Arteriolar diameter and spontaneous vasomotion: Importance of potassium channels and nitric oxide

•Spontaneous rhythmic arteriolar diameter oscillation, termed vasomotion, is not solely related to vascular tone.•Interplay between vascular tone and membrane currents is necessary to modulate vasomotion.•Vasomotion could also be modulated by nitric oxide (but not cGMP) and KATP channels.•In addition, our results point to dissociation between vasomotion frequency and amplitude.

Arterioles display cyclic variations in diameter, termed vasomotion initiated by smooth muscle cells (SMCs), but the endothelium should also be evaluated due to its modulatory role on vessel tone. Since nitric oxide (NO) and prostacyclin (PGI2) regulate SMC tone and activate K+ currents, we have investigated their role on vasomotion, by observing effects of topical application of Nω-nitro-l-arginine (L-NA, NO synthesis inhibitor), glibenclamide (KATP channel inhibitor), sodium nitroprusside (SNP, NO donor), iloprost (PGI2 analogue) and methylene blue (MB, cGMP production inhibitor) on the cheek pouch preparation of anesthetized male hamsters. L-NA (10− 10–10− 6 M) induced vasoconstriction, reduction and abolition of vasomotion. MB (10− 7 to 10− 5 M) reduced mean arteriolar diameter with no changes on vasomotion. In the presence of 10− 6 M of MB, addition of 10− 6 L-NA totally abolished vasomotion without further constriction. Glibenclamide (10− 6 M) in the presence of L-NA at equimolar concentration restored both vasomotion frequency and amplitude. This effect was not observed in the presence of TEA 5 mM. SNP (10− 10–10− 6 M) induced a dose-dependent increase of arteriolar diameter and decreased vasomotion. Iloprost (10− 12–10− 6 M) induced a concentration dependent increase of arteriolar diameter, reduced vasomotion frequency, but in lower concentrations (10− 12–10− 10 M) increased its amplitude and in higher concentrations (10− 9–10− 6 M) decreased it. SNP and iloprost inhibited vasomotion at 10− 7 M; however, at this concentration SNP and iloprost induced an increment of 35% and 50% of the initial arteriolar diameter, respectively. In the presence of L-NA (10− 6 M), vasomotion was restored by SNP at 10− 10 M and iloprost 10− 12 M, which corresponded to 80% of the initial diameter value. Around the initial (control) arteriolar diameter value, vasomotion presented its highest frequencies and amplitudes. Cessation of vasomotion occurred with L-NA (10− 6 M) in the presence of SNP (10− 6 M) and iloprost (10− 7 M) when arteriolar diameter reached 150% and 120% of its initial value, respectively. In conclusion, the present study strongly suggests that vasomotion (1) is not solely related to vascular tone, (2) needs an interplay between vascular tone and membrane currents and (3) could be modulated by NO (but not cGMP) and KATP channels. In addition, our results point to the existence of dissociation between vasomotion frequency and amplitude.