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. 2012 Jan 20;302(6):H1274–H1284. doi: 10.1152/ajpheart.01067.2011

Fig. 2.

Fig. 2.

Pial arteriolar diameter changes (expressed as a percentage of the baseline diameter) elicited by SNS or suffusions of specific activators of high-conductance Ca2+-operated K+ (BKCa) and K+ inward rectifier (Kir) channels in control and T1DM rats. A: pial arteriolar diameter changes in response to the BKCa agonist NS-1619 (10 and 50 μM). *P < 0.001 for both concentrations; n = 8. B: pial arteriolar responses to the Kir agonist K+ (6 and 12 mM). *P < 0.002 for both concentrations; n = 8–9. C: effects of the BKCa specific inhibitor paxilline (PAX, 10 μM) on SNS-induced pial arteriolar dilation. In controls, paxilline blocked ∼70% of the response (n = 9, *P < 0.001); but, in T1DM rats (n = 6), it did not interfere with the vasodilation. D: effects of the Kir blocker barium (Ba2+, 100 μM) on SNS-linked vascular responses in control (40% decrease, n = 9, *P = 0.003) and T1DM (60% decrease, n = 5, *P = 0.004) rats.