Activation of Rho-associated kinase during augmented contraction of the basilar artery to serotonin after subarachnoid hemorrhage

Yoshimasa Watanabe; Frank M Faraci; Donald D Heistad

doi:10.1152/ajpheart.00923.2004

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Activation of Rho-associated kinase during augmented contraction of the basilar artery to serotonin after subarachnoid hemorrhage

Journal article

Peer reviewed

Activation of Rho-associated kinase during augmented contraction of the basilar artery to serotonin after subarachnoid hemorrhage

Yoshimasa Watanabe, Frank M Faraci and Donald D Heistad

American journal of physiology. Heart and circulatory physiology, Vol.288(6), pp.H2653-2658

06/2005

DOI: 10.1152/ajpheart.00923.2004

PMID: 15665056

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Abstract

Delayed cerebral vasospasm after subarachnoid hemorrhage (SAH) may be due, in part, to altered regulation of arterial smooth muscle contraction. Contraction of cerebral arteries to serotonin is augmented after experimental SAH. We hypothesized that activation of Rho-associated kinase (Rho kinase) contributes to augmented contraction of cerebral arteries to serotonin after SAH. Autologous arterial blood (SAH) or artificial cerebrospinal fluid (control) was injected into the cisterna magna of anesthetized rabbits. At 2 days after injection, the basilar artery was excised and isometric contraction of arterial rings was recorded. Maximum contraction of the basilar artery to serotonin was augmented about fourfold in SAH compared with control rabbits (P < 0.01). Contraction to histamine was similar in the two groups. Fasudil hydrochloride (3 mumol/l), an inhibitor of Rho kinase, markedly attenuated serotonin-induced contraction. Fasudil had little effect on contractions induced by histamine or phorbol 12,13-dibutyrate. In addition, phosphorylation of myosin phosphatase, a major target of Rho kinase in regulation of smooth muscle contraction, in the basilar artery was examined by Western blotting. In basilar arteries of SAH, but not control, rabbits, serotonin increased phosphorylation of myosin phosphatase about twofold at Thr(853) of the myosin-targeting subunit. These results suggest that enhanced activation of Rho kinase contributes to augmented contraction of the basilar artery to serotonin after SAH.

Motor Activity - physiology

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives

Motor Activity - drug effects

Male

Serotonin - pharmacology

Muscle, Smooth, Vascular - physiopathology

Basilar Artery - physiopathology

rho-Associated Kinases

Subarachnoid Hemorrhage - enzymology

Basilar Artery - physiology

Muscle, Smooth, Vascular - physiology

Protein-Serine-Threonine Kinases - metabolism

Disease Models, Animal

Muscle, Smooth, Vascular - drug effects

Basilar Artery - enzymology

Rabbits

Basilar Artery - drug effects

Histamine - pharmacology

Intracellular Signaling Peptides and Proteins

Animals

Muscle Contraction - drug effects

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology

Muscle Contraction - physiology

Enzyme Activation

Muscle, Smooth, Vascular - enzymology

Details

Title: Subtitle: Activation of Rho-associated kinase during augmented contraction of the basilar artery to serotonin after subarachnoid hemorrhage
Creators: Yoshimasa Watanabe - Dept. of Internal Medicine, Univ. of Iowa College of Medicine, 200 Hawkins Dr., Iowa City, IA 52242, USA
Frank M Faraci
Donald D Heistad
Resource Type: Journal article
Publication Details: American journal of physiology. Heart and circulatory physiology, Vol.288(6), pp.H2653-2658
Publisher: United States
DOI: 10.1152/ajpheart.00923.2004
PMID: 15665056
ISSN: 0363-6135
eISSN: 1522-1539
Grant note: HL-16066 / NHLBI NIH HHS HL-62984 / NHLBI NIH HHS NS-24621 / NINDS NIH HHS
Language: English
Date published: 06/2005
Academic Unit: Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
Record Identifier: 9984040220102771

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