Fig. 5.

NO/cGMP/vasodilator-stimulated phosphoprotein (VASP) pathway activation in isolated Ca²⁺-deprived canine mesenteric arteries. A: NO production was measured in vessel incubation media. BK- and EPI-treated mesenteric arteries under regular Ca²⁺ conditions showed substantial amounts of NO production. In contrast, in the Ca²⁺-deprived vessels, BK is unable to induce NO increase; however, EPI is still cable to induce a discrete but sustained NO amount in the vessel under these conditions, in both conditions the induced NO production was blocked by pretreatment of the blood vessels with N^G-nitro-l-arginine methyl ester (l-NAME). B: cGMP accumulation was measured in homogenized vessels. BK as well as EPI-treated mesenteric arteries under regular Ca²⁺ conditions showed a large amount of cGMP. In Ca²⁺-deprived vessels, EPI is able to induce discrete increases in cGMP but BK does not. There is no cGMP increase in vessels pretreated with l-NAME. C: protein extracts from EPI or l-NAME plus EPI-treated and untreated mesenteric arteries under regular Ca²⁺ and Ca²⁺-deprived conditions were assessed by Western blot for VASP and p-VASP. Data are expressed as means ± SD (n = 3, and analyzed by t-test *P < 0.05).