Prostaglandins participate in the late phase of the vascular response to acetylcholine iontophoresis in humans

The participation of prostaglandins (PGs) in the cutaneous vasodilatation to acetylcholine (ACh) applied via iontophoresis is under debate. Using laser Doppler flowmetry, we studied the long lasting effect (20 min) of iontophoretic application (30 s; 0.1 mA) of ACh on the human forearm. Experiments were repeated (1) using deionized water instead of ACh to test the effect of current application, (2) after scopolamine treatment to inhibit muscarinic cholinergic receptors, and (3) 2 h, 3 days and 10 days following inhibition of PG synthesis with aspirin or a placebo control. Cutaneous vascular conductance (CVC) was calculated at rest (CVC rest ), at peak vasodilatation in the first 5 min following ACh iontophoresis (CVC peak ), and 20 min after iontophoresis (CVC 20 ). The minimal CVC (CVC min ) following iontophoresis was also determined. Cutaneous response to ACh displayed a biphasic pattern with an early and transient peak (CVC peak : 62 ± 8% of the maximal CVC induced by local heating (MVC)) followed by a long lasting slower vasodilatation (CVC min : 44 ± 6; CVC 20 : 56 ± 5%MVC). The current itself had no major effect. Scopolamine almost abolished both phases. The long lasting phase was aspirin sensitive but not the transient phase. At hour 2 post-aspirin, CVC peak was 61 ± 10, CVC min 26 ± 6 and CVC 20 29 ± 6%MVC. At day 3, CVC peak was 53 ± 9, CVC min 22 ± 3 and CVC 20 25 ± 4%MVC. At day 10, CVC peak was 67 ± 10, CVC min 47 ± 7 and CVC 20 50 ± 8%MVC. Placebo had no effect. We conclude that PGs participate in the vasodilator response following ACh iontophoresis. Previous non-steroidal anti-inflammatory drug treatments must be taken into account when studying the effect of ACh iontophoresis.