Figure 4.

SKA-31 evoked inhibition of myogenic tone is not blunted in the presence of the NO synthase inhibitor L-NAME. Following development of stable myogenic tone, brief exposure of a cannulated cremaster artery to 3 μM SKA-31, 0.5 μM ACh and 10 μM SNP produced robust and reversible inhibition of developed tone (panel A). Re-exposure to SKA-31, ACh and SNP was then carried out in the presence of 100 μM L-NAME, as indicated by the horizontal bar beneath the tracing. Washout (W/O) of L-NAME from the bath is also marked by a horizonatal bar. Panel B displays the same experimental protocol applied to a cannulated middle cerebral artery. Quantification of the effect of L-NAME treatment on the SKA-31, ACh and SNP-evoked inhibition of myogenic tone in cremaster and middle cerebral arteries is shown in panel C. The left-hand columns display the control dilatory responses to SKA-31, ACh and SNP, whereas the middle columns describe responses to repeated exposures to these dilators in the presence 100 μM L-NAME (n = 3–10 for cremaster, n = 3–8 for middle cerebral arteries). The right-hand columns display the responses to SKA-31 and ACh in vessels treated with the saline vehicle used for L-NAME suspension (n = 4 for both vessel types). The asterisk (*) indicates a statistically significant difference in the magnitude of inhibition compared with the initial drug-evoked response, as determined by one-way ANOVA and a Tukey’s post-hoc test (P < 0.05).