否归因于肾上腺对血管紧张素II反应性的改变。通过向正常受试者和原发性高血压患者输注分级剂量的血管紧张素II，并测量输注后血浆醛固酮水平的变化，来确定肾上腺对血管紧张素II的反应性。为了尽量减少内源性血管紧张素II和促肾上腺皮质激素的影响，在输注前给予补充钠和地塞米松。在速尿和直立姿势这一用于提高内源性血管紧张素II水平的操作联合刺激后，测定正常受试者和同一批患者的血浆醛固酮水平和血浆肾素活性。为了确定血管紧张素II输注期间血浆醛固酮水平的变化是否归因于醛固酮代谢清除率的改变，在血管紧张素II输注前和输注期间测量醛固酮代谢清除率。在钠负荷、地塞米松治疗和仰卧姿势后，正常受试者和原发性高血压患者的血浆醛固酮水平受到同等程度的抑制。对血管紧张素II输注的反应中，低肾素性原发性高血压患者的血浆醛固酮水平显著高于正常受试者或正常肾素性原发性高血压患者。速尿和直立姿势后，低肾素性原发性高血压患者的血浆醛固酮水平显著高于正常肾素性原发性高血压患者，尽管低肾素性原发性高血压患者的血浆肾素活性反应减弱。血管紧张素II输注期间，正常肾素性原发性高血压患者和低肾素性原发性高血压患者的醛固酮代谢清除率下降相似，且仅占低肾素性原发性高血压患者血浆醛固酮水平显著升高的一小部分。得出的结论是，低肾素性原发性高血压患者肾上腺对血管紧张素II的敏感性增加。这种增加的敏感性可能解释了低肾素性原发性高血压中醛固酮与血浆肾素活性的分离。
