Involvement of constitutive nitric oxide synthase in the portal-systemic collaterals of portal hypertensive rats

Ching Chih Chang; Hui Chun Huang; Sun Sang Wang; Fa Yauh Lee; Full Young Chang; Han Chieh Lin; Ming Chieh Hou; Shou Dong Lee

doi:10.1016/S1726-4901(09)70144-3

Involvement of constitutive nitric oxide synthase in the portal-systemic collaterals of portal hypertensive rats

Ching Chih Chang, Hui Chun Huang, Sun Sang Wang, Fa Yauh Lee^*, Full Young Chang, Han Chieh Lin, Ming Chieh Hou, Shou Dong Lee

^*Corresponding author for this work

Department of Internal Medicine

Research output: Contribution to journal › Article › peer-review

3 Scopus citations

Abstract

Background: Recent studies have shown that endothelial nitric oxide (NO) is involved in modulating the vascular response to vasoconstrictors in portal-systemic collaterals of portal hypertensive rats. This study investigated which isoform of NO synthase is involved in the collateral circulation of portal hypertensive rats. Methods: The relaxation response to acetylcholine (10^-8 M, 10^-7 M and 10^-6 M) in norepinephrine (NE)-preconstricted portal-systemic collaterals was investigated after incubation with vehicle (Krebs solution), a preferential inducible NO synthase inhibitor (aminoguanidine [AG]), or a non-selective NO synthase inhibitor (N^ω-nitro-L-arginine [NNA]), in rats with partial portal vein ligation. Mean arterial pressure was measured before the perfusion experiments. Results: Bodyweight and mean arterial pressure before the perfusion studies were similar in the vehicle, AG and NNA groups. Preincubation with NNA, but not AG, produced a significant increase in baseline perfusion pressure compared with the vehicle group (p < 0.05). The increase in perfusion pressure in response to NE was enhanced in the presence of NNA (p < 0.05), but not AG. In addition, preincubation with NNA, but not AG, significantly suppressed acetylcholine-induced relaxation in the portal-systemic collaterals (p < 0.05). Conclusion: These results suggest that constitutive, rather than inducible, NO synthase is involved in the vascular response to vasoconstrictors in the portal-systemic collaterals of portal hypertensive rats.

Original language	English
Pages (from-to)	245-249
Number of pages	5
Journal	Journal of the Chinese Medical Association
Volume	68
Issue number	6
DOIs	https://doi.org/10.1016/S1726-4901(09)70144-3
State	Published - Jun 2005

Keywords

Aminoguanidine
Nitric oxide
Nω-nitro-L-arginine
Portal hypertension
Portal-systemic collaterals

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10.1016/S1726-4901(09)70144-3

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@article{8b9004e9071d41b09a9c442d81a5a8e6,

title = "Involvement of constitutive nitric oxide synthase in the portal-systemic collaterals of portal hypertensive rats",

abstract = "Background: Recent studies have shown that endothelial nitric oxide (NO) is involved in modulating the vascular response to vasoconstrictors in portal-systemic collaterals of portal hypertensive rats. This study investigated which isoform of NO synthase is involved in the collateral circulation of portal hypertensive rats. Methods: The relaxation response to acetylcholine (10-8 M, 10-7 M and 10-6 M) in norepinephrine (NE)-preconstricted portal-systemic collaterals was investigated after incubation with vehicle (Krebs solution), a preferential inducible NO synthase inhibitor (aminoguanidine [AG]), or a non-selective NO synthase inhibitor (Nω-nitro-L-arginine [NNA]), in rats with partial portal vein ligation. Mean arterial pressure was measured before the perfusion experiments. Results: Bodyweight and mean arterial pressure before the perfusion studies were similar in the vehicle, AG and NNA groups. Preincubation with NNA, but not AG, produced a significant increase in baseline perfusion pressure compared with the vehicle group (p < 0.05). The increase in perfusion pressure in response to NE was enhanced in the presence of NNA (p < 0.05), but not AG. In addition, preincubation with NNA, but not AG, significantly suppressed acetylcholine-induced relaxation in the portal-systemic collaterals (p < 0.05). Conclusion: These results suggest that constitutive, rather than inducible, NO synthase is involved in the vascular response to vasoconstrictors in the portal-systemic collaterals of portal hypertensive rats.",

keywords = "Aminoguanidine, Nitric oxide, Nω-nitro-L-arginine, Portal hypertension, Portal-systemic collaterals",

author = "Chang, {Ching Chih} and Huang, {Hui Chun} and Wang, {Sun Sang} and Lee, {Fa Yauh} and Chang, {Full Young} and Lin, {Han Chieh} and Hou, {Ming Chieh} and Lee, {Shou Dong}",

note = "Funding Information: The authors gratefully acknowledge Chun-Ching Tai, Shwu-Ling Wu, and I-Nien Lai for their excellent technical assistance. This work was supported by grants from the National Science Council (NSC93-2314-B-075-060) and Taipei Veterans General Hospital (VGH93-212), Taiwan, R.O.C.",

year = "2005",

month = jun,

doi = "10.1016/S1726-4901(09)70144-3",

language = "English",

volume = "68",

pages = "245--249",

journal = "Journal of the Chinese Medical Association",

issn = "1726-4901",

publisher = "Elsevier Taiwan LLC",

number = "6",

}

TY - JOUR

T1 - Involvement of constitutive nitric oxide synthase in the portal-systemic collaterals of portal hypertensive rats

