Purpose: We studied the effect of angiotensin II (AngII), a vosoconstrictor hormone, on bovine retinal pericytes pre-relaxed with sodium nitroprusside (SNP). Pure cultures of pericytes appear in a fully contracted state, because they are not exposed to nitric oxide (NO) released by endothelial cells. Therefore, we applied SNP as a donor of NO. Methods: Bovine retinal pericytes were cultured on the surface of silicone rubber sheets. Changes in the contractile tone of pericytes were quantified as the changes in the length of wrinkles induced by cells on the silicone surface. Contamination of the pericyte culture by endothelium was ruled out by absence of any cells that take up low-density lipoprotein by endocytosis. Results: After pre-relaxation with SNP(10-6 M), AngII (10-5 M) produced a transient contractile effect. The maximal contraction was 22%, which occurred at 3 minutes (n=5). Angiotensin I (AngI; 10-5 M) also caused contractions of pre-relaxed pericytes. The maximal contraction induced by Angl was 18% at 1 minute (n=6). AngII (10-5 M) did not contract the cells without pre-relaxation. Saralasin (10-5M), an AngII receptor antagonist, significantly inhibited the contractile effects of both AngII and AngI. Saralasin (10-5 M) itself did not affect basal tone of pericytes. Conclusion: We found contractile responses of pericytes to both AngII and AngI. AngII causes contraction through the activation of AngII receptors that are competitively inhibited by saralasin. Contractibility of pericytes to AngII may contribute to the regulation of retinal blood flow under physiological condition. In pericyte culture, AngI is probably converted into AngII, but details of this conversion require further investigation.
|Original language||English (US)|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Feb 15 1996|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience