NDLI: The Rho kinase inhibitor azaindole-1 has long-acting vasodilator activity in the pulmonary vascular bed of the intact chest rat.

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The Rho kinase inhibitor azaindole-1 has long-acting vasodilator activity in the pulmonary vascular bed of the intact chest rat.

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The Rho kinase inhibitor azaindole-1 has long-acting vasodilator activity in the pulmonary vascular bed of the intact chest rat.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Pankey, Edward A. Byun, Ryuk J. Smith, William B. Bhartiya, Manish Bueno, Franklin R. Badejo, Adeleke M. Stasch, Johannes-Peter Murthy, Subramanyam N. Nossaman, Bobby D. Kadowitz, Philip J.
Description	Country affiliation: United States Author Affiliation: Pankey EA ( Department of Pharmacology, Tulane University School of Medicine, New Orleans, Louisiana 70112-2699, USA.)
Abstract	Responses to a selective azaindole-based Rho kinase (ROCK) inhibitor (azaindole-1) were investigated in the rat. Intravenous injections of azaindole-1 (10-300 µg/kg), produced small decreases in pulmonary arterial pressure and larger decreases in systemic arterial pressure without changing cardiac output. Responses to azaindole-1 were slow in onset and long in duration. When baseline pulmonary vascular tone was increased with U46619 or L-NAME, the decreases in pulmonary arterial pressure in response to the ROCK inhibitor were increased. The ROCK inhibitor attenuated the increase in pulmonary arterial pressure in response to ventilatory hypoxia. Azaindole-1 decreased pulmonary and systemic arterial pressures in rats with monocrotaline-induced pulmonary hypertension. These results show that azaindole-1 has significant vasodilator activity in the pulmonary and systemic vascular beds and that responses are larger, slower in onset, and longer in duration when compared with the prototypical agent fasudil. Azaindole-1 reversed hypoxic pulmonary vasoconstriction and decreased pulmonary and systemic arterial pressures in a similar manner in rats with monocrotaline-induced pulmonary hypertension. These data suggest that ROCK is involved in regulating baseline tone in the pulmonary and systemic vascular beds, and that ROCK inhibition will promote vasodilation when tone is increased by diverse stimuli including treatment with monocrotaline.
File Format	HTM / HTML
ISSN	00084212
e-ISSN	12057541
Journal	Canadian Journal of Physiology and Pharmacology
Issue Number	7
Volume Number	90
Language	English
Publisher	Canadian Science Publishing
Publisher Date	2012-07-01
Publisher Place	Canada
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Pharmacology Cardiovascular System Drug Effects Protein Kinase Inhibitors Pharmacology Pulmonary Circulation Vasodilator Agents Rho-associated Kinases Antagonists & Inhibitors 15-hydroxy-11 Alpha,9 Alpha-(epoxymethano)prosta-5,13-dienoic Acid Animals Blood Pressure Cardiac Output Hypertension, Pulmonary Chemically Induced Drug Therapy Anoxia Monocrotaline Ng-nitroarginine Methyl Ester Nitric Oxide Synthase Pulmonary Artery Rats, Sprague-dawley Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Pharmacology

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