Figure 4.

(A) Effect of endothelium-specific damage on the diameter and fluorescence responses to agonists. Perfusion of air bubbles through the lumen of arterioles changed resting diameter from 64.9 ± 4.9 to 60.5 ± 10.5 μm (n = 4). The responses to ACh were abolished (n = 4), whereas PE-mediated vasoconstriction was unaffected, yet the increase in fluorescence was markedly attenuated (n = 4). (B) Effect of nifedipine on changes in vessel diameter and endothelial cell [Ca²⁺] in response to agonists. Addition of nifedipine (10⁻⁶ M) to the superfusion solution resulted in near maximal dilation of the arteriole (Δ diameter 64 ± 4 to 84 ± 5 μm, n = 8). In the presence of nifedipine, the rise in [Ca²⁺]_i in response to ACh was not affected (106.3 ± 27.6% of control) despite an absence of vasodilation (−8.1 ± 8.1% of control, n = 5). In contrast, both the rise in [Ca²⁺]_i and vasoconstriction in response to PE were reduced (30.9 ± 14.8%, 37.1 ± 9.6% of control, respectively, n = 4) and were markedly reduced in response to KCl (23.4 ± 9.2%, 25.7 ± 10.4% of control, respectively, n = 5). For all agents, values are means ± SE of paired responses before and after each treatment. The stimulation pipette was positioned at the same arteriolar location to obtain each pair of responses.