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Abstract
Introduction Stimulation of nitrergic neurons and endothelial cells in the erectile tissue results in release of NO that diffuse to surrounding smooth muscle cells where it activates the soluble guanylate cyclase (sGC), facilitating the conversion of GTP to cGMP. This second messenger diminishes the intracellular levels of calcium thereby causing penile smooth muscle relaxation and penile erection [1]. Epidemiological studies have shown a strong association between erectile dysfunction (ED) and arterial hypertension [2], where the deficiency of the NO-cGMP pathway seems to greatly contribute to such association [3]. Regular physical exercise has been shown to increase the NO production thus ameliorating cardiovascular diseases [2,4]. Recently, we have shown that prior physical conditioning improves the erectile function in normotensive rats [5] and prevents the impaired corpus cavernosum relaxation secondary to chronic NO blockade in rats [2].
Highlights
Stimulation of nitrergic neurons and endothelial cells in the erectile tissue results in release of NO that diffuse to surrounding smooth muscle cells where it activates the soluble guanylate cyclase, facilitating the conversion of GTP to cGMP
Wistar rats were divided into control sedentary (C-SD), control trained (C-TR), L-NAME sedentary (LN-SD) and L-NAME trained (LN-TR) groups
The in vitro and in vivo nitrergic-dependent relaxing responses were significantly reduced in LN-SD group compared with C-SD, as expected
Summary
Stimulation of nitrergic neurons and endothelial cells in the erectile tissue results in release of NO that diffuse to surrounding smooth muscle cells where it activates the soluble guanylate cyclase (sGC), facilitating the conversion of GTP to cGMP. This second messenger diminishes the intracellular levels of calcium thereby causing penile smooth muscle relaxation and penile erection [1]. We have shown that prior physical conditioning improves the erectile function in normotensive rats [5] and prevents the impaired corpus cavernosum relaxation secondary to chronic NO blockade in rats [2].
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