Renal denervation ameliorated salt-induced hypertension by improving cardiac work, cardiac enzyme and oxidative balance in Sprague-Dawley rats

IF 1.9 Q3 PERIPHERAL VASCULAR DISEASE
Abdullahi Adejare, Ahmed Oloyo, Yusuf Dahud, Morufat Adeshina, Abiola Agbaje, Clinton Ejim, Khadijah Ismail-Badmus, Smith Jaja
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Abstract

Background

Hypertension is associated with cardiovascular dysfunction, dysregulation of the antioxidant system and alteration of the level of some enzymes in the metabolic pathway. The possible modulatory effect of acute renal denervation (ARD) on cardiovascular function and the antioxidant system is still a subject of intense debate. This study sought to ascertain the ameliorative effects of ARD on cardiovascular parameters, antioxidant system, creatine kinase and lactate dehydrogenase levels.

Methods

Thirty-six Sprague-Dawley rats (5–6 weeks old) were divided into 6 groups of 6 animals each consisting of Normal Salt, High Salt, Normal Salt + Sham Denervation, High Salt + Sham Denervation, Normal Salt + Renal Denervation and High Salt + Renal Denervation. Induction of hypertension with 8 % salt in the diet lasted for 8 weeks. Renal or Sham denervation was thereafter done on selected groups. At the end of the experimental period, cardiovascular parameters, plasma antioxidant status, plasma creatine kinase (CK) and lactate dehydrogenase (LDH) levels were assessed. Significance level was set at p < 0.05.

Results

Salt-loading significantly increased systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MABP), rate pressure product (RPP) while reducing superoxide dismutase (SOD), reduced glutathione (GSH) and catalase (CAT). Acute renal denervation significantly (p < 0.0001) reduced SBP, DBP, MABP, RPP, LDH and norepinephrine level while increasing SOD, GSH and CAT. ARD did not significantly alter CK level.

Conclusion

Acute renal denervation, by reducing sympathetic activity, ameliorates cardiovascular and antioxidant functions as well as reduces LDH level without significantly altering CK level in salt-induced hypertension.

通过改善 Sprague-Dawley 大鼠的心脏功、心肌酶和氧化平衡,去神经肾脏可改善盐引起的高血压
背景高血压与心血管功能障碍、抗氧化系统失调和代谢途径中某些酶的水平改变有关。急性肾脏去神经(ARD)对心血管功能和抗氧化系统可能产生的调节作用仍是一个激烈争论的话题。方法将 36 只 Sprague-Dawley 大鼠(5-6 周龄)分为 6 组,每组 6 只,包括正常盐组、高盐组、正常盐 + 假去神经组、高盐 + 假去神经组、正常盐 + 肾去神经组和高盐 + 肾去神经组。在饮食中加入 8% 的盐诱发高血压,持续 8 周。然后对选定的组别进行肾脏或假肾脏去神经支配。实验结束时,对心血管参数、血浆抗氧化状态、血浆肌酸激酶(CK)和乳酸脱氢酶(LDH)水平进行评估。结果盐负荷明显增加了收缩压(SBP)、舒张压(DBP)、平均动脉血压(MABP)和速率压力积(RPP),同时降低了超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)和过氧化氢酶(CAT)。急性肾脏去神经化可明显(p < 0.0001)降低 SBP、DBP、MABP、RPP、LDH 和去甲肾上腺素水平,同时增加 SOD、GSH 和 CAT。结论 急性肾脏神经支配通过降低交感神经活性,改善了盐诱导高血压患者的心血管和抗氧化功能,并降低了 LDH 水平,但没有明显改变 CK 水平。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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