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48例原发性高血压(EH)患者于快速静注生理盐水1000ml后及口服速尿40mg后二小时内舒张压分别升、降≥10mmHg的盐敏感患者,探索血压调控激素、红细胞膜结构及离子转运功能机制。发现:(1)约50%患者对负荷盐升压及(或)削减钠(Na)降压敏感。(2)在盐升压组速尿有效的9例血浆类地高辛物质(EDLS)较无效的4例高,(P<0.05);EDLS/心房肽(ANP)也较高(P<0.05);在盐不升压组速尿有效的11例负荷盐水期尿Na排量低于无效的14例(P<0.05),提示速尿有效的存在潴Na、容量扩张倾向。(3)在盐升压的速尿有效组红细胞内向Na“漏”较无效的高(P<0.05);在盐不升压的速尿有效组在盐水负荷前后膜芘I~m/I~e(322nm、272nm时)均较无效的低(P<0.01),血浆醛固酮(PA)也较低(P<0.05)。(4)在速尿有效组盐升压的9例负荷盐水后PA较不升压的11例高(P<0.05),负荷盐水期尿Na排量也偏高(P=0.05),在速尿无效组盐升压的4例内向Na“漏”较盐不升压的14例高(P<0.01)。以上提示红细胞膜功能与结构改变和血压调控激素的平衡失调和盐敏感机制有关。
Forty-eight patients with essential hypertension (EH) under rapid intravenous infusion of normal saline 1000ml and oral furosemide 40mg diastolic blood pressure were increased or decreased 10mmHg salt sensitive patients, to explore the blood pressure regulating hormone, membrane structure of erythrocyte and Ion transport mechanism. It was found that: (1) About 50% of patients were sensitive to pressure-induced salt stress and / or reduced sodium (Na) blood pressure. (2) The EDLS of 9 cases of effective furosemide in the group of elevated pressure were higher than that of 4 cases of ineffective (P <0.05), EDLS / ANP was also higher (P <0.05) ); In the non-hypertensive saline group, the urinary Na excretion was lower than that of ineffective in 11 cases of saline load (P <0.05), suggesting that there is effectively retention of Na in the fasting urine and the capacity expansion tendency. (3) The “leak” of Na to erythrocytes in the hypertensive group was higher than that of ineffective (P <0.05); in the furosemide-effective group, the pyrene I ~ m / I ~ e (322 nm, 272 nm) were lower (P <0.01) and plasma aldosterone (PA) were lower (P <0.05). (4) In the group of 9 cases of saline with elevated urinary pressure, the PA was higher in the PA than in the 11 cases (P <0.05) and the urinary Na in the loaded saline phase was also higher (P = 0.05) Urinary ineffective group of salt pressure in 4 cases of Na leakage "than the salt does not increase the pressure of 14 cases (P <0.01). The above suggests that the function of erythrocyte membrane and structural changes and the balance of blood pressure regulating hormones and salt sensitivity mechanism.