Effect of palmitoleic acid on bradykinin-induced endothelium-dependent relaxation in isolated pig ciliary artery.

BACKGROUND

Endothelial-dependent relaxation has been reported to be impaired in some normal tension glaucoma patients. The present study investigates whether the gap junction uncoupling agent palmitoleic acid (PA) affects bradykinin-induced endothelium-dependent relaxation in isolated pig ciliary artery.

MATERIAL AND METHODS

In a myograph system (isometric force measurement), vessels precontracted with the thromboxane A2 agonist U 46619 ( approximately 0.1 micrometer) were relaxed by increasing concentrations (cumulative) of bradykinin (0.003 - 3 micrometer). Experiments were repeated in the presence of 100 micrometer L-NAME (inhibitor of nitric oxide formation) and/or 100 micrometer PA. Some experiments were conducted in vessels with a non-functional endothelium (intentionally and mechanically damaged). All experiments were conducted in the presence of 10 microM indomethacin (cyclooxygenase inhibitor).

RESULTS

In a concentration-dependent manner, bradykinin evoked a relaxation (101 +/- 2 %) that was abolished in vessels with a non-functional endothelium (maximal relaxation: 7 +/- 1 %, p < 0.001). In the presence of L-NAME, relaxations induced by bradykinin were almost completely inhibited (maximal relaxation: 25 +/- 5 %, p < 0.001). Relaxations evoked by bradykinin were not significantly affected by PA (either in the presence or in the absence of L-NAME).

CONCLUSIONS

The bradykinin-induced relaxation, known to be associated in porcine ciliary arteries with an electrical coupling between endothelial and smooth muscle cells, appears to be unaffected by the gap junction uncoupling agent palmitoleic acid. Further investigations are needed to understand the physiology of the endothelium-dependent ocular blood flow modulation that is considered to be dysregulated in some glaucoma patients.