Receptor activation induces short-term modulation of arterial contractions: memory in vascular smooth muscle.

This study examined the hypothesis that arteries retain a memory of receptor activation, resulting in temporary modulation of stimulus-contraction coupling. When pretreated for 30 min with 10(-5) M phenylephrine (PE), histamine, or prostaglandin F2 alpha (PGF2 alpha) and then relaxed fully for 10 min, steady-state increases in stress (S/So) and myosin light-chain phosphorylation (MLC20P/MLC20) produced by KCl in femoral arteries were weaker (0.33-0.57 S/So and 0.29-0.30 MLC20P/MLC20) than control responses (approximately 0.91 S/So and approximately 0.41 MLC20P/MLC20). The inhibitory effect lasted for at least 2 h and was not as strong in tissues pretreated for a 10-fold shorter duration or a 10-fold lower concentration of PE. When pretreated with low concentrations of PE (10(-7) M) and PGF2 alpha (10(-6) M), the early portion of subsequent KCl-induced contractile responses reached levels higher than control responses (0.79-0.86 S/So compared with approximately 0.70 S/So). These data support the hypothesis that receptor activation of arteries not only caused contractions but also stimulated another system, a response modulator that appeared to serve as memory of receptor activation.