AU - Chang, Ching Chih

AU - Huang, Hui Chun

AU - Wang, Sun Sang

AU - Lee, Fa Yauh

AU - Chang, Full Young

AU - Lin, Han Chieh

AU - Hou, Ming Chieh

AU - Lee, Shou Dong

N1 - Funding Information: The authors gratefully acknowledge Chun-Ching Tai, Shwu-Ling Wu, and I-Nien Lai for their excellent technical assistance. This work was supported by grants from the National Science Council (NSC93-2314-B-075-060) and Taipei Veterans General Hospital (VGH93-212), Taiwan, R.O.C.

PY - 2005/6

Y1 - 2005/6

N2 - Background: Recent studies have shown that endothelial nitric oxide (NO) is involved in modulating the vascular response to vasoconstrictors in portal-systemic collaterals of portal hypertensive rats. This study investigated which isoform of NO synthase is involved in the collateral circulation of portal hypertensive rats. Methods: The relaxation response to acetylcholine (10-8 M, 10-7 M and 10-6 M) in norepinephrine (NE)-preconstricted portal-systemic collaterals was investigated after incubation with vehicle (Krebs solution), a preferential inducible NO synthase inhibitor (aminoguanidine [AG]), or a non-selective NO synthase inhibitor (Nω-nitro-L-arginine [NNA]), in rats with partial portal vein ligation. Mean arterial pressure was measured before the perfusion experiments. Results: Bodyweight and mean arterial pressure before the perfusion studies were similar in the vehicle, AG and NNA groups. Preincubation with NNA, but not AG, produced a significant increase in baseline perfusion pressure compared with the vehicle group (p < 0.05). The increase in perfusion pressure in response to NE was enhanced in the presence of NNA (p < 0.05), but not AG. In addition, preincubation with NNA, but not AG, significantly suppressed acetylcholine-induced relaxation in the portal-systemic collaterals (p < 0.05). Conclusion: These results suggest that constitutive, rather than inducible, NO synthase is involved in the vascular response to vasoconstrictors in the portal-systemic collaterals of portal hypertensive rats.

AB - Background: Recent studies have shown that endothelial nitric oxide (NO) is involved in modulating the vascular response to vasoconstrictors in portal-systemic collaterals of portal hypertensive rats. This study investigated which isoform of NO synthase is involved in the collateral circulation of portal hypertensive rats. Methods: The relaxation response to acetylcholine (10-8 M, 10-7 M and 10-6 M) in norepinephrine (NE)-preconstricted portal-systemic collaterals was investigated after incubation with vehicle (Krebs solution), a preferential inducible NO synthase inhibitor (aminoguanidine [AG]), or a non-selective NO synthase inhibitor (Nω-nitro-L-arginine [NNA]), in rats with partial portal vein ligation. Mean arterial pressure was measured before the perfusion experiments. Results: Bodyweight and mean arterial pressure before the perfusion studies were similar in the vehicle, AG and NNA groups. Preincubation with NNA, but not AG, produced a significant increase in baseline perfusion pressure compared with the vehicle group (p < 0.05). The increase in perfusion pressure in response to NE was enhanced in the presence of NNA (p < 0.05), but not AG. In addition, preincubation with NNA, but not AG, significantly suppressed acetylcholine-induced relaxation in the portal-systemic collaterals (p < 0.05). Conclusion: These results suggest that constitutive, rather than inducible, NO synthase is involved in the vascular response to vasoconstrictors in the portal-systemic collaterals of portal hypertensive rats.

KW - Aminoguanidine

KW - Nitric oxide

KW - Nω-nitro-L-arginine

KW - Portal hypertension

KW - Portal-systemic collaterals

UR - http://www.scopus.com/inward/record.url?scp=20744446624&partnerID=8YFLogxK

U2 - 10.1016/S1726-4901(09)70144-3

DO - 10.1016/S1726-4901(09)70144-3

M3 - Article

C2 - 15984816

AN - SCOPUS:20744446624

SN - 1726-4901

VL - 68

SP - 245

EP - 249

JO - Journal of the Chinese Medical Association

JF - Journal of the Chinese Medical Association

IS - 6

ER -

Involvement of constitutive nitric oxide synthase in the portal-systemic collaterals of portal hypertensive rats

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