Bautista-Pérez Rocio, Franco Martha
Department of Molecular Biology, Instituto Nacional de Cardiología Ignacio Chávez, México City 14080, Mexico.
Department of Cardio-Renal Pathophysiology, Instituto Nacional de Cardiología Ignacio Chávez, México City 14080, Mexico.
Pharmaceuticals (Basel). 2024 Aug 13;17(8):1060. doi: 10.3390/ph17081060.
The treatment of hypertension has improved in the last century; attention has been directed to restoring several altered pathophysiological mechanisms. However, regardless of the current treatments, it is difficult to control blood pressure. Uncontrolled hypertension is responsible for several cardiovascular complications, such as chronic renal failure, which is frequently observed in hypertensive patients. Therefore, new approaches that may improve the control of arterial blood pressure should be considered to prevent serious cardiovascular disorders. The contribution of purinergic receptors has been acknowledged in the pathophysiology of hypertension; this review describes the participation of these receptors in the alteration of kidney function in hypertension. Elevated interstitial ATP concentrations are essential for the activation of renal purinergic receptors; this becomes a fundamental pathway that leads to the development and maintenance of hypertension. High ATP levels modify essential mechanisms implicated in the long-term control of blood pressure, such as pressure natriuresis, the autoregulation of the glomerular filtration rate and renal blood flow, and tubuloglomerular feedback responses. Any alteration in these mechanisms decreases sodium excretion. ATP stimulates the release of vasoactive substances, causes renal function to decline, and induces tubulointerstitial damage. At the same time, a deleterious interaction involving angiotensin II and purinergic receptors leads to the deterioration of renal function.
在上个世纪，高血压的治疗已经有所改善；人们已将注意力转向恢复几种改变的病理生理机制。然而，不管目前的治疗方法如何，血压都很难得到控制。未得到控制的高血压会引发多种心血管并发症，比如慢性肾衰竭，这在高血压患者中很常见。因此，应该考虑采用可能改善动脉血压控制的新方法，以预防严重的心血管疾病。嘌呤能受体在高血压病理生理学中的作用已得到认可；本综述描述了这些受体在高血压患者肾功能改变中的参与情况。间质ATP浓度升高对于肾嘌呤能受体的激活至关重要；这成为导致高血压发生和维持的一条基本途径。高ATP水平改变了与血压长期控制相关的重要机制，如压力性利钠、肾小球滤过率和肾血流量的自身调节以及管球反馈反应。这些机制中的任何改变都会减少钠排泄。ATP刺激血管活性物质的释放，导致肾功能下降，并引起肾小管间质损伤。与此同时，涉及血管紧张素II和嘌呤能受体的有害相互作用会导致肾功能恶化。
