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Cardiovascular Research Advance Access [Accepted Manuscript] published online on January 6, 2009
Cardiovascular Research, doi:10.1093/cvr/cvn359
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

TIROFIBAN INCREASES SOLUBLE GUANYLATE CYCLASE IN RAT VASCULAR WALLS: PHARMACOLOGICAL AND PATHOPHYSIOLOGICAL CONSEQUENCES

Maria P. Ruiz-Torres1, Mercedes Griera1, Aránzazu Chamorro1, Maria L. Diez-Marques1, Diego Rodriguez-Puyol2,3,4 and Manuel Rodriguez-Puyol1

1 Physiology and "Príncipe de Asturias" Hospital, Alcalá de Henares, Madrid, Spain
2 Medicine Departments, Universidad de Alcala, "Príncipe de Asturias" Hospital, Alcalá de Henares, Madrid, Spain
3 Research Unit and "Príncipe de Asturias" Hospital, Alcalá de Henares, Madrid, Spain
4 Nephrology Section, "Príncipe de Asturias" Hospital, Alcalá de Henares, Madrid, Spain

Corresponding author: María Piedad Ruiz Torres Physiology Department Alcala University Campus Universitario s/n Alcalá de Henares. 28805-Madrid. Spain. Phone: 34 91 8854519 Fax: 34 91 8854590 E-mail: mpiedad.ruiz{at}uah.es

Aims: Our aim was to evaluate whether tirofiban, which mimics the structure of arginine-glycine-aspartic acid- peptides (RGD), up-regulates soluble guanylate cyclase β1 subunit (sGC-β1) expression in vascular smooth muscle cells (VSMC) and in aorta from rats, and to investigate the pharmacological and pathophysiological consequences of this up-regulation.

Methods: Wistar, Wistar Kyoto and spontaneously hypertensive rats (SHR) were used. sGC-β1 content was assessed by immunoblotting. Arterial pressure was recorded using a tail-cuff sphygmomanometer. Sodium nitroprusside (SNP) and isosorbide dinitrate (IDN) were used as nitric oxide (NO) donors.

Results: Tirofiban increased the sGC-β1 content in VSMC and in aortic walls from rats after six hours of treatment. Rats treated with tirofiban experienced a more pronounced decrease in their arterial pressure after acute SNP treatment than vehicle treated rats. Isolated rat aortic rings incubated with tirofiban showed a higher relaxing response to SNP than control rings as well as an increased sGC-β1 content and SNP-induced cGMP synthesis. Animals receiving IDN for one week showed decreased sGC-β1 in aortic walls, and did not respond to SNP treatment with changes in arterial pressure. Tirofiban restored the decreased sGC-β1 content in IDN-treated rats and promoted a decreased arterial pressure in response to SNP administration. SHR rats showed reduced sGC-β1 levels, and tirofiban increased these levels and led to a higher response to SNP.

Conclusions: Tirofiban increased the sGC-β1 content in contractile cells and aortic walls of rats, enhancing the response to SNP and reversing the NO donor tachyphylaxis.

Time for primary review: 17 Days

Ruiz-Torres, Tirofiban increases sGC in vivo


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