Microtubule depolymerization facilitates contraction of rat aorta via activation of Rho-kinase

Kanchan Chitaley, R. Clinton Webb

Research output: Contribution to journalArticle

15 Scopus citations

Abstract

This study tests the hypothesis that microtubule (MT) depolymerization facilitates contraction of rat aorta via activation of Rho-kinase. Aortic rings from Sprague-Dawley rats were placed in a muscle bath for the measurement of isometric force generation. Bath temperature was decreased from 37 to 10-20°C (30 min), inducing MT depolymerization. Some vessels were treated with nocodazole (10-5 M) or colchicine (10-8-10-5 M) to stabilize the MTs in the depolymerized state, and the remaining vessels were treated with dimethyl sulfoxide (DMSO: vehicle). Warming of vessels to 37°C induced a significantly greater contraction in nocodazole- and colchicine-treated vessels as compared with controls, and this increase was blocked by pretreatment with taxol (10-5 M; a MT stabilizing agent) [force (mg): NOC 1159±93; COL 1138±69; DMSO 578±14; TAX+NOC 526±43; TAX+COL 538±90]. Following the sustained contraction in response to rewarming, Rho-kinase inhibition with Y-27632 (10-5 M) relaxed nocodazole- and colchicine-treated rings to a significantly greater extent as compared to DMSO-treated vessels (percent relaxation: NOC 64±2; COL 65±5; DMSO 33±5). These results support the hypothesis that MT depolymerization facilitates contraction of rat aorta via activation of Rho-kinase.

Original languageEnglish (US)
Pages (from-to)157-161
Number of pages5
JournalVascular Pharmacology
Volume38
Issue number3
DOIs
StatePublished - Mar 1 2002

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Keywords

  • Microtubule depolymerization
  • Rho-kinase
  • Vasoconstriction

ASJC Scopus subject areas

  • Physiology
  • Molecular Medicine
  • Pharmacology

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