A transient dilatation of pressurised rat cerebral arteries during rapid pressure increases is mediated by nitric oxide

Abstract

 In pressurised resistance arteries in vitro, rapid pressure increases cause a transient ”peak” dilatation, followed by a myogenic constriction. The mechanism of transient dilatation was investigated in isolated rat cerebral arteries in vitro using pressure myography. The peak increased with the amplitude of the pressure step. A near-maximal dilatation to 118±1.6% (SEM, n=20) of the diameter at 30 mmHg was produced by pressure steps from 30 to 75 mmHg. N ^ω-nitro-l-arginine methyl ester (L-NAME, 20 μM) depressed the peak at the onset of a 30 to 75 mmHg pressure step to 49.8±14% of the control (n=6; P=0.04). D-NAME (20 μM) had no significant effect (82.1±13%; n=4; P=0.13). l-Arginine (400 μM) enhanced the peak (164±17% of control; n=8; P=0.01). Oxadiazolol (4,3-a) quinoxalin-1-one (ODQ, 2 μM) depressed the peak to 33.2±12% of control (n=5; P=0.012). 6-Anilino-5,8-quinolinedone (LY 83583, 10 μM) depressed the peak to 18.8±2.9% of control (n=3; P=0.01). Removing the endothelium decreased the peak to 15.3±11% of control (n=3; P=0.04). In conclusion, in rat cerebral arteries, the initial dilatation at the onset of a rapid step increase in pressure is an active dilatation involving endothelial NO release.