给药后局部血流的重新分布在盐枯竭的狗。

C S Liang, H Gavras, H R Brunner
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引用次数: 3

摘要

1. 5只狗通过低盐饮食和每天服用氟塞胺5天产生盐消耗;对照组的5只狗被置于同样的饮食中,其中添加了2.5克氯化钠。2. 撒拉拉西素输注(0.5微克min-1 kg-1)降低了盐耗竭犬的平均主动脉压和总外周血管阻力,增加了心输出量,但不影响心率和左心室dP/dt。3.注射萨拉拉西素使正常犬的平均主动脉压略有升高;其他全身血流动力学参数无明显变化。4. salalasin在正常犬和缺盐犬中均降低肝动脉流量,但仅在缺盐犬中增加左心室和肾脏的血流量。5. 这些结果表明,salalasin在正常犬中发挥部分激动剂作用以增加动脉血压,但在盐消耗期间引起降压反应,因为它逆转了血管紧张素II的血管收缩作用,特别是对肾脏和冠状动脉循环。
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Redistribution of regional blood flow after administration of saralasin in salt-depleted dogs.

1. Salt depletion was produced in five dogs by a low salt diet and daily administration of frusemide for 5 days; a control group of five dogs was placed on the same diet, to which 2.5 g of sodium chloride was added. 2. Saralasin infusion (0.5 microgram min-1 kg-1) reduced mean aortic blood pressure and total peripheral vascular resistance and increased cardiac output in salt-depleted dogs, but did not affect the heart rate and left ventricular dP/dt. 3. Saralasin infusion increased mean aortic blood pressure slightly in normal dogs; other systemic haemodynamic parameters did not change significantly. 4. Saralasin decreased hepatic arterial flow in both normal and salt-depleted dogs, but increased blood flow to left ventricle and kidneys only in salt-depleted dogs. 5. These results suggest that saralasin exerts a partial agonist effect in normal dogs to increase arterial blood pressure, but causes a depressor response during salt depletion because it reverses the vasoconstrictor effect of angiotensin II, particularly on the renal and coronary circulations.

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Proceedings of the Fifth Meeting of the International Society of Hypertension, Paris, 12-14 June 1978. Brain catecholamines and catecholamine-synthesizing enzymes in renovascular hypertension in the rat. Enhanced hypothalamic noradrenaline biosynthesis in Goldblatt I renovascular hypertension. Definitive evidence for renin in rat brain by affinity chromatographic separation from protease. Renal release of active and inactive renin in essential and renovascular hypertension.
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