3.5 Basal oxidative and nitrosative stress
The inhibitors of cyclooxygenases, NO-synthases and antioxidant enzymes
and the scavengers of reactive oxygen species that we used, did not
cause contraction in the isolated pericardial resistance arteries.
L-NAME significantly increased contractile responses
to 32 mM
K+ by 48 ± 11 %
(P < 0.0001; N = 28) (Figure 6). It did not increase
the potency of ET-1 further; 3.1 ± 0.8 and 2.4 ± 0.6 nM ET-1 were needed
to cause contractions similar to those stimulated by 32 mM
K+ in the presence and absence of L-NAME, respectively
(P = 0.1754; N = 27) (Suppl. Figure 1). In contrast to the
non-selective NOS-inhibitor L-NAME, the selective inhibitors of nNOS
7-NI and NPLA did not increase contractile responses to 32 mM
K+ (Figure 6). Also, c-PTIO and DETCA, which abolished
relaxing responses to SNP (Figure 4), did not increase contractile
responses to 32 mM K+ (Figure 6). Although exogenous
catalase did not significantly modify contractile responses, amitrole (a
putative inhibitor of catalase) reduced K+-induced
contractions by -48 ± 9 % (P < 0.001; N = 11).