title: Suppression of CO2-induced relaxation of bovine retinal pericytes by angiotensin II.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami School of Medicine, Florida, USA.
authors.forename: T
authors.initials: T
authors.lastname: Matsugi
authors.forename: Q
authors.initials: Q
authors.lastname: Chen
authors.forename: D R
authors.initials: DR
authors.lastname: Anderson
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D002196:Capillaries / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D002245:Carbon Dioxide / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D002417:Cattle; D002465:Cell Movement / Q000187:drug effects*; D002478:Cells, Cultured; D006863:Hydrogen-Ion Concentration; D011945:Receptors, Angiotensin / Q000378:metabolism; D012171:Retinal Vessels / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D012504:Saralasin / Q000494:pharmacology; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D011945:Receptors, Angiotensin; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D002245:Carbon Dioxide; D012504:Saralasin