Campese V M, Karubian F, Chervu I, Parise M, Sarkies N, Bigazzi R
Department of Medicine, University of Southern California, Los Angeles.
Hypertension. 1993 Mar;21(3):301-7. doi: 10.1161/01.hyp.21.3.301.
The mechanisms responsible for increased blood pressure in response to a high dietary sodium intake in salt-sensitive patients with essential hypertension are only partially understood. The possibility that increased reactivity to pressor hormones might contribute to hypertension in these patients has not been adequately investigated. We studied 11 salt-sensitive and 15 salt-resistant patients with essential hypertension while they were ingesting a diet with 20 meq/day sodium for 9 days or one with 200 meq/day sodium for 14 days. During the last 4 days of each dietary regimen, they received 30 mg/day of slow-release nifedipine. Blood pressure response to increasing doses of norepinephrine and angiotensin II (Ang II) was studied at the end of each of four phases of the study. Salt-sensitive patients exhibited a greater blood pressure response to norepinephrine than salt-resistant patients, irrespective of the dietary sodium intake and whether we took into account the dose infused or the actual plasma levels of norepinephrine achieved during the infusion. The blood pressure response to Ang II, on the other hand, was greater in salt-sensitive than salt-resistant patients during low but not during high sodium intake. The blood levels of norepinephrine achieved during the infusion of this hormone were lower in salt-sensitive than in salt-resistant patients. These studies indicate that an increased reactivity to the pressor action of norepinephrine might contribute to the maintenance of hypertension in salt-sensitive patients. The increased reactivity appears to be specific for norepinephrine. In fact, we observed increased reactivity to Ang II during low but not during high sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS)
对于原发性高血压盐敏感患者而言，高钠饮食导致血压升高的机制仅得到部分理解。这些患者对升压激素反应性增加可能导致高血压这一可能性尚未得到充分研究。我们研究了11名盐敏感和15名盐抵抗的原发性高血压患者，他们分别摄入每日20毫当量钠的饮食9天，或每日200毫当量钠的饮食14天。在每种饮食方案的最后4天，他们接受每日30毫克的缓释硝苯地平。在研究的四个阶段结束时，研究了对递增剂量去甲肾上腺素和血管紧张素II（Ang II）的血压反应。无论饮食钠摄入量如何，也无论我们是否考虑输注剂量或输注期间实际达到的去甲肾上腺素血浆水平，盐敏感患者对去甲肾上腺素的血压反应均大于盐抵抗患者。另一方面，在低钠摄入时盐敏感患者对Ang II的血压反应大于盐抵抗患者，但在高钠摄入时并非如此。输注该激素期间盐敏感患者达到的去甲肾上腺素血水平低于盐抵抗患者。这些研究表明，对去甲肾上腺素升压作用反应性增加可能有助于维持盐敏感患者的高血压状态。这种反应性增加似乎对去甲肾上腺素具有特异性。事实上，我们观察到在低钠摄入而非高钠摄入期间对Ang II的反应性增加。（摘要截选至250字）
