Relaxation of the bovine retractor penis muscle by a small K+ excess and the role of K+ in its neurogenic relaxation.

The mechanism of the relaxation of the bovine retractor penis muscle induced by 6.7 mM K+ as well as the role of K+ in the neurogenic relaxation of this muscle induced by nicotine, acetylcholine or electrical field stimulation, was studied. The relaxation induced by 6.7 mM K+ was, contrary to that induced by nicotine or electrical field stimulation, abolished by 10(-7) M ouabain. 15 min exposure to 10(-5) M NG-nitro-L-arginine, 3.2 x 10(-6) M tetrodotoxin, 5.0 x 10(-4) M hexamethonium, 5.3 x 10(-4) M methylene blue or hypoxia, all known to inhibit the neurogenic relaxation, did not affect the relaxation induced by 6.7 mM K+, which was also unaffected by 10(-5) M apamin, 3 x 10(-3) M 4-aminopyridine, 2.6 x 10(-2) M tetraethylammonium and 7.3 x 10(-4) M Ba2+. Exposure to K(+)-free solution reversibly abolished the neurogenic relaxations. The relaxations caused by 5.0 x 10(-7) M cromakalim and 2.0 x 10(-6) M pinacidil were totally blocked by 10(-5) M glibenclamide. Glibenclamide and apamin did not affect the tone of the muscle or its neurogenic relaxations. 4-Aminopyridine 4.0 x 10(-5) to 3.0 x 10(-3) M and tetraethylammonium 10(-4) to 2.6 x 10(-2) M raised the tone and enhanced the relaxations elicited by electrical field stimulation. The results indicate that the relaxation induced by 6.7 mM K+ is partly mediated by activation of Na(+)-K(+) ATPase and that its mechanism is thoroughly different from that of the neurogenic relaxations.(ABSTRACT TRUNCATED AT 250 WORDS)