Endothelium-Dependent and -Independent Vascular Dysfunction in Type 1 Diabetes
Objective— Defective NO release/response may contribute to increased coronary risk and the loss of sex difference in coronary heart disease in diabetes. We aimed to determine whether NO release/response is impaired in type 1 diabetes and whether any defects are greater in women than men. Methods and...
Published in: | Arteriosclerosis, Thrombosis, and Vascular Biology |
---|---|
Main Authors: | , , |
Format: | Article in Journal/Newspaper |
Language: | English |
Published: |
Ovid Technologies (Wolters Kluwer Health)
2003
|
Subjects: | |
Online Access: | http://dx.doi.org/10.1161/01.atv.0000072968.00157.6b https://www.ahajournals.org/doi/full/10.1161/01.ATV.0000072968.00157.6B |
id |
crovidcr:10.1161/01.atv.0000072968.00157.6b |
---|---|
record_format |
openpolar |
spelling |
crovidcr:10.1161/01.atv.0000072968.00157.6b 2023-12-03T10:23:42+01:00 Endothelium-Dependent and -Independent Vascular Dysfunction in Type 1 Diabetes Role of Conventional Risk Factors, Sex, and Glycemic Control Chan, Norman Nor Vallance, Patrick Colhoun, Helen Martina 2003 http://dx.doi.org/10.1161/01.atv.0000072968.00157.6b https://www.ahajournals.org/doi/full/10.1161/01.ATV.0000072968.00157.6B en eng Ovid Technologies (Wolters Kluwer Health) Arteriosclerosis, Thrombosis, and Vascular Biology volume 23, issue 6, page 1048-1054 ISSN 1079-5642 1524-4636 Cardiology and Cardiovascular Medicine journal-article 2003 crovidcr https://doi.org/10.1161/01.atv.0000072968.00157.6b 2023-11-05T13:57:20Z Objective— Defective NO release/response may contribute to increased coronary risk and the loss of sex difference in coronary heart disease in diabetes. We aimed to determine whether NO release/response is impaired in type 1 diabetes and whether any defects are greater in women than men. Methods and Results— Forearm blood flow response to vasoactive drugs was assessed by venous plethysmography in 88 diabetic and 69 control subjects aged 30 to 53 years. In diabetic patients, response was 18% lower for acetylcholine (ACh) ( P =0.002), 6% lower for bradykinin ( P =0.14), and 17% lower for glyceryl trinitrate (GTN) ( P <0.001). Women had a higher response to ACh than men (17%, P =0.006). The diabetes-associated defect in ACh was greater in women (25% lower, P =0.01) than men (13% lower, P =0.08), although not significantly ( P =0.26 for the interaction). Poorer glycemic control was associated with ACh response ( P =0.003) and contributed to the greater defect in diabetic women than men. Conclusions— The diabetes-associated defect in GTN response was similar in men and women. Established coronary heart disease risk factors did not explain any of the defects in ACh or GTN response associated with diabetes. Type 1 diabetes is associated with impaired responsiveness to NO and with an impairment in ACh-stimulated NO release. Article in Journal/Newspaper GTN-P Ovid (via Crossref) Arteriosclerosis, Thrombosis, and Vascular Biology 23 6 1048 1054 |
institution |
Open Polar |
collection |
Ovid (via Crossref) |
op_collection_id |
crovidcr |
language |
English |
topic |
Cardiology and Cardiovascular Medicine |
spellingShingle |
Cardiology and Cardiovascular Medicine Chan, Norman Nor Vallance, Patrick Colhoun, Helen Martina Endothelium-Dependent and -Independent Vascular Dysfunction in Type 1 Diabetes |
topic_facet |
Cardiology and Cardiovascular Medicine |
description |
Objective— Defective NO release/response may contribute to increased coronary risk and the loss of sex difference in coronary heart disease in diabetes. We aimed to determine whether NO release/response is impaired in type 1 diabetes and whether any defects are greater in women than men. Methods and Results— Forearm blood flow response to vasoactive drugs was assessed by venous plethysmography in 88 diabetic and 69 control subjects aged 30 to 53 years. In diabetic patients, response was 18% lower for acetylcholine (ACh) ( P =0.002), 6% lower for bradykinin ( P =0.14), and 17% lower for glyceryl trinitrate (GTN) ( P <0.001). Women had a higher response to ACh than men (17%, P =0.006). The diabetes-associated defect in ACh was greater in women (25% lower, P =0.01) than men (13% lower, P =0.08), although not significantly ( P =0.26 for the interaction). Poorer glycemic control was associated with ACh response ( P =0.003) and contributed to the greater defect in diabetic women than men. Conclusions— The diabetes-associated defect in GTN response was similar in men and women. Established coronary heart disease risk factors did not explain any of the defects in ACh or GTN response associated with diabetes. Type 1 diabetes is associated with impaired responsiveness to NO and with an impairment in ACh-stimulated NO release. |
format |
Article in Journal/Newspaper |
author |
Chan, Norman Nor Vallance, Patrick Colhoun, Helen Martina |
author_facet |
Chan, Norman Nor Vallance, Patrick Colhoun, Helen Martina |
author_sort |
Chan, Norman Nor |
title |
Endothelium-Dependent and -Independent Vascular Dysfunction in Type 1 Diabetes |
title_short |
Endothelium-Dependent and -Independent Vascular Dysfunction in Type 1 Diabetes |
title_full |
Endothelium-Dependent and -Independent Vascular Dysfunction in Type 1 Diabetes |
title_fullStr |
Endothelium-Dependent and -Independent Vascular Dysfunction in Type 1 Diabetes |
title_full_unstemmed |
Endothelium-Dependent and -Independent Vascular Dysfunction in Type 1 Diabetes |
title_sort |
endothelium-dependent and -independent vascular dysfunction in type 1 diabetes |
publisher |
Ovid Technologies (Wolters Kluwer Health) |
publishDate |
2003 |
url |
http://dx.doi.org/10.1161/01.atv.0000072968.00157.6b https://www.ahajournals.org/doi/full/10.1161/01.ATV.0000072968.00157.6B |
genre |
GTN-P |
genre_facet |
GTN-P |
op_source |
Arteriosclerosis, Thrombosis, and Vascular Biology volume 23, issue 6, page 1048-1054 ISSN 1079-5642 1524-4636 |
op_doi |
https://doi.org/10.1161/01.atv.0000072968.00157.6b |
container_title |
Arteriosclerosis, Thrombosis, and Vascular Biology |
container_volume |
23 |
container_issue |
6 |
container_start_page |
1048 |
op_container_end_page |
1054 |
_version_ |
1784271930200686592 |