TY - JOUR
T1 - Role of ERK and Rho kinase pathways in central pressor action of urotensin II
AU - Lin, Yingzi
AU - Matsumura, Kiyoshi
AU - Tsuchihashi, Takuya
AU - Fukuhara, Masayo
AU - Fujii, Koji
AU - Iida, Mitsuo
PY - 2004/5
Y1 - 2004/5
N2 - 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.
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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U2 - 10.1097/00004872-200405000-00021
DO - 10.1097/00004872-200405000-00021
M3 - Article
C2 - 15097239
AN - SCOPUS:2542449375
VL - 22
SP - 983
EP - 988
JO - Journal of Hypertension
JF - Journal of Hypertension
SN - 0263-6352
IS - 5
ER -