Department of Cardiology, Daping Hospital, The Third Military Medical University, Chongqing, P.R. China.
Division of Renal Diseases & Hypertension, Departments of Medicine and Pharmacology/Physiology, The George Washington University School of Medicine and Health Sciences, Washington, DC, USA.
Clin Exp Hypertens. 2019;41(8):739-746. doi: 10.1080/10641963.2018.1545850. Epub 2018 Nov 18.
The aim of this study was to investigate the effect of long-term low salt diet on blood pressure and its underlying mechanisms. Male Sprague-Dawley (SD) rats were divided into normal salt diet group (0.4%) and low salt diet group (0.04%). Blood pressure was measured with the non-invasive tail-cuff method. The contractile response of isolated mesenteric arteries was measured using a small vessel myograph. The effects on renal function of the intrarenal arterial infusion of candesartan (10 μg/kg/min), an angiotensin II receptor type 1 (ATR) antagonist, were also measured. The expressions of renal ATR and mesenteric arterial α, α, and α adrenergic receptors were quantified by immunoblotting. Plasma levels of angiotensin II were also measured. Systolic blood pressure was significantly increased after 8 weeks of low salt diet. There were no obvious differences in the renal structure between the low and normal salt diet groups. However, the plasma angiotensin II levels and renal ATR expression were higher in low than normal salt diet group. The intrarenal arterial infusion of candesartan increased urine flow and sodium excretion to a greater extent in the low than normal salt diet group. The expressions of α and α but not α, adrenergic receptors, and phenylephrine-induced contraction were increased in mesenteric arteries from the low salt, relative to the normal salt diet group. Activation of the renin-angiotensin and sympathetic nervous systems may be involved in the pathogenesis of long-term low salt diet-induced hypertension.
本研究旨在探讨长期低盐饮食对血压的影响及其潜在机制。雄性 Sprague-Dawley（SD）大鼠分为正常盐饮食组（0.4%）和低盐饮食组（0.04%）。采用非侵入性尾套法测量血压。使用小血管肌动描记仪测量分离的肠系膜动脉的收缩反应。还测量了血管紧张素 II 受体 1（ATR）拮抗剂坎地沙坦（10μg/kg/min）经肾内动脉输注对肾功能的影响。通过免疫印迹定量肾 ATR 和肠系膜动脉α、α和α肾上腺素能受体的表达。还测量了血管紧张素 II 的血浆水平。低盐饮食 8 周后，收缩压显著升高。低盐和正常盐饮食组之间肾脏结构没有明显差异。然而，低盐饮食组的血浆血管紧张素 II 水平和肾 ATR 表达高于正常盐饮食组。坎地沙坦经肾内动脉输注可增加低盐饮食组的尿量和钠排泄量，而正常盐饮食组则无明显增加。与正常盐饮食组相比，低盐饮食组肠系膜动脉中α和α但不是α肾上腺素能受体的表达增加，且去氧肾上腺素诱导的收缩增加。肾素-血管紧张素和交感神经系统的激活可能参与了长期低盐饮食诱导的高血压的发病机制。
