Potassium (K
+) channels could be involved in the RRF relaxation, because bovine retinal arteries relax less when contracted with a 120 mM K
+ KRB solution.
4 It even changes the biphasic RRF-induced relaxation into a monophasic one.
15 Lee et al. tested different K
+ channels inhibitors and observed that blocking voltage-dependent K
+ (K
V) channels with 4-aminopyridine (4-AP) inhibited the RRF-induced relaxation on rat aortas (
Fig. 1). A more general K
+ channel blocker, tetraethylammonium (TEA), did the same.
5 However, Takir et al. could not confirm these observations for bovine RRF, because 4-AP and TEA were unable to block the RRF-induced relaxation.
15 The contradictory results about the involvement of K
V channels could be attributed to the use of different contractile substances (phenylephrine versus PGF
2α) and different species or arteries (rat aorta versus bovine retinal artery).
15 Both studies also tested ATP-sensitive K
+ (K
ATP) channels with the blocker glibenclamide and concluded that it had no effect. Calcium-actived K
+ (K
Ca) channels were tested by using iberiotoxin on rat retina and charybdotoxin (big and intermediate K
Ca blocker) and apamin (small K
Ca blocker) on bovine retina. All these blockers did not reduce the RRF-induced relaxation. However, inward rectifier K
+ (K
ir) channels seem to be involved (
Fig. 1). Their inhibition with barium chloride (BaCl
2) reduced the RRF-induced relaxation and changed the biphasic relaxation in a monophasic one.
16