Figure 1.

Time course of changes in vessel diameter and endothelial cell [Ca²⁺] in response to abluminal pressure-pulse application of agonists to isolated perfused resistance arterioles. (A) ACh (10⁻⁴ M, 1.2-sec pulse, n = 15) and sodium nitroprusside (NP 5 × 10⁻⁵ M, 1.2-sec pulse, n = 3) both stimulated vasodilation, but had opposite effects on [Ca²⁺]_i. (Right) The rapid rise in [Ca²⁺]_i in response to ACh, but not sodium nitroprusside, at the same arteriolar location suggests changes in fluorescence intensity relate to changes in endothelial cell rather than smooth muscle [Ca²⁺]_i (typical trace). (B) PE (10⁻⁵ M, 1.2-sec pulse, n = 11) and KCl (250 mM, 2.2-sec pulse, n = 8) both stimulated vasoconstriction and rises in endothelial cell [Ca²⁺]_i. In contrast, indolactam (10⁻⁵ M, 1.2-sec pulse, n = 4) caused vasoconstriction without a change in [Ca²⁺]_i. (Right) No increase in [Ca²⁺]_i was observed in association with indolactam-stimulated vasoconstriction at the same arteriolar location shown to be responsive to PE (typical trace). (C) For each agonist, changes in endothelial cell [Ca²⁺]_i occurred well in advance of changes in arteriolar diameter. Values are means ± SE; ▴ denotes time at which agonist application commenced.