Alterations of calcium handling and other second messenger cascades including protein kinase C (PKC) and A (PKA) were suggested to be responsible for abnormal vascular function in spontaneously hypertensive rats (SHR). However, the relative contribution of these pathways to vasoconstriction is still not completely understood. We investigated the effect of Ro 31-8220 (PKC inhibitor) and H89 (PKA inhibitor) on vasoconstriction induced by 120 mM KCl or by addition of 10 μM noradrenaline (NA) in isolated femoral arteries of control Wistar rats and SHR. Moreover, we investigated these responses in the presence and absence of Ca2+ ions in the incubation medium in order to assess the role of calcium influx in these contractions. We observed that while the vasoconstriction in the presence of calcium was not different between Wistar and SHR, the difference between constriction elicited by NA addition in the absence and presence of external calcium was larger in SHR. The inhibition of PKC had no effect on constrictions in SHR, but diminished constrictions in Wistar rats. PKA inhibition slightly enhanced constrictions in Wistar rats, but reduced them in the presence of calcium in SHR. We conclude that vasoconstriction elicited by adrenergic stimulation is more dependent on extracellular calcium influx in SHR compared to Wistar rats. Moreover, the activation of PKA contributes to this calcium-dependent vasoconstriction in SHR but not in Wistar. On the other hand, PKC activation seems to play a less important role in vasoconstriction in SHR than in Wistar rats., M. S. Bal ... [et al.]., and Obsahuje seznam literatury
In functional arterial studies using wire myography, the determination of a vessel’s standardized normalization factor (factor k) is an essential step to ensure optimal contraction and relaxation by the arteries when stimulated with their respective vasoactive agents and to obtain reproducible results. The optimal factor k for several arteries have been determined, however, the optimal initial tension and factor k for the arteries involved in erection remains unknown. Hence, in the present study we set out to determine the optimal factor k for the internal iliac artery, proximal and distal internal pudendal artery (IPA), and dorsal penile artery. After isolating, harvesting, and mounting the arteries from male Sprague-Dawley rats on a multi wire myograph, we tested arterial responsivity to high K+-stimulation when the factor k was set at 0.7, 0.8, 0.85, 0.9, 0.95, 1.0, 1.1, and 1.2 to determine the factor k setting that results in the greatest K+-induced active force production for each vessel type. The data showed the optimal factor k is 0.90-0.95 for the dorsal penile, distal internal pudendal and internal iliac arteries while it is 0.85-0.90 for proximal internal pudendal artery. These optimal values corresponded to initial passive tension settings of 1.10±0.16 - 1.46±0.23, 1.28±0.20 - 1.69±0.34, 1.03±0.27 - 1.33±0.31, and 1.33±0.31 - 1.77±0.43 mN/mm for the dorsal penile, distal IP, proximal IP, and internal iliac arteries, respectively.