Cytoplasmic microtubules serve as a network by which vesicles and membrane-bounded organelles can travel. In addition, microtubules regulate cell shape and movement. In vascular smooth muscle (VSM), microtubules may play a role in regulating reactivity, as has been demonstrated by the potentiation of agonist-induced contraction in isolated rat pulmonary arteries. In this study, we tested the hypothesis that microtubule disruption enhance endothelium-independent relaxation in VSM. Tail artery rings from normotensive Sprague-Dawley rats (n=3) were placed in isolated organ baths for the measurement of isometric contractions using standard muscle bath techniques. The tail artery rings were contracted with serotonin (0.1 μM 5-HT) in physiological buffer. After maximal contractions were induced with 5-HT, VSM relaxation was mediated with sodium nitroprusside (0.1 μM). Microtubular disassembly with 10 μM nocodazole potentiated nitroprusside-mediated relaxation in isolated rat tail arteries. Before nocodazole treatment, tail arteries relaxed 72±3%. Relaxation to nitroprusside after nocodazole treatment was significantly enhanced to 89±2% (p<0.05). This study demonstrates that disassembly of microtubules enhances endothelium-independent VSM relaxation, implying that microtubules play a role in antagonizing NO-mediated relaxation in the VSM.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology