Department of Experimental Genomics, Institute of Genetics and Animal Biotechnology, Polish Academy of Sciences, Postępu 36A, Jastrzębiec, 05-552 Magdalenka, Poland.
British Heart Foundation Centre for Excellence, Institute of Cardiovascular and Medical Sciences, University of Glasgow, University Place 126, Glasgow G12 8TA, UK.
Int J Mol Sci. 2021 Apr 17;22(8):4179. doi: 10.3390/ijms22084179.
The opioid system is well-known for its role in modulating nociception and addiction development. However, there are premises that the endogenous opioid system may also affect blood pressure. The main goal of the present study was to determine the impact of different endogenous opioid system activity and its pharmacological blockade on blood pressure. Moreover, we examined the vascular function in hyper- and hypoactive states of the opioid system and its pharmacological modification. In our study, we used two mouse lines which are divergently bred for high (HA) and low (LA) swim stress-induced analgesia. The obtained results indicated that individuals with low endogenous opioid system activity have higher basal blood pressure compared to those with a hyperactive opioid system. Additionally, naloxone administration only resulted in the elevation of blood pressure in HA mice. We also showed that the hypoactive opioid system contributes to impaired vascular relaxation independent of endothelium, which corresponded with decreased guanylyl cyclase levels in the aorta. Together, these data suggest that higher basal blood pressure in LA mice is a result of disturbed mechanisms in vascular relaxation in smooth muscle cells. We believe that a novel mechanism which involves endogenous opioid system activity in the regulation of blood pressure will be a promising target for further studies in hypertension development.
阿片系统以其在调节痛觉和成瘾发展中的作用而闻名。然而,有前提表明内源性阿片系统也可能影响血压。本研究的主要目的是确定不同内源性阿片系统活性及其药理学阻断对血压的影响。此外,我们还检查了阿片系统高活性和低活性状态及其药理学修饰对血管功能的影响。在我们的研究中,我们使用了两种经过不同培育的小鼠品系,分别对高(HA)和低(LA)游泳应激诱导的镇痛进行选育。研究结果表明,与高阿片系统活性的个体相比,内源性阿片系统活性较低的个体的基础血压更高。此外,纳洛酮给药仅导致 HA 小鼠的血压升高。我们还表明,低阿片系统活性会导致血管舒张受损,与主动脉中环鸟苷酸水平降低有关,这种血管舒张受损与内皮无关。总之,这些数据表明,LA 小鼠的基础血压较高是由于平滑肌细胞中血管舒张机制紊乱所致。我们认为,涉及内源性阿片系统活性调节血压的新机制将成为高血压发展进一步研究的有前途的靶点。