Alteration of the soluble guanylate cyclase system in coronary arteries of high cholesterol diet‐fed rabbits
Abstract This study aimed to investigate how atherosclerosis affects the soluble guanylate cyclase (sGC) system in coronary arteries. Rabbits were fed a normal diet for 12 weeks (N group) or a diet containing high cholesterol (1%) for 4 weeks (S‐HC group) and 12 weeks (L‐HC group). Cholesterol depos...
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Wiley
2021-08-01
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Online Access: | https://doi.org/10.1002/prp2.838 |
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author | Masashi Tawa Katsuya Nakano Yuka Yamashita Qiang He Takayoshi Masuoka Tomio Okamura Takaharu Ishibashi |
author_facet | Masashi Tawa Katsuya Nakano Yuka Yamashita Qiang He Takayoshi Masuoka Tomio Okamura Takaharu Ishibashi |
author_sort | Masashi Tawa |
collection | DOAJ |
description | Abstract This study aimed to investigate how atherosclerosis affects the soluble guanylate cyclase (sGC) system in coronary arteries. Rabbits were fed a normal diet for 12 weeks (N group) or a diet containing high cholesterol (1%) for 4 weeks (S‐HC group) and 12 weeks (L‐HC group). Cholesterol deposition in the intima of coronary arteries was observed in the S‐HC group, but the formation of an atherosclerotic plaque was not observed. In contrast, a major plaque developed in the L‐HC group. The relaxant response of isolated coronary arteries to sodium nitroprusside (SNP, nitric oxide donor) was not different between the N and S‐HC groups, whereas the response in the L‐HC group was markedly attenuated. The relaxation induced by BAY 60‐2770 (sGC activator) tended to be augmented in the S‐HC group, but it was significantly impaired in the L‐HC group compared to that in the N group. sGC β1 immunostaining was equally detected in the medial layer of the arteries among the N, S‐HC, and L‐HC groups. In addition, a strong staining was observed in the plaque region of the L‐HC group. cGMP levels in the arteries stimulated with SNP were identical in the N and S‐HC groups and slightly lower in the L‐HC group than the other groups. BAY 60‐2770‐stimulated cGMP formation tended to be increased in the S‐HC and L‐HC groups. These findings suggest that the sGC system was not normal in atherosclerotic coronary arteries. The redox state of sGC and the distribution pattern are likely to change with the progression of atherosclerosis. |
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issn | 2052-1707 |
language | English |
last_indexed | 2024-12-16T12:46:06Z |
publishDate | 2021-08-01 |
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spelling | doaj.art-0829004e01484892b846003fa7e160c12022-12-21T22:31:17ZengWileyPharmacology Research & Perspectives2052-17072021-08-0194n/an/a10.1002/prp2.838Alteration of the soluble guanylate cyclase system in coronary arteries of high cholesterol diet‐fed rabbitsMasashi Tawa0Katsuya Nakano1Yuka Yamashita2Qiang He3Takayoshi Masuoka4Tomio Okamura5Takaharu Ishibashi6Department of Pharmacology Kanazawa Medical University Kahoku Ishikawa JapanDepartment of Pharmacology Kanazawa Medical University Kahoku Ishikawa JapanDepartment of Pharmacology Kanazawa Medical University Kahoku Ishikawa JapanDepartment of Pharmacology Kanazawa Medical University Kahoku Ishikawa JapanDepartment of Pharmacology Kanazawa Medical University Kahoku Ishikawa JapanShiga University of Medical Science Otsu Shiga JapanDepartment of Pharmacology Kanazawa Medical University Kahoku Ishikawa JapanAbstract This study aimed to investigate how atherosclerosis affects the soluble guanylate cyclase (sGC) system in coronary arteries. Rabbits were fed a normal diet for 12 weeks (N group) or a diet containing high cholesterol (1%) for 4 weeks (S‐HC group) and 12 weeks (L‐HC group). Cholesterol deposition in the intima of coronary arteries was observed in the S‐HC group, but the formation of an atherosclerotic plaque was not observed. In contrast, a major plaque developed in the L‐HC group. The relaxant response of isolated coronary arteries to sodium nitroprusside (SNP, nitric oxide donor) was not different between the N and S‐HC groups, whereas the response in the L‐HC group was markedly attenuated. The relaxation induced by BAY 60‐2770 (sGC activator) tended to be augmented in the S‐HC group, but it was significantly impaired in the L‐HC group compared to that in the N group. sGC β1 immunostaining was equally detected in the medial layer of the arteries among the N, S‐HC, and L‐HC groups. In addition, a strong staining was observed in the plaque region of the L‐HC group. cGMP levels in the arteries stimulated with SNP were identical in the N and S‐HC groups and slightly lower in the L‐HC group than the other groups. BAY 60‐2770‐stimulated cGMP formation tended to be increased in the S‐HC and L‐HC groups. These findings suggest that the sGC system was not normal in atherosclerotic coronary arteries. The redox state of sGC and the distribution pattern are likely to change with the progression of atherosclerosis.https://doi.org/10.1002/prp2.838atherosclerosiscoronary arterynitric oxideredox statesoluble guanylate cyclase |
spellingShingle | Masashi Tawa Katsuya Nakano Yuka Yamashita Qiang He Takayoshi Masuoka Tomio Okamura Takaharu Ishibashi Alteration of the soluble guanylate cyclase system in coronary arteries of high cholesterol diet‐fed rabbits Pharmacology Research & Perspectives atherosclerosis coronary artery nitric oxide redox state soluble guanylate cyclase |
title | Alteration of the soluble guanylate cyclase system in coronary arteries of high cholesterol diet‐fed rabbits |
title_full | Alteration of the soluble guanylate cyclase system in coronary arteries of high cholesterol diet‐fed rabbits |
title_fullStr | Alteration of the soluble guanylate cyclase system in coronary arteries of high cholesterol diet‐fed rabbits |
title_full_unstemmed | Alteration of the soluble guanylate cyclase system in coronary arteries of high cholesterol diet‐fed rabbits |
title_short | Alteration of the soluble guanylate cyclase system in coronary arteries of high cholesterol diet‐fed rabbits |
title_sort | alteration of the soluble guanylate cyclase system in coronary arteries of high cholesterol diet fed rabbits |
topic | atherosclerosis coronary artery nitric oxide redox state soluble guanylate cyclase |
url | https://doi.org/10.1002/prp2.838 |
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