Khoyi M A, Smith M A, Buxton I L, Westfall D P
Department of Pharmacology, University of Nevada, School of Medicine, Reno 89557.
Cell Signal. 1989;1(6):599-605. doi: 10.1016/0898-6568(89)90068-5.
A large number of studies indicate that K(+)-induced contractions of smooth muscle depend on extracellular calcium. If these contractions depend exclusively on extracellular calcium then contractile responses to 140 mM K+, which are larger than the response to 35 mM K+, should be associated with a larger influx of 45Ca. This is not the case in the vas deferens from reserpine pretreated rats. During a 2 min interval, 45Ca influx induced by 140 mM K+ was identical to that produced by 35 mM K+. This suggests that a second mechanism may be involved in responses to high K+. Indeed, 140 mM K+ caused an approximately 300% increase above control in the formation of inositol trisphosphate (IP3) in tissues prelabelled with 3H-myoinositol whereas 35 mM K+ did not increase IP3. IP3 is thought to cause the release of calcium from internal stores which is consistent with our finding of an increase in 45Ca efflux into calcium-free medium from tissues prelabelled with 45Ca and stimulated with 140 mM K+. Stimulation with 35 mM K+ did not influence 45Ca efflux. We conclude that in the rat vas deferens high K+ promotes tension development by smooth muscle by a dual mechanism: influx of extracellular calcium and release of calcium from internal stores via an IP3 mechanism.