Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava 81108, Slovak Republic; 3rd Department of Internal Medicine, Faculty of Medicine, Comenius University, Bratislava 83305, Slovak Republic; Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava 84505, Slovak Republic.
Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava 81108, Slovak Republic; Department of Pneumology, Phthisiology and Functional Diagnostics, Slovak Medical University and Bratislava University Hospital, Bratislava, Slovak Republic.
Biomed Pharmacother. 2024 Apr;173:116391. doi: 10.1016/j.biopha.2024.116391. Epub 2024 Mar 11.
This study investigated whether sacubitril/valsartan or valsartan are able to prevent left ventricular (LV) fibrotic remodelling and dysfunction in two experimental models of pre-hypertension induced by continuous light (24 hours/day) exposure or by chronic lactacystin treatment, and how this potential protection interferes with the renin-angiotensin-aldosterone system (RAAS). Nine groups of three-month-old male Wistar rats were treated for six weeks as follows: untreated controls (C), sacubitril/valsartan (ARNI), valsartan (Val), continuous light (24), continuous light plus sacubitril/valsartan (24+ARNI) or valsartan (24+Val), lactacystin (Lact), lactacystin plus sacubitil/valsartan (Lact+ARNI) or plus valsartan (Lact+Val). Both the 24 and Lact groups developed a mild but significant systolic blood pressure (SBP) increase, LV hypertrophy and fibrosis, as well as LV systolic and diastolic dysfunction. Yet, no changes in serum renin-angiotensin were observed either in the 24 or Lact groups, though aldosterone was increased in the Lact group compared to the controls. In both models, sacubitril/valsartan and valsartan reduced elevated SBP, LV hypertrophy and fibrosis and attenuated LV systolic and diastolic dysfunction. Sacubitril/valsartan and valsartan increased the serum levels of angiotensin (Ang) II, Ang III, Ang IV, Ang 1-5, Ang 1-7 in the 24 and Lact groups and reduced aldosterone in the Lact group. We conclude that both continuous light exposure and lactacystin treatment induced normal-to-low serum renin-angiotensin models of pre-hypertension, whereas aldosterone was increased in lactacystin-induced pre-hypertension. The protection by ARNI or valsartan in the hypertensive heart in either model was related to the Ang II blockade and the protective Ang 1-7, while in lactacystin-induced pre-hypertension this protection seems to be additionally related to the reduced aldosterone level.
本研究旨在探讨沙库巴曲缬沙坦(ARNI)或缬沙坦是否能够预防持续光照(24 小时/天)暴露或慢性乳清酸处理引起的两种高血压前期实验模型中的左心室(LV)纤维化重塑和功能障碍,以及这种潜在的保护作用如何干扰肾素-血管紧张素-醛固酮系统(RAAS)。将 9 组 3 个月大的雄性 Wistar 大鼠分别用以下方法处理 6 周:未处理对照组(C)、沙库巴曲缬沙坦(ARNI)、缬沙坦(Val)、持续光照(24)、持续光照加沙库巴曲缬沙坦(24+ARNI)或缬沙坦(24+Val)、乳清酸处理(Lact)、乳清酸加沙库巴曲缬沙坦(Lact+ARNI)或加缬沙坦(Lact+Val)。24 小时和 Lact 组大鼠均出现轻度但显著的收缩压(SBP)升高、LV 肥大和纤维化以及 LV 收缩和舒张功能障碍。然而,24 小时和 Lact 组大鼠的血清肾素-血管紧张素均未发生变化,尽管与对照组相比,Lact 组大鼠的醛固酮增加。在这两种模型中,沙库巴曲缬沙坦和缬沙坦均降低了升高的 SBP、LV 肥大和纤维化,并减轻了 LV 收缩和舒张功能障碍。沙库巴曲缬沙坦和缬沙坦增加了 24 小时和 Lact 组大鼠血清中血管紧张素(Ang)II、Ang III、Ang IV、Ang 1-5、Ang 1-7 的水平,并降低了 Lact 组大鼠的醛固酮水平。我们得出结论,持续光照暴露和乳清酸处理均可诱导正常至低血清肾素-血管紧张素的高血压前期模型,而在乳清酸诱导的高血压前期模型中,醛固酮增加。ARNI 或缬沙坦在两种模型中对高血压心脏的保护作用与 Ang II 阻断和保护性的 Ang 1-7 有关,而在乳清酸诱导的高血压前期模型中,这种保护作用似乎还与降低的醛固酮水平有关。