Orchidectomy attenuates high-salt diet-induced increases in blood pressure, renovascular resistance, and hind limb vascular dysfunction: role of testosterone.
Orchidectomy attenuates high-salt diet-induced increases in blood pressure, renovascular resistance, and hind limb vascular dysfunction: role of testosterone.
复制标题
睾丸切除术可减轻高盐饮食引起的血压升高、肾血管阻力和后肢血管功能障碍：睾酮的作用。
DOI：
10.1111/1440-1681.12595
复制
发表时间：
2016
影响因子：
2.9
通讯作者：
Yakubu,MomohA
中科院分区：
文献类型：
--
作者：
Oloyo,AhmedK;Sofola,OlusogaA;Yakubu,MomohA
Sex hormone‐dependent vascular reactivity is an underlying factor contributing to sex differences in salt‐dependent hypertension. This study evaluated the role of androgens (testosterone) in high salt‐induced increase in blood pressure (BP) and altered vascular reactivity in renal blood flow and perfused hind limb preparation. Weanling male rats (8 weeks old, 180–200 g) were bilaterally orchidectomised or sham operated with or without testosterone replacement (Sustanon 250, 10 mg/kg intramuscularly once in 3 weeks) and placed on a normal (0.3%) or high (4.0%) NaCl diet for 6 weeks. The high‐salt diet (HSD) increased arterial BP, renal vascular resistance (RVR) and positive fluid balance (FB). These changes were accompanied by decreased plasma nitric oxide levels. The increased BP, RVR and FB observed in the rats fed a HSD were reversed by orchidectomy while testosterone replacement prevented the reversal. Phenylephrine (PE)‐induced increased vascular resistance in the perfused hind limb vascular bed was enhanced by HSD, the enhanced vascular resistance was prevented by orchidectomy and testosterone replacement reversed orchidectomy effect. Vasorelaxation responses to acetylcholine (ACh) and sodium nitroprusside (SNP) were impaired in HSD groups, orchidectomy attenuated the impairment, while testosterone replacement prevented the orchidectomy attenuation. These data suggested that eNOS‐dependent and independently‐mediated pathways were equally affected by HSD in vascular function impairment and this effect is testosterone‐dependent in male Sprague‐Dawley rats.
