Abstract
The vascular effects of bradykinin were studied in rat perfused mesenteric vascular beds with active tone. Bolus injections of bradykinin (1-1000 pmol) but not des-Arg9-bradykinin (bradykinin B1 receptor agonist) induced triphasic vascular responses: the initial sharp vasodilation followed by transient vasoconstriction and subsequent gradual vasodilation. The triphasic vascular responses to bradykinin were abolished by FR 172357 (3-bromo-8-[2,6-dichloro-3-[N-[(E)-4-(N,N-dimethylcarbamoyl) cinnamidoacetyl]-N-methylamino]benzyloxy]-2-metylimidazo[1,2-a]pyridine) (bradykinin B2 receptor antagonist, 0.1 μM). Endothelium removal with sodium deoxycholate and Nw-nitro-L-arginine (300 μM) abolished the bradykinin-induced initial sharp vasodilation. Indomethacin (0.5 μM) and seratrodast (thromboxane A2 receptor antagonist, 0.5 and 5 μM) abolished the bradykinin-induced second vasoconstriction. The bradykinin-induced third vasodilation was abolished by capsaicin (1 μM) and calcitonin gene-related peptide (CGRP)-(8-37) (CGRP receptor antagonist, 0.5 μM). These findings suggest that the bradykinin-induced initial sharp vasodilation is endothelium dependent, that endogenous thromboxane A2 is involved in the second vasoconstriction, and that the third slow vasodilation is produced by activation of capsaicin-sensitive CGRP-containing nerves.
| Original language | English |
|---|---|
| Pages (from-to) | 105-113 |
| Number of pages | 9 |
| Journal | European Journal of Pharmacology |
| Volume | 433 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Dec 14 2001 |
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Keywords
- Bradykinin
- CGRP (calcitonin gene-related peptide)
- Endothelium dependent
- Mesenteric resistance artery, (Rat)
- Thromboxane A
- Vasodilation
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience
- Pharmacology
Cite this
Triphasic vascular responses to bradykinin in the mesenteric resistance artery of the rat. / Nawa, Hideki; Kawasaki, Hiromu; Nakatsuma, Akira; Isobe, Sachiko; Kurosaki, Yuji.
In: European Journal of Pharmacology, Vol. 433, No. 1, 14.12.2001, p. 105-113.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Triphasic vascular responses to bradykinin in the mesenteric resistance artery of the rat
AU - Nawa, Hideki
AU - Kawasaki, Hiromu
AU - Nakatsuma, Akira
AU - Isobe, Sachiko
AU - Kurosaki, Yuji
PY - 2001/12/14
Y1 - 2001/12/14
N2 - The vascular effects of bradykinin were studied in rat perfused mesenteric vascular beds with active tone. Bolus injections of bradykinin (1-1000 pmol) but not des-Arg9-bradykinin (bradykinin B1 receptor agonist) induced triphasic vascular responses: the initial sharp vasodilation followed by transient vasoconstriction and subsequent gradual vasodilation. The triphasic vascular responses to bradykinin were abolished by FR 172357 (3-bromo-8-[2,6-dichloro-3-[N-[(E)-4-(N,N-dimethylcarbamoyl) cinnamidoacetyl]-N-methylamino]benzyloxy]-2-metylimidazo[1,2-a]pyridine) (bradykinin B2 receptor antagonist, 0.1 μM). Endothelium removal with sodium deoxycholate and Nw-nitro-L-arginine (300 μM) abolished the bradykinin-induced initial sharp vasodilation. Indomethacin (0.5 μM) and seratrodast (thromboxane A2 receptor antagonist, 0.5 and 5 μM) abolished the bradykinin-induced second vasoconstriction. The bradykinin-induced third vasodilation was abolished by capsaicin (1 μM) and calcitonin gene-related peptide (CGRP)-(8-37) (CGRP receptor antagonist, 0.5 μM). These findings suggest that the bradykinin-induced initial sharp vasodilation is endothelium dependent, that endogenous thromboxane A2 is involved in the second vasoconstriction, and that the third slow vasodilation is produced by activation of capsaicin-sensitive CGRP-containing nerves.
AB - The vascular effects of bradykinin were studied in rat perfused mesenteric vascular beds with active tone. Bolus injections of bradykinin (1-1000 pmol) but not des-Arg9-bradykinin (bradykinin B1 receptor agonist) induced triphasic vascular responses: the initial sharp vasodilation followed by transient vasoconstriction and subsequent gradual vasodilation. The triphasic vascular responses to bradykinin were abolished by FR 172357 (3-bromo-8-[2,6-dichloro-3-[N-[(E)-4-(N,N-dimethylcarbamoyl) cinnamidoacetyl]-N-methylamino]benzyloxy]-2-metylimidazo[1,2-a]pyridine) (bradykinin B2 receptor antagonist, 0.1 μM). Endothelium removal with sodium deoxycholate and Nw-nitro-L-arginine (300 μM) abolished the bradykinin-induced initial sharp vasodilation. Indomethacin (0.5 μM) and seratrodast (thromboxane A2 receptor antagonist, 0.5 and 5 μM) abolished the bradykinin-induced second vasoconstriction. The bradykinin-induced third vasodilation was abolished by capsaicin (1 μM) and calcitonin gene-related peptide (CGRP)-(8-37) (CGRP receptor antagonist, 0.5 μM). These findings suggest that the bradykinin-induced initial sharp vasodilation is endothelium dependent, that endogenous thromboxane A2 is involved in the second vasoconstriction, and that the third slow vasodilation is produced by activation of capsaicin-sensitive CGRP-containing nerves.
KW - Bradykinin
KW - CGRP (calcitonin gene-related peptide)
KW - Endothelium dependent
KW - Mesenteric resistance artery, (Rat)
KW - Thromboxane A
KW - Vasodilation
UR - http://www.scopus.com/inward/record.url?scp=0035861916&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035861916&partnerID=8YFLogxK
U2 - 10.1016/S0014-2999(01)01513-8
DO - 10.1016/S0014-2999(01)01513-8
M3 - Article
C2 - 11755140
AN - SCOPUS:0035861916
VL - 433
SP - 105
EP - 113
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
SN - 0014-2999
IS - 1
ER -