Orchidectomy attenuates impaired endothelial effects of a high-salt diet in Sprague–Dawley rats

Abstract

The effect of sex hormones on vascular reactivity is considered one of the underlying factors contributing to gender differences in cardiovascular functions and diseases. Experiments were designed to investigate the role of androgens in salt-induced hypertension by assessing the relaxation response of isolated aortic rings to acetylcholine and sodium nitroprusside in the presence or absence of l-nitroarginine methyl ester in Sprague-Dawley rats. The rats were either orchidectomized or sham-operated, with or without testosterone replacement, and were placed on a normal or high-salt diet for 6 weeks. The results indicate a significant increase (p < 0.001) in the mean arterial blood pressure of rats on the high-salt diet, when compared with control or orchidectomized rats. Orchidectomy elicited a reduction in mean arterial blood pressure (p < 0.01), while testosterone replacement normalized mean arterial blood pressure to values seen in intact rats on the high-salt diet. The high-salt diet reduced the relaxation response to acetylcholine both in the presence and absence of inhibition of endothelial nitric oxide synthase with l-nitroarginine methyl ester. Bilateral orchidectomy attenuated the impaired endothelial function induced by the high-salt diet in rats, but this was reversed by concomitant administration of testosterone, suggesting a role for androgens in enhancing long-term vascular smooth muscle tone and hence maintenance of high blood pressure in salt-induced hypertension.

Orchidectomy attenuates high‐salt diet‐induced increases in blood pressure, renovascular resistance, and hind limb vascular dysfunction: role of testosterone

“…These findings are consistent with our previous report which showed that testosterone promoted impaired reactivity of aortic rings from male Sprague-Dawley rats fed a HSD. 10 Attenuation by orchidectomy of the elevated RVR observed in rats fed HSD suggests that testosterone did not only promote BPelevating effect of a HSD, but may also enhance the impairment of renovascular function that could be present in rats fed a HSD. Renovascular dysfunction is associated with enhanced renal vasoconstriction, decreased renal blood flow and in some cases, increased plasma volume.…”

“…16 We have previously demonstrated that testosterone increases vascular reactivity of the aorta from male rats fed a HSD. 10 But effects of testosterone on arterioles are yet to be fully understood considering the importance of arterioles in the overall systemic vascular resistance and regulation of BP under normal and pathological conditions. Salt sensitivity exhibits sexual dimorphism with male rats developing higher BP compared to female rats when fed a HSD.…”

Relaxation response of abdominal aorta to androgens in orchidectomised Sprague–Dawley rats fed a high-salt diet

“…Ltd., Bangalore, India) that already contained 0.3% NaCl, to give 8% NaCl (Adegunloye and Sofola 1997). All of the rats that underwent surgery received an injection of penicillin (300 000 IU/kg body mass) at the time of surgery to prevent infections, and were allowed a 3 day recovery period before the beginning of the experiments (Oloyo et al 2011a). After recovery from anesthesia, all animals were returned to their cages.…”

“…One of the mechanisms by which a high-salt diet induces hypertension includes impairment of vascular functions (Oloyo et al 2011a). For instance, increased dietary salt intake has been demonstrated to impair the relaxation response to vasodilator agents in several vascular beds in laboratory animals (Zhu et al 2007).…”

l-arginine Supplementation Increased Only Endothelium-Dependent Relaxation in Sprague-Dawley Rats Fed a High-Salt Diet by Enhancing Abdominal Aorta Endothelial Nitric Oxide Synthase Gene Expression

“…[2][3][4] Vascular function impairment is known to be part of the key mechanisms by which high-salt diet leads to the increase in blood pressure. [5][6][7] In the endothelial cells, endothelial nitric oxide synthase (eNOS) helps in the production of citrulline and nitric oxide from l-arginine. 8 The eNOS mRNA expression has, however, been reported to be a key modulator of vascular tone, and its uncoupling has been shown to contribute to development of hypertension.…”