Nitroxidergic (nitrergic) nerve and erectile dysfunction.

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  • AYAJIKI Kazuhide
    Department of Pharmacology, Shiga University of Medical Science
  • TODA Noboru
    Department of Pharmacology, Shiga University of Medical Science
  • OKAMURA Tomio
    Department of Pharmacology, Shiga University of Medical Science

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  • ＮＯの病態生理　　創薬への展開　　ＮＯ作動性神経と勃起障害
  • NO作動性神経と勃起障害
  • NO サドウセイ シンケイ ト ボッキ ショウガイ

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Description

In vascular tissues including the corpus cavernosum, the organ function is reciprocally regulated by noradrenergic and non-adrenergic, non-cholinergic (NANC) nerves. NANC nerves innervating the corpus cavernosum is thought to be nitroxidergic (nitrergic) nerves which liberate nitric oxide (NO) produced by neuronal NO synthase, and liberated NO activates soluble guanylate cyclase (sGC) in cavernous smooth muscle cells. Intracellular increase in cyclic (c) GMP by activation of sGC dilates cavernous smooth muscle and then induces penile erection. Nitroxidergic (nitrergic) vasodilator nerves also innervate cavernous arteries and veins which regulate the blood volume in the corpus cavernosum. The order of potency of nitroxidergic nerve functions in these tissues (cavernosum>artery>>vein) may be suitable for producing the erection. Therefore, obstruction of the arteries and impairment of nitroxidergic (nitrergic) nerve function are speculated to be one of the causes for erectile dysfunction (ED). On the other hand, NO derived from the cavernous endothelium may partly contribute to erectile function. Sildenafil (Viagra) is one of the potent therapeutics for ED. The agent is a selective phosphodiesterase type 5 (PDE-V) inhibitor that inhibits degradation of cGMP elevated by NO mainly derived from the nerves. To develop more selective and safer therapeutics for ED, further systematic investigations are required.<br>

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