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HEAT SHOCK‐INDUCED AUGMENTATION OF VASCULAR CONTRACTILITY IS INDEPENDENT OF RHO‐KINASE
Author(s) -
Seok YoungMi,
Kim Jee In,
Ito Masaaki,
Kureishi Yasuko,
Nakano Takeshi,
Kim SiOh,
Lim Dong Gun,
Park Wee Hyun,
Kim InKyeom
Publication year - 2006
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2006.04356.x
Subject(s) - contractility , phenylephrine , shock (circulatory) , vascular smooth muscle , contraction (grammar) , heat shock protein , heat shock , aorta , medicine , rho associated protein kinase , endocrinology , kinase , chemistry , biochemistry , blood pressure , smooth muscle , gene
SUMMARY1 In a previous study, we demonstrated that heat shock augments the contractility of vascular smooth muscle through the stress response. 2 In the present study, we investigated whether Rho‐kinases play a role in heat shock‐induced augmentation of vascular contractility in rat isolated aorta. 3 Rat aortic strips were mounted in organ baths, exposed to 42C for 45 min and subjected to contractile or relaxant agents 5 h later. 4 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. 5 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. 6 The results of the present study suggest that Rho‐kinases are unlikely to be involved in heat shock‐induced augmentation of vascular contractility.