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Modification of tumour blood flow using the hypertensive agent, angiotensin II.
The effects of different doses of angiotensin II (0.02 to 0.5 microgram kg-1 min-1 on mean arterial blood pressure, tissue blood flow and tissue vascular resistance were investigated in BD9 rats. Blood flow was measured using the uptake of 125I- or 14C-labelled iodoantipyrine (125I-IAP and 14C-IAP)....
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
1993
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1968475/ https://www.ncbi.nlm.nih.gov/pubmed/8494732 |
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author | Tozer, G. M. Shaffi, K. M. |
author_facet | Tozer, G. M. Shaffi, K. M. |
author_sort | Tozer, G. M. |
collection | PubMed |
description | The effects of different doses of angiotensin II (0.02 to 0.5 microgram kg-1 min-1 on mean arterial blood pressure, tissue blood flow and tissue vascular resistance were investigated in BD9 rats. Blood flow was measured using the uptake of 125I- or 14C-labelled iodoantipyrine (125I-IAP and 14C-IAP). Spatial heterogeneity of blood flow within tumours, before and after angiotensin II infusion, was also measured using 14C-IAP and an autoradiographic procedure. Mean arterial blood pressure rose steeply with angiotensin II dose. Blood flow to skeletal muscle, skin overlying the tumour, contralateral skin, small intestine and kidney tended to decline in a dose-dependent manner. Blood flow to the tumour was also reduced (to 80% of control values) but there was no dose response. Blood flow to the heart was slightly increased and blood flow to the brain was unaffected by angiotensin II. Vascular resistance, in all tissues, was increased by angiotensin II infusion. The increase in tumour tissue was similar to that found in skeletal muscle and small intestine and is likely to be caused by a direct vasoconstricting effect of the drug rather than autoregulation of tumour blood flow in the face of an increase in perfusion pressure. The reduction in overall blood flow at the highest perfusion pressure was due to a preferential effect of angiotensin II at the tumour periphery. These results show that some tumours, at least, can respond directly to the effects of vasoactive agents. IMAGES: |
format | Text |
id | pubmed-1968475 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1993 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-19684752009-09-10 Modification of tumour blood flow using the hypertensive agent, angiotensin II. Tozer, G. M. Shaffi, K. M. Br J Cancer Research Article The effects of different doses of angiotensin II (0.02 to 0.5 microgram kg-1 min-1 on mean arterial blood pressure, tissue blood flow and tissue vascular resistance were investigated in BD9 rats. Blood flow was measured using the uptake of 125I- or 14C-labelled iodoantipyrine (125I-IAP and 14C-IAP). Spatial heterogeneity of blood flow within tumours, before and after angiotensin II infusion, was also measured using 14C-IAP and an autoradiographic procedure. Mean arterial blood pressure rose steeply with angiotensin II dose. Blood flow to skeletal muscle, skin overlying the tumour, contralateral skin, small intestine and kidney tended to decline in a dose-dependent manner. Blood flow to the tumour was also reduced (to 80% of control values) but there was no dose response. Blood flow to the heart was slightly increased and blood flow to the brain was unaffected by angiotensin II. Vascular resistance, in all tissues, was increased by angiotensin II infusion. The increase in tumour tissue was similar to that found in skeletal muscle and small intestine and is likely to be caused by a direct vasoconstricting effect of the drug rather than autoregulation of tumour blood flow in the face of an increase in perfusion pressure. The reduction in overall blood flow at the highest perfusion pressure was due to a preferential effect of angiotensin II at the tumour periphery. These results show that some tumours, at least, can respond directly to the effects of vasoactive agents. IMAGES: Nature Publishing Group 1993-05 /pmc/articles/PMC1968475/ /pubmed/8494732 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Research Article Tozer, G. M. Shaffi, K. M. Modification of tumour blood flow using the hypertensive agent, angiotensin II. |
title | Modification of tumour blood flow using the hypertensive agent, angiotensin II. |
title_full | Modification of tumour blood flow using the hypertensive agent, angiotensin II. |
title_fullStr | Modification of tumour blood flow using the hypertensive agent, angiotensin II. |
title_full_unstemmed | Modification of tumour blood flow using the hypertensive agent, angiotensin II. |
title_short | Modification of tumour blood flow using the hypertensive agent, angiotensin II. |
title_sort | modification of tumour blood flow using the hypertensive agent, angiotensin ii. |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1968475/ https://www.ncbi.nlm.nih.gov/pubmed/8494732 |
work_keys_str_mv | AT tozergm modificationoftumourbloodflowusingthehypertensiveagentangiotensinii AT shaffikm modificationoftumourbloodflowusingthehypertensiveagentangiotensinii |