Physiological Sciences Post-Graduation Program, Federal University of Espírito Santo, Vitoria, ES, Brazil.
Center for Biological and Health Sciences, Federal University of Western Bahia, Barreiras, BA, Brazil.
Biol Trace Elem Res. 2024 Jun;202(6):2645-2656. doi: 10.1007/s12011-023-03851-5. Epub 2023 Sep 12.
Chronic cadmium exposure is known to be associated with vascular changes and increased blood pressure, but its short-term effects on the cardiovascular system remain poorly understood. This study aimed to investigate the pressoric and vascular effects of a 7-day exposure to CdCl in Wistar rats. The rats were divided in control group (Ct), which received tap water, and the Cd group, which received a 100 mg/L CdCl solution via drinking water for 7 days. We analyzed body weight, plasma Cadmium concentration, systolic blood pressure (SBP), and vascular responses. Despite relatively low plasma Cadmium concentration, the Cd group exhibited elevated SBP and increased contractile response to phenylephrine. Endothelium removal and NOS inhibition increased contractions in both groups. In the Cd group's aorta, we observed enhanced levels of phospho-eNOS (Ser and basal NO release. Cd group showed reduced Catalase expression and increased basal release of HO, with catalase reducing the contractile response. In arteries pre-contracted with phenylephrine, Cd group showed impaired endothelium-dependent (Acetylcholine) and independent (sodium nitroprussiate-SNP) relaxation responses. However, responses to SNP were similar after pre-contraction with KCl in both groups. These data suggest early effects of Cadmium on blood pressure and aortic function, indicating impaired HO-scavenging by catalase. Increased HO due to Cadmium exposure might explain heightened responses to phenylephrine and weakened relaxation responses mediated by the NO-K-channels pathway. Our findings shed light on Cadmium's short-term impact on the cardiovascular system, providing insights into potential mechanisms underlying its effects on blood pressure regulation and vascular function.
慢性镉暴露已知与血管变化和血压升高有关，但它对心血管系统的短期影响仍知之甚少。本研究旨在研究 7 天暴露于 CdCl2 对 Wistar 大鼠的血压和血管效应。大鼠分为对照组（Ct），给予自来水，Cd 组给予含 100mg/L CdCl2 的水溶液通过饮水 7 天。我们分析了体重、血浆镉浓度、收缩压（SBP）和血管反应。尽管血浆镉浓度相对较低，但 Cd 组的 SBP 升高，对苯肾上腺素的收缩反应增强。内皮去除和 NOS 抑制增加了两组的收缩。在 Cd 组的主动脉中，我们观察到磷酸化 eNOS（Ser 和基础 NO 释放增加。Cd 组的 Catalase 表达减少，基础 HO 释放增加，Catalase 减少收缩反应。在预先用苯肾上腺素收缩的动脉中，Cd 组表现出受损的内皮依赖性（乙酰胆碱）和非依赖性（硝普酸钠-SNP）松弛反应。然而，两组在预先用 KCl 收缩后，对 SNP 的反应相似。这些数据表明镉对血压和主动脉功能的早期影响，表明 Catalase 对 HO 清除的损害。由于镉暴露增加的 HO 可能解释了对苯肾上腺素反应增强和由 NO-K 通道途径介导的松弛反应减弱。我们的研究结果揭示了镉对心血管系统的短期影响，为其对血压调节和血管功能的影响的潜在机制提供了深入了解。
