HEAT SHOCK‐INDUCED AUGMENTATION OF VASCULAR CONTRACTILITY IS INDEPENDENT OF RHO‐KINASE

Clinical and Experimental Pharmacology and Physiology - Tập 33 Số 3 - Trang 264-268 - 2006
Young Mi Seok1, Jee In Kim2, Masaaki Ito3, Yasuko Kureishi3, Takeshi Nakano3, Si‐Oh Kim4, Dong Gun Lim4, Wee Hyun Park5, Inkyeom Kim2
1Department of Pharmacology, Kyungpook National University School of Medicine, Daegu, Republic of Korea
2Departments of Pharmacology
3First Department of Internal Medicine, Mie University School of Medicine, Tsu, Mie, Japan
4Anesthesiology, and
5Internal Medicine, Kyungpook National University School of Medicine, Daegu, Republic of Korea and

Tóm tắt

SUMMARY In a previous study, we demonstrated that heat shock augments the contractility of vascular smooth muscle through the stress response. In the present study, we investigated whether Rho‐kinases play a role in heat shock‐induced augmentation of vascular contractility in rat isolated aorta. Rat aortic strips were mounted in organ baths, exposed to 42C for 45 min and subjected to contractile or relaxant agents 5 h later. The level of expression of Rho‐kinases in heat shock‐exposed tissues was no different to that of control tissues, whereas heat shock induced heat shock protein (Hsp) 72 at 3 and 5 h. Heat shock resulted in an increase in vascular contractility in response to phenylephrine 5 h later. The Rho‐kinase inhibitors Y27632 (30 nmol/L‐10 mmol/L) or HA 1077 (10 nmol/L‐10 mmol/L) relaxed 1.0 mmol/L phenylephrine‐precontracted vascular strips in a concentration‐dependent manner; these effects were attenuated in heat shock‐exposed strips. Pretreatment with Y27632 resulted in greater inhibition of the maximum contraction in control strips compared with those in heat shock‐exposed strips. The results of the present study suggest that Rho‐kinases are unlikely to be involved in heat shock‐induced augmentation of vascular contractility.

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Clinical and Experimental Pharmacology and Physiology

Tập 33 Số 3

264-268

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