Oxygen reactivity of the feline isolated ophthalmociliary artery

The goal of this study was to investigate the modulating role of oxygen tension on noradrenaline (NA) and KCl responses in the ophthalmociliary artery and to ascertain whether these effects are mediated by the endothelial cells.

The isometric tension generated by myograph ring segments activated by NA or KCl was measured as the PO2 of the bathing solution was decreased in discrete steps from 506.1 +/- 16.0 mmHg to 29.4 +/- 1.4 mmHg in preparations with and without endothelial cells.

Vessels pre-activated with K+ Krebs solution were insensitive to oxygen tensions between 506.1 +/- 16.0 mmHg and 124.6 +/- 4.2 mmHg. Lower PO2s caused a graded and increasing contraction that reached 176 +/- 12% of the contraction at the highest PO2. Vessels pre-activated with NA had a dichotomous response to reductions in oxygen tension: 44% of vessels showed a graded contraction, whereas a graded relaxation was observed for the remaining 56% of vessels as bath PO2 was reduced. In all cases, a functional endothelium was demonstrated. However, deliberate disruption of the endothelium caused all vessels pre-activated with NA to exhibit a consistent graded contraction for PO2s below 124.6 +/- 4.2 mmHg, similar to that observed for endothelial intact vessels pre-activated with K+ Krebs. The acetylcholine dose-response curve and passive tension were not affected by changes in oxygen tension.

Endothelial cells modify the intrinsic smooth muscle response to a gradual reduction in PO2 by releasing relaxing and contracting factors, causing the observed dichotomous response in NA-activated vessels. However, the KCl-induced response is modulated only by low oxygen tensions.