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Length‐Dependent Regulation of ROK Activity During KCl‐Induced Tonic Force in Rabbit Epigastric Artery Involves Microtubule Depolymerization

Vascular smooth muscle contraction can be divided temporally into early (phasic) and late (tonic) phases. ROK regulates tonic force by phosphorylating the regulatory subunit of myosin light chain (MLC20) phosphatase (MLCP), MYPT1. Whether alterations in muscle length can regulate ROK activity has yet to be determined. Epigastric Artery (EA) showed increasing tonic‐to‐peak force ratios with increasing circumferential (length) stretch of the vessel, indicating that the degree of tonic force was selectively muscle length‐dependent. The ROK inhibitor, Y‐27632, completely abolished tonic force at all lengths examined. Femoral artery (FA) showed no significant differences in basal and KCl‐stimulated MLC20 ‐p and MYPT‐p levels when comparing muscles at slack length (Ls) to those preloaded by stretching to 1.2‐fold the optimal length for muscle contraction (Lp). This is in contrast to EA, in which an increase in muscle stretch from Ls to Lp caused increased basal levels of MLC20‐p (Ls: 9.40±1.71; Lp: 16.70±3.42 p<0.05) and MYPT‐p at Thr 850 (Lp: 1.4‐fold Ls p<0.05). Increased stretch of the vessel also elevated the KCl‐stimulated MLC20‐p at 5′ (Ls: 27.78±2.23; Lp: 34.15±1.48). Additionally, the tonic‐to‐peak force ratio increased 2.2‐fold in Lp tissues incubated with colchicine vs. 1.1‐fold in Ls tissues. EA appears to have a unique regulatory mechanism controlled by the degree of stretch applied to the artery which is distinct from FA. These data support the conclusion that increases in muscle length modulate tonic force maintenance in rabbit EA but not the upstream FA via a RhoA/ROK signaling pathway.