Abstract
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.
Highlights
Dietary salt consumption in high quantity is the commonest environmental risk factor for hypertension [1] as dietary salt intake correlates positively with blood pressure (BP)
The increase in the heart and kidney weight indices due to HSD was restored by testosterone replacement as the cardiac and renal weight indices of the testosterone replacement plus HSD group were comparable to that of the sham plus HSD group, whereas it was significantly higher (p
There was a reduction in weight gain, a phenomenon that was linked to an increase in body metabolism rate and an increase in energy expenditure, thence a decrease in body weight [31]
Summary
Dietary salt consumption in high quantity is the commonest environmental risk factor for hypertension [1] as dietary salt intake correlates positively with blood pressure (BP). The mechanisms linking salt to hypertension are not well-understood. An abnormal baroreflex control of heart rate has been linked to the pathogenesis of essential hypertension [2], [3] and impaired baroreflex sensitivity (BRS) has been demonstrated in salt-sensitive hypertension [4]-[6]. A sudden increase in BP usually leads to reflex slowing of the heart rate and a reduction in the arterial tone due to enhanced vagal tone and attenuated sympathetic efferent activity [8]. BRS is a measure of the gain of the reflex [8] and factors that reduce BRS include ageing, hypertension, diabetes, and myocardial infarction [9], [10]. HSD is reported to reduce or blunt BRS via mechanism involving
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