Voltage-dependent potassium channels (Kv channels) have been reported to be involved in a variety of contractile responses of small arteries. In small arteries of the systemic circulation the expression of Kv1 and Kv2 subunits has been detected. However, due to a lack of specific inhibitors the functional role of individual Kv subunits is incompletely understood. Recently, a specific inhibitor of Kv2 subunits, stromatoxin, was discovered. Thus, the hypothesis was tested that Kv2 subunits contribute to the regulation of myogenic tone of Wistar rat posterior cerebral small arteries by employing PCR, the patch-clamp technique and isobaric myography.

In homogenates from intact cerebral small arteries the expression of Kv2.1 (n=8) but not Kv2.2 subunits (n=10) was detected. In freshly isolated smooth muscle cells from these vessels, expression of Kv2.1 subunits was verified in 10 out of a total of 11 cell samples; expression of Kv2.2 subunits was not found in the same samples. Further, an outward current with biophysical and pharmacological properties similar to recently described Kv currents of rat and mouse small arteries was found in the cells studied. Stromatoxin inhibited the Kv current in a concentration-dependent manner with an ED₅₀ of 36 nM and a maximum effect of 61.2%. At 100 nM, stromatoxin produced a fast, reversible reduction of the Kv current. The voltage-dependence of activation of the Kv current in the presence of 100 nM stromatoxin was characterized by a potential of half-maximal activation of -6.22.3 mV (n=10) that is not different from the potential of half maximal activation of -4.41.9 mV (n=10) obtained in the absence of stromatoxin. The inactivation of the Kv current in the presence of 100 nM stromatoxin was characterized by a potential of half maximal inactivation of -45.12.5 mV (n=10) that is different from the potential of half maximal inactivation of -37.91.4 mV (n=10; p<0.05, t-test) in the absence of stromatoxin. Furthermore, in intact endothelium-denuded and capsaicin-pretreated vessels stromatoxin produced complex responses: (i) in vessels with weak myogenic tone, stromatoxin did not evoke any effect (n=6), (ii) in vessels with strong myogenic tone, it induced vasomotion. In many cases, this vasomotion was regular without changes of the level of the myogenic tone (n=8) or of the strength of the myogenic response (n=7). In contrast, in other cases vasomotion was irregular with large diameter fluctuations and a complete destruction of the myogenic response (n=6).

Thus, the presented data show that in rat posterior cerebral small arteries (i) Kv2.1 but not Kv2.2 subunits are expressed, (ii) a stromatoxin-sensitive current contributes considerably to the Kv current in smooth muscle cells and (iii) this current prevents vasomotion protecting the myogenic response.