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).