High Salt Diet Blunted Baroreflex Sensitivity (BRS) to Bilateral Common Carotid Artery Occlusion (BCCO) in Male Sprague –Dawley Rats – Permissive Effect of Testosterone
التفاصيل البيبلوغرافية
العنوان:
High Salt Diet Blunted Baroreflex Sensitivity (BRS) to Bilateral Common Carotid Artery Occlusion (BCCO) in Male Sprague –Dawley Rats – Permissive Effect of Testosterone
Autonomic dysfunction is involved in the onset of salt-sensitive hypertension as baroreflex sensitivity (BRS) is blunted in salt-sensitive hypertension. However, salt sensitivity exhibits sex disparity because in salt-sensitive hypertension, blood pressure (BP) is usually higher in males when compared with females. The mechanism(s) underlying this sexual dimorphism is not clear. We, therefore, designed this study to determine BRS in weanling male Sprague – Dawley rats that were either bilaterally orchidectomized or sham-operated (under ketamine and xylazine anaesthesia (90 mg and 10 mg/kg/body weight i.m) respectively, with or without testosterone replacement (10 mg/kg sustanon 250® i.m once in 3 weeks) and were placed on normal (0.3%) or high (8%) NaCl diet for 6 weeks. Blood pressure (BP) and heart rate (HR) were measured via arterial cannulation under urethane and α-chloralose anesthesia (5 ml/kg body weight i.p). BRS was determined as change in HR per unit change in BP in response to 30 seconds bilateral common carotid artery occlusion (BCCO). Serum concentration of testosterone was measured using enzyme-linked immunosorbent assay (ELISA). High salt diet (HSD) increased both the basal BP and peak BP after BCCO when compared with control. Orchidectomy attenuated but testosterone replacement restored the elevated BP in rats fed HSD. HSD blunted BRS to BCCO. However, this effect of HSD was lost in the absence of testosterone as there was no significant difference in BRS between rat fed a normal or high salt diet. Our results suggest that blunting of the BRS may be one of the mechanisms by which testosterone promotes salt-induced hypertension and serves as one of the bases for sex disparity in salt-sensitive hypertension.
