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心房利钠肽参与游泳训练引起的而不是跑步训练引起的高血压大鼠动脉血压降低。

Involvement of the atrial natriuretic peptide in the reduction of arterial pressure induced by swimming but not by running training in hypertensive rats.

机构信息

Department of Physiological Sciences, Health Sciences Center, Federal University of Espírito Santo, Espírito Santo, Vitória-ES, Brazil.

出版信息

Peptides. 2011 Aug;32(8):1706-12. doi: 10.1016/j.peptides.2011.06.027. Epub 2011 Jul 5.

Abstract

The aim of this study was to compare, under resting conditions, the influence of chronic training in swimming or running on mean arterial pressure (MAP) and the involvement of the natriuretic peptide system in this response. Two-month-old male spontaneously hypertensive rats (SHR) were divided into three groups-sedentary (SD), swimming (SW) and running (RN)-and were trained for eight weeks under regimens of similar intensities. Atria tissue and plasma atrial natriuretic peptide (ANP) concentrations were measured by radioimmunoassay. ANP mRNA levels in the right and left atria as well as the natriuretic peptide receptors (NPR), NPR-A and NPR-C, mRNA levels in the kidney were determined by real-time PCR. Autoradiography was used to quantify NPR-A and NPR-C in mesenteric adipose tissue. Both training modalities, swimming and running, reduced the mean arterial pressure (MAP) of SHR. Swimming, but not running, training increased plasma levels of ANP compared to the sedentary group (P<0.05). Expression of ANP mRNA in the left atrium was reduced in the RN compared to the SD group (P<0.05). Expression of NPR-A and NPR-C in the kidneys of the SW group decreased significantly (P<0.05) compared to the SD group. Although swimming increased (125)I-ANP binding to mesenteric adipose tissue, displacement by c-ANF was reduced, indicating a reduction of NPR-C. These results suggest that the MAP reduction induced by exercise in SHR differs in its mechanisms between the training modalities, as evidenced by the finding that increased levels of ANP were only observed after the swimming regimen.

摘要

本研究旨在比较慢性游泳或跑步训练对静息状态下平均动脉压(MAP)的影响,并探讨利钠肽系统在此反应中的作用。将 2 月龄雄性自发性高血压大鼠(SHR)分为 3 组:安静组(SD)、游泳组(SW)和跑步组(RN),并进行 8 周的类似强度训练。采用放射免疫法测定心房组织和血浆心钠肽(ANP)浓度。实时 PCR 测定右心房和左心房的 ANP mRNA 水平以及肾脏中的利钠肽受体(NPR)、NPR-A 和 NPR-C mRNA 水平。采用放射自显影技术定量肠系膜脂肪组织中的 NPR-A 和 NPR-C。游泳和跑步两种训练方式均可降低 SHR 的平均动脉压(MAP)。与安静组相比,游泳训练组(P<0.05)血浆 ANP 水平升高,但跑步训练组无此变化。与 SD 组相比,RN 组左心房 ANP mRNA 表达减少(P<0.05)。与 SD 组相比,SW 组肾脏中 NPR-A 和 NPR-C 的表达显著降低(P<0.05)。尽管游泳训练增加了 125I-ANP 与肠系膜脂肪组织的结合,但 c-ANF 的置换减少,表明 NPR-C 减少。这些结果表明,运动引起的 SHR 平均动脉压降低的机制在两种训练方式之间存在差异,因为仅在游泳方案后才观察到 ANP 水平升高。

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