Role of ERK and Rho kinase pathways in central pressor action of urotensin II

Yingzi Lin, Kiyoshi Matsumura, Takuya Tsuchihashi, Masayo Fukuhara, Koji Fujii, Mitsuo Iida

Research output: Contribution to journalArticle

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Abstract

Background: It has been shown that central urotensin II acts on the central nervous system to increase arterial pressure in conscious rats. Objective: To investigate the intracellular signal transduction mechanisms of the central cardiovascular action of urotensin II. Methods: The effects of intracerebroventricular (i.c.v.) administration of the extracellular signal-regulated protein kinase (ERK) inhibitor, PD 98059 (20 nmol), the phosphatidylinositol 3 (PI3) kinase inhibitor, wortmannin (20 nmol), or the Rho kinase inhibitor, Y-27632 (20 nmol), on cardiovascular responses to i.c.v. urotensin II (10 nmol) were determined in conscious rats. Results: I.c.v. injection of urotensin II increased both arterial pressure and heart rate (14.9 ± 1.5 mmHg and 94.6 ± 12.8 beats/min, respectively; P < 0.05 for each). Pretreatment with PD 98059 or Y-27632 significantly (P < 0.01 and P < 0.05, respectively) attenuated the pressor response induced by i.c.v. urotensin II (6.6 ± 1.4 and 6.9 ± 1.2 mmHg, respectively). Pretreatment with a mixed solution of PD 98059 and Y-27632 failed to cause further suppression of the urotensin II-induced pressor responses (4.5 ± 0.9 mmHg). In contrast, pretreatment with i.c.v. wortmannin failed to influence the pressor response induced by i.c.v. urotensin II (12.6 ± 1.3 mmHg). The tachycardiac response induced by i.c.v. urotensin II was not influenced by pretreatment with PD 98059, Y-27632 or wortmannin. Conclusions: These findings suggest that the ERK and Rho kinase pathways, but not the PI3 pathway, may be involved in the central pressor action of urotensin II in conscious rats.

Original languageEnglish
Pages (from-to)983-988
Number of pages6
JournalJournal of hypertension
Volume22
Issue number5
DOIs
Publication statusPublished - May 1 2004

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rho-Associated Kinases
Arterial Pressure
Phosphatidylinositol 3-Kinase
urotensin II
Extracellular Signal-Regulated MAP Kinases
Protein Kinase Inhibitors
Phosphatidylinositols
Signal Transduction
Central Nervous System
Heart Rate
Injections
2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one
Y 27632

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Lin, Y., Matsumura, K., Tsuchihashi, T., Fukuhara, M., Fujii, K., & Iida, M. (2004). Role of ERK and Rho kinase pathways in central pressor action of urotensin II. Journal of hypertension, 22(5), 983-988. https://doi.org/10.1097/00004872-200405000-00021

Role of ERK and Rho kinase pathways in central pressor action of urotensin II. / Lin, Yingzi; Matsumura, Kiyoshi; Tsuchihashi, Takuya; Fukuhara, Masayo; Fujii, Koji; Iida, Mitsuo.

In: Journal of hypertension, Vol. 22, No. 5, 01.05.2004, p. 983-988.

Research output: Contribution to journalArticle

Lin, Y, Matsumura, K, Tsuchihashi, T, Fukuhara, M, Fujii, K & Iida, M 2004, 'Role of ERK and Rho kinase pathways in central pressor action of urotensin II', Journal of hypertension, vol. 22, no. 5, pp. 983-988. https://doi.org/10.1097/00004872-200405000-00021
Lin, Yingzi ; Matsumura, Kiyoshi ; Tsuchihashi, Takuya ; Fukuhara, Masayo ; Fujii, Koji ; Iida, Mitsuo. / Role of ERK and Rho kinase pathways in central pressor action of urotensin II. In: Journal of hypertension. 2004 ; Vol. 22, No. 5. pp. 983-988.
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AU - Iida, Mitsuo

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AB - Background: It has been shown that central urotensin II acts on the central nervous system to increase arterial pressure in conscious rats. Objective: To investigate the intracellular signal transduction mechanisms of the central cardiovascular action of urotensin II. Methods: The effects of intracerebroventricular (i.c.v.) administration of the extracellular signal-regulated protein kinase (ERK) inhibitor, PD 98059 (20 nmol), the phosphatidylinositol 3 (PI3) kinase inhibitor, wortmannin (20 nmol), or the Rho kinase inhibitor, Y-27632 (20 nmol), on cardiovascular responses to i.c.v. urotensin II (10 nmol) were determined in conscious rats. Results: I.c.v. injection of urotensin II increased both arterial pressure and heart rate (14.9 ± 1.5 mmHg and 94.6 ± 12.8 beats/min, respectively; P < 0.05 for each). Pretreatment with PD 98059 or Y-27632 significantly (P < 0.01 and P < 0.05, respectively) attenuated the pressor response induced by i.c.v. urotensin II (6.6 ± 1.4 and 6.9 ± 1.2 mmHg, respectively). Pretreatment with a mixed solution of PD 98059 and Y-27632 failed to cause further suppression of the urotensin II-induced pressor responses (4.5 ± 0.9 mmHg). In contrast, pretreatment with i.c.v. wortmannin failed to influence the pressor response induced by i.c.v. urotensin II (12.6 ± 1.3 mmHg). The tachycardiac response induced by i.c.v. urotensin II was not influenced by pretreatment with PD 98059, Y-27632 or wortmannin. Conclusions: These findings suggest that the ERK and Rho kinase pathways, but not the PI3 pathway, may be involved in the central pressor action of urotensin II in conscious rats.

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