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

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. Nomega-nitro-l-arginine methyl ester (L-NAME, 20 microM) 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 microM) had no significant effect (82.1+/-13%; n=4; P=0.13). L-Arginine (400 microM) enhanced the peak (164+/-17% of control; n=8; P=0.01). Oxadiazolol (4,3-a) quinoxalin-1-one (ODQ, 2 microM) depressed the peak to 33.2+/-12% of control (n=5; P=0.012). 6-Anilino-5, 8-quinolinedone (LY 83583, 10 microM) 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.