IOVS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Matsugi, T.
Right arrow Articles by Anderson, D. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Matsugi, T.
Right arrow Articles by Anderson, D. R.

Investigative Ophthalmology & Visual Science, Vol 38, 652-657, Copyright © 1997 by Association for Research in Vision and Ophthalmology

ARTICLES AND REPORTS

Suppression of CO2-induced relaxation of bovine retinal pericytes by angiotensin II

T Matsugi, Q Chen and DR Anderson
Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami School of Medicine, Florida, USA.

PURPOSE: To determine whether angiotensin II (Ang II), a vasoconstrictive peptide, changes the relaxation effect of elevated partial pressure of carbon dioxide (PCO2) on pericytes. METHODS: The contractile tone of cultured bovine retinal pericytes was measured when the ambient PCO2 was elevated in the absence or the presence of Ang II. All experiments were performed in the bicarbonate-buffered solution at 37 degrees C. RESULTS: Ang II (10(-6) M) by itself did not increase the baseline tone of the pericytes. Raising the PCO2 from 5% to 20% acidified the solution (pH dropped 0.51 +/- 0.02 U) and caused a sustained and statistically significant 22.9% +/- 4.6% relaxation of pericytes within 5 minutes (n = 8). In the presence of Ang II (10(-6) M), the maximum relaxation induced by 20% PCO2 was only 12.6% +/- 4.5% (n = 6) at 3 minutes, and the relaxation was not sustained. The effect of Ang II was statistically significant. Pretreatment with the competitive Ang II receptor antagonist saralasin (10(-6) M) for 10 minutes completely abolished the effect of Ang II (10(-6) M) on the response of pericytes to 20% PCO2. Saralasin by itself had no effect. CONCLUSIONS: Ang II attenuated the relaxing response of pericytes to elevated PCO2 through saralasin-sensitive Ang II receptors. Results suggest that some vasoactive agents, such as Ang II, could affect the pericyte responses to metabolic needs as signaled by local PCO2. This experimental design may permit further investigation of the altered physiology of local blood flow regulation.


This article has been cited by other articles:


Home page
 HypertensionHome page
Y. Kim, R. Y. Imdad, A. H. Stephenson, R. S. Sprague, and A. J. Lonigro
Vascular Endothelial Growth Factor mRNA in Pericytes Is Upregulated by Phorbol Myristate Acetate
Hypertension, January 1, 1998; 31(1): 511 - 515.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1997 by the Association for Research in Vision and Ophthalmology