Physiology Exercise Laboratory, Department of Physiology, Federal University of Sao Paulo (UNIFESP), Sao Paulo, Brazil.
Human Movement Laboratory, Sao Judas Tadeu University (USJT), Sao Paulo, SP, Brazil.
Biol Sex Differ. 2020 Apr 7;11(1):15. doi: 10.1186/s13293-020-00290-y.
Studies have presented conflicting findings regarding the association between both fluctuation and deprivation of ovarian hormones and cardiovascular autonomic modulation and oxidative stress and their potential impact on resting arterial pressure (AP) and cardiovascular risk. This study aimed to assess cardiovascular autonomic modulation, baroreflex sensitivity (BRS), and oxidative stress in male rats (M) and in female rats during ovulatory (FOV) and non-ovulatory phases (FNOV) of the estrous cycle and after deprivation of ovarian hormones (FO). Direct AP was recorded, and BRS was assessed by using increasing doses of phenylephrine and sodium nitroprusside. AP and heart rate variability were assessed by spectral analysis. Oxidative stress profile was evaluated in cardiac, renal, and muscle tissues. In females, the ovulatory phase and ovarian hormone deprivation induced an increase in AP (FOV and FO ~ 9 mmHg) when compared to the non-ovulatory phase. Ovariectomy promoted increased cardiac sympathovagal balance (~ 17-37%) when compared to other groups. Both FOV and FO groups presented impaired BRS, associated with higher AP variability. In general, antioxidant capacity was higher in the FNOV than in the M group. Ovarian hormone deprivation induced a decrease in catalase activity in cardiac and renal tissues and an increase in lipid peroxidation in all tissues analyzed. Positive correlations (p < 0.05) were found between vascular sympathetic modulation and lipid peroxidation in cardiac (r = 0.60), renal (r = 0.60), and muscle (r = 0.57) tissues. In conclusion, both oscillation and deprivation of ovarian hormones play an important role in cardiovascular autonomic control and oxidative stress profile in target organs, which is reflected in AP changes.
研究提出了关于卵巢激素波动和剥夺与心血管自主调节、氧化应激及其对静息动脉压(AP)和心血管风险的潜在影响之间的关联的相互矛盾的发现。本研究旨在评估雄性大鼠(M)和雌性大鼠在发情周期的排卵(FOV)和非排卵(FNOV)阶段以及卵巢激素剥夺(FO)后的心血管自主调节、压力感受反射敏感性(BRS)和氧化应激。直接记录 AP,并用苯肾上腺素和硝普钠递增剂量评估 BRS。通过频谱分析评估 AP 和心率变异性。评估心脏、肾脏和肌肉组织的氧化应激谱。在女性中,与非排卵阶段相比,排卵阶段和卵巢激素剥夺导致 AP 升高(FOV 和 FO9mmHg)。与其他组相比,卵巢切除术促进了心脏交感神经-迷走神经平衡的增加(17-37%)。FOV 和 FO 组均表现出 BRS 受损,与 AP 变异性增加相关。总的来说,非排卵组的抗氧化能力高于 M 组。卵巢激素剥夺导致心脏和肾脏组织中的过氧化氢酶活性降低,所有分析的组织中的脂质过氧化作用增加。在心脏(r=0.60)、肾脏(r=0.60)和肌肉(r=0.57)组织中,血管交感神经调节与脂质过氧化之间存在正相关(p<0.05)。总之,卵巢激素的波动和剥夺对靶器官的心血管自主控制和氧化应激谱起着重要作用,这反映在 AP 的变化上。