3.2 General properties of resistance arteries
The lumen diameter of isolated and distended pericardial small arteries averaged 243 ± 19 μm (mean of means; n=225 segments, N=53 patients). The contractile response of these preparations to depolarization with 32 mM K+ was 1.47 ± 0.40 N.m-1 and exhibited a weak statistically significant positive relationship to the lumen diameter of the vessels (Figure 1A, 1B and 1D). In 3/53 experiments, 1 µM BK failed to induce a noticeable arterial relaxation. These arterial preparations were not investigated further. In the remaining experiments, the relaxing response to 1 µM BK averaged -65 ± 12% (mean of means; n = 205, N = 50). It differed considerably between patients (Figure 1C) but was not significantly related to the absolute amplitude (N.m-1) of the pre-contraction. It was significantly (but not markedly) smaller for patients with coronary artery disease (-57 ± 4%; n = 86, N = 21) compared to those needing replacement of cardiac valves (-71 ± 5%; n = 91, N = 22, P = 0.041). In a small number of dedicated experiments, gentle mechanical damage to the luminal surface of the arterial segments abolished the relaxing response to 1 µM BK during contraction induced by 32 mM K+ (Figure 2).
In arteries that contracted in response to depolarizing solution, contraction was also stimulated by ET-1. This agonist can increase oxidative stress(Davenport et al., 2016) and has been proposed to shift the mediator of endothelium-dependent relaxation from NO to H2O2(Leurgans et al., 2016). On average, 3.36 ± 0.72 nM ET-1 resulted in contractions that were comparable to those stimulated by 32 mM K+ in the same arterial segments (2.10 ± 0.19 N.m-1 vs.1.52 ± 0.17 N.m-1, respectively, n = 36, N = 36). In the presence of ET-1, relaxations induced by 1 µM BK were significantly larger than during K+-stimulated contraction (-78 ± 2% vs. -68 ± 3% respectively, N = 36, P = 0.034) and were also endothelium-dependent (Figure 2).