Myogenic tone is an important autoregulatory mechanism ensuring that blood flow is kept constant despite alterations in perfusion pressure. Its existence has been demonstrated in vitro using isolated pressurized small arteries where increases in transmural pressure (TmP) have been obtained by increasing intravascular pressure (IvP). In vivo, however, coronary vessels are subject to compressive forces of the surrounding contractile cardiac muscle. Transmural pressure will thus be determined by both intra- and extravascular pressure (EvP) changes. It is unclear whether IvP and EvP have similar effects on active arterial diameter. This study describes a new technique that allows the effect of variations in both intra- and extravascular pressures on isolated arterial diameter to be investigated.

Wistar rats were humanely killed by cervical dislocation and septal coronary arteries (200Ð250 µm diameter) were dissected out. Each artery was mounted on a modified pressure myograph where they were constantly superfused with physiological salt solution (pH 7.4, 37 °C, 95 % air and 5 % CO₂). A lid was secured over the myograph chamber, which allowed EvP to be altered (via a 95 % air and 5 % CO₂ source). The internal diameter of vessels was determined using a video dimension analyser.

At an IvP of 60 mmHg, and thus an outward TmP of 60 mmHg, coronary arteries (mean internal diameter of 223 ± 9 µm, n = 5) developed myogenic tone (124 ± 21.39 µm). Elevation of EvP to 40 mmHg, which effectively reduced the outward TmP to 20 mmHg, reduced the diameter of all vessels by 25 ± 3.9 %. Subsequent elevation of IvP to 100 mmHg, at a maintained EvP of 40 mmHg, to return TmP to 60 mmHg increased arterial diameter to 99.6 ± 1.9 % of that observed at the original TmP of 60 mmHg (due to IvP of 60 mmHg and EvP of 0 mmHg).

The effect of different IvPs on arterial diameter was also assessed when EvP was 0 mmHg, n = 8 (IvP range = 20Ð60 mmHg) and when EvP was maintained at 40 mmHg, n = 4 (IvP range = 60Ð100 mmHg), such that similar TmPs were obtained. Arterial diameters were similar at each TmP regardless of the relative contribution of IvP and EvP to it (0.77 ± 0.13 and 0.87 ± 0.09 for 20 mmHg; 0.88 ± 0.09 and 0.95 ± 0.07 for 40 mmHg and 0.94 ± 0.05 and 0.97 ± 0.04; data are means ± S.E.M.) for a TmP of 60 mmHg observed at an EvP of 40 and 0 mmHg, respectively (Student’s unpaired t test, P > 0.05) (data normalised to diameter at IvP of 60 and EvP of 0 mmHg for each vessel).

Thus we demonstrate for the first time that changes in both intra- and extravascular pressure may modify coronary artery diameter. Furthermore we have shown that it is the outward transmural pressure that is important in determining arterial diameter, which may be determined by a combination of intra-and extravascular pressures.

This work was supported by the British Heart Foundation.

All procedures accord with current UK legislation.