Relaxin increased blood pressure and sympathetic activity in paraventricular nucleus of hypertensive rats via enhancing oxidative stress.

摘要: Abstract Relaxin, an ovarian polypeptide hormone, is found in the hypothalamic paraventricular nucleus (PVN) which important central integrative site for control of blood pressure and sympathetic outflow. The aim this study was to determine if superoxide anions modulate effects relaxin PVN. Experiments were performed normotensive Wistar-Kyoto (WKY) rats spontaneously hypertensive (SHRs). Relaxin mRNA protein, its receptor, family peptide receptor 1 (RXFP1) levels PVN 3.24, 3.17, 3.64 times higher SHRs than WKY rats, respectively. Microinjection relaxin-2 into dose-dependently increased mean arterial (MAP), renal nerve activity (RSNA) heart rate (HR) both SHRs, although on MAP (16.87 ± 1.99 vs. 8.97 ± 1.48 mm Hg 100 nmol), RSNA (22.60 ± 2.15 11.77 ± 1.43 % 100 nmol) HR (22.85 ± 3.13 12.62 ± 2.83 beats/min greater SHRs. Oxidative stress level enhanced after microinjection Pretreatment with anion scavengers or NADPH oxidase inhibitor blocked, dismutase potentiated MAP, HR. RXFP1 knockdown significantly attenuated inhibited increases atrial natriuretic peptide, brain collagen I, III fibronectin These results demonstrated that expressed PVN, contributes hypertension overdrive via oxidative stress. Down-regulation could attenuate cardiac remodeling.