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Sympathectomy-induced blood pressure reduction in adult normotensive and hypertensive rats is counteracted by enhanced cardiovascular sensitivity to vasoconstrictors
Hypertension Research ( IF 4.3 ) Pub Date : 2019-09-17 , DOI: 10.1038/s41440-019-0319-2
Anna Vavřínová 1, 2 , Michal Behuliak 1 , Michal Bencze 1 , Martin Vodička 1, 2 , Peter Ergang 1 , Ivana Vaněčková 1 , Josef Zicha 1
Affiliation  

The effect of chemical sympathectomy on cardiovascular parameters and the compensatory role of adrenal hormones, the renin–angiotensin system, and cardiovascular sensitivity to vasoconstrictors were studied in spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats. Sympathectomy was induced in 20-week-old rats by daily intraperitoneal guanethidine administration (30 mg/kg b.w.) for 2 weeks. Basal blood pressure (BP), heart rate (HR), and restraint stress-induced cardiovascular changes were measured by radiotelemetry. The BP response to catecholamines was determined in rats with implanted catheters. Sympathectomy decreased BP only transiently, and after 14-day guanethidine treatment, BP returned to basal values in both strains. Sympathectomy permanently lowered HR, improved baroreflex sensitivity, and decreased the low-frequency domain of systolic blood pressure variability (a marker of vascular sympathetic activity). Guanethidine also attenuated the BP and HR responses to restraint stress. On the other hand, the BP response to catecholamines was augmented in sympathectomized rats, and this was not due to the de novo synthesis of vascular adrenergic receptors. Sympathectomy caused adrenal enlargement, enhanced the expression of adrenal catecholamine biosynthetic enzymes, and elevated plasma adrenaline levels in both strains, especially in WKY rats. Guanethidine also increased the plasma levels of aldosterone and corticosterone in WKY rats only. In conclusion, sympathectomy produced a transient decrease in BP, a chronic decrease in HR and improvement in baroreflex sensitivity. The effect of sympathectomy on BP was counteracted by increased vascular sensitivity to catecholamines in WKY rats and SHRs and/or by the enhanced secretion of adrenal hormones, which was more pronounced in WKY rats.

中文翻译:

交感神经切除术引起的成年血压正常和高血压大鼠的血压降低被心血管对血管收缩剂的敏感性增强所抵消

在自发性高血压大鼠 (SHR) 和血压正常的 Wistar-Kyoto (WKY) 大鼠中研究了化学交感神经切除术对心血管参数的影响以及肾上腺激素、肾素-血管紧张素系统和心血管对血管收缩剂的敏感性的代偿作用。通过每日腹腔注射胍乙啶 (30 mg/kg bw) 在 20 周龄大鼠中诱导交感神经切除术,持续 2 周。通过无线电遥测法测量基础血压 (BP)、心率 (HR) 和约束压力引起的心血管变化。在植入导管的大鼠中测定 BP 对儿茶酚胺的反应。交感神经切除术只是暂时降低了血压,经过 14 天胍乙啶治疗后,两种菌株的血压都恢复到了基础值。交感神经切除术永久降低心率,提高压力反射敏感性,并降低收缩压变异性的低频域(血管交感神经活动的标志)。胍乙啶还减弱了 BP 和 HR 对约束压力的反应。另一方面,交感神经切除大鼠的 BP 对儿茶酚胺的反应增强,这不是由于血管肾上腺素能受体的从头合成。交感神经切除术导致肾上腺增大,增强了肾上腺儿茶酚胺生物合成酶的表达,并提高了两种菌株的血浆肾上腺素水平,尤其是在 WKY 大鼠中。Guanethidine 也仅增加 WKY 大鼠的血浆醛固酮和皮质酮水平。总之,交感神经切除术导致血压短暂下降、心率慢性下降和压力反射敏感性改善。
更新日期:2019-09-17
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