Biological effectsVIP elevates platelet cyclic AMP (cAMP) levels and inhibits in vitro platelet activation induced by platelet-activating factor (PAF)
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Cited by (53)
The specific VPAC2 agonist Bay 55-9837 increases neuronal damage and hemorrhagic transformation after stroke in type 2 diabetic rats
2013, NeuropeptidesCitation Excerpt :Thus, imposing vasodilation and hypotension by VPAC-2 receptor activation (Grant et al., 2006; Ishizuka et al., 1992; Nandha et al., 1991) to the brittle state of GK rat vasculature could have contributed to the negative effect on survival and stroke outcome in our study. Finally, since VIP has been previously reported to potently inhibit platelet-activating factor (PAF) (Cox et al., 1984), the reduced aggregation of thrombocytes by inhibiting the PAF could potentially contribute to brain hemorrhage and will require further scrutiny. In conclusion, our results show that daily systemic administration of the VPAC-2 receptor agonist Bay 55-9837 in type 2 diabetic GK rats, at a dose previously shown to induce insulin secretion, does not produce anti-diabetic efficacy.
Immune and inflammatory mechanisms in pulmonary arterial hypertension
2012, Progress in Cardiovascular DiseasesCitation Excerpt :Other actions may be mediated by inositol trisphosphate synthesis and calcium mobilization. Some of the actions of VIP include, but are not limited to, relaxation of vascular SMC,47 inhibition of PA-SMC proliferation in vitro,48 reduction of pulmonary vasoconstriction induced by endothelin,49 and antithrombotic effects.50 Genetic deletion of VIP results in overexpression of genes that promote pulmonary vascular SMC proliferation, downregulation of antiproliferative genes, as well as upregulation of pro-inflammatory genes51 suggesting a preponderant role of VIP in pulmonary vascular remodeling and inflammatory response in the setting of PAH.
Therapeutic targets in pulmonary arterial hypertension
2009, Pharmacology and TherapeuticsPACAP: A new player in thrombopoiesis
2008, BloodPathogenic mechanisms of pulmonary arterial hypertension
2008, Journal of Molecular and Cellular CardiologyCitation Excerpt :Downregulation of vasoactive intestinal peptide (VIP) may also play a pathogenic role. VIP is a pulmonary vasodilator, an inhibitor of proliferation of vascular smooth muscle cells, and an inhibitor of platelet aggregation [152,153]. Decreased concentrations of VIP have been reported in serum and lung tissue of patients with PAH [154].
Pathobiologic Mechanisms of Pulmonary Arterial Hypertension
2006, Pulmonary Vascular Disease