Renal hemodynamics in acute and chronic angiotensin II hypertension.
Renal hemodynamics in acute and chronic angiotensin II hypertension.
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急性和慢性血管紧张素 II 高血压中的肾血流动力学。
DOI：
10.1152/ajprenal.1978.235.3.f174
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发表时间：
1978
期刊：
影响因子：
--
通讯作者：
J. Balfe
中科院分区：
文献类型：
--
作者：
J. Hall;A. C. Guyton;H. Salgado;R. McCaa;J. Balfe
约翰·霍尔，亚瑟C.赫利奥·盖顿罗伯特·萨加多McCAA和J.威廉姆森Balfe。急性和慢性血管紧张素II高血压的肾血流动力学。Am. J. Physiol.235（3）：F174-F179，1978或Am.生理学杂志：肾液电解质生理学4（3）：F174-F179，1978年。在8只清醒的狗中，在维持103 meq/天钠摄入的急性和慢性静脉输注血管紧张素II（Au）（10 ng/kg/min）期间，检查动脉压（AP）、肾血流动力学、体液和电解质平衡以及血浆醛固酮浓度（PAC）的顺序变化。在AI 1输注开始后20分钟内，AP增加24 ± 2 mmHg;在接下来的4天内，AP进一步增加，稳定在高于对照组的38 ± 4 mmHg。与第1天和第2天AP上升相一致的是水和钠的显著保留，碘酞酸钠空间分别上升至对照值的108 t-1和111 t-2%。有效肾血浆流量（ERPF）下降到对照组的85 2 5%，并在整个研究中保持在这个水平，但肾小球滤过率下降只有5-8%，在急性输注和慢性AI 1输注过程中没有显着改变。虽然PAC在AI 1输注的前100分钟内显著增加，但1天后PAC下降至仅略高于对照组的值。这些观察结果表明，在慢性AI 1高血压期间，AII的直接肾血流动力学（ERPF降低和滤过分数增加）或肾小管效应，而不是PAC的变化，可能是导致钠和水潴留趋势的主要原因，直到AP增加到足以实现钠和水平衡。血管紧张素系统;肾小球滤过率;醛固酮;电解质排泄;体液;动脉血压已广泛研究了肾素-血管紧张素系统在高血压，特别是肾血管性高血压的发展中的重要性（2，21）。几项研究表明，输注生理量的血管紧张素II（5-25 rig/kg/min）会导致高血压的逐渐发展，其严重程度随钠摄入量而变化（2，4，21）。虽然血管紧张素II（AII）对外周小动脉的直接影响已被广泛认可，但最初降压的血管紧张素II剂量逐渐发展为高血压表明涉及其他机制（7，24）。此外，最近的理论和实验证据表明，
HALL, JOHN E., ARTHUR C. GUYTON, HELIO C. SALGADO, ROBERT E. MCCAA, AND J. WILLIAMSON BALFE. Renal hemodynamics in acute and chronic angiotensin II hypertension. Am. J. Physiol. 235 (3): F174-F179, 1978 or Am. J. Physiol.: Renal Fluid Electrolyte Physiol. 4 (3): F174-F179, 1978.-Sequential changes in arterial pressure (AP), renal hemodynamics, body fluid and electrolyte balance, and plasma aldosterone concentration (PAC) were examined during acute and chronic intravenous infusions of angiotensin II (AU)(10 ng/kg per min) in eight conscious dogs maintained on 103 meq/day sodium intake. Within 20 min after the start of AI1 infusion, AP increased 24* 2 mmHg; during the next 4 days AP increased further, stabilizing at 38 t 4 mmHg above control. Coinciding with the rise in AP on days 1 and 2 was a marked retention of water and sodium and a rise in sodium iothalamate space to 108 t 1 and 111 t 2%, respectively, of control value. Effective renal plasma flow (ERPF) decreased to 85 2 5% of control and remained at this level throughout the study, but glomerular filtration rate decreased only 5-8% during acute infusions and was not significantly altered during chronic AI1 infusion. Although PAC increased markedly during the first 100 min of AI1 infusion, after 1 day PAC declined to values only slightly greater than control. These observations suggest that during chronic AI1 hypertension, the direct renal hemodynamic (decreased ERPF and increased filtration fraction) or tubular effects of AII, rather than changes in PAC, may be primarily responsible for the tendency toward sodium and water retention that occurs until AP increases enough to achieve sodium and water balance. renin-angiotensin system; glomerular filtration rate; aldosterone; electrolyte excretion; body fluids; arterial blood pressureTHE IMPORTANCE OF THE renin-angiotensin system in the development of hypertension, especially renovascular hypertension, has been widely investigated (2, 21). Several studies have demonstrated that infusion of physiologic amounts of angiotensin II (5-25 rig/kg per min) causes a gradual development of hypertension, the severity of which varies with the sodium intake (2, 4, 21). While the direct effects of angiotensin II (AII) on the peripheral arterioles are widely recognized, the gradual development of hypertension with doses of angiotensin II that are initially subpressor suggests that additional mechanisms are involved (7, 24). Additionally, recent theoretical and experimental evidence