Increased expression of Ndufa10, a subunit of mitochondrial complex 1 in the paraventricular nucleus of the SHR

Abstract

PVN integrates signals from circulating angiotensin II (AngII), transmits them to the RVLM and increases sympathetic nerve activity and blood pressure (BP). Although oxidative stress (OS) in the PVN has been implicated in this process, little is known regarding as mechanism. Our proteomic studies have established that Ndufa10, a subcomplex of mitochondrial NADH dehydrogenas involved in ROS and OS is increased in the PVN of the SHR. This observation, coupled with central role of mitochondria in OS, led us to propose that Ndufa10 is the key protein whose expression is critical in the establishment of neurogenic hypertension. Thus, we compared levels of Ndufa10 in the PVN of WKY rats and SHR, and determined if its expression is linked to the genetic aspects of hypertension. PVN from the SHR showed a ~1.8‐fold increase in the mRNA and protein levels of Ndufa10 compared to WKY rat PVN. Neuronal cells in primary culture from prehypertensive SHR brain were used next to determine if this increase was genetically linked or was a result of chronic exposure of the rat to high BP. Both mRNA and protein levels of Ndufa10 were 1.3‐to 2‐fold higher in neuronal culture of the SHR compared to the WKY rat. Together, these observations suggest that an increase in the expression of Ndufa10 is linked to the genetic aspects of hypertension and may be responsible for increased OS in the PVN of the SHR.