Abluminal plasma induces vasoconstriction meditated by serotonin and counterbalanced by endothelial nitric oxide synthase in healthy and malarial mouse arteries

Table 1 and 2. Raw data for vascular function of middle cerebral arteries (MCAs) from ECM and control animals evaluated ex vivo using pressure myographyThis table contains raw internal and external diameter measurements of MCAs from experimental cerebral malaria (ECM) and uninfected control mice during stimulation with serotonin (5-HT), methacholine (MCh), and sodium nitroprusside (SNP). Diameter data are presented as percentage change from basal diameter values. Data include concentration–response values and individual biological replicates. Also, this table contains raw internal and external diameter measurements of MCAs from ECM and uninfected mice stimulated with MCh or SNP in the presence or absence of the NOS inhibitor L-NAME. Diameter data are presented as percentage change from basal diameter values. Data include concentration–response values and individual vessel replicates.Table 3. Raw data for plasma-induced vascular reactivity of aortic ringsThis table contains raw vascular tension measurements from aortic rings exposed to increasing concentrations (0.1%, 0.3%, 1%, and 3%) of plasma from ECM or uninfected control mice. Tension data are presented as variation from basal tension values. Data include individual replicate measurements obtained during concentration–response experiments.Table 4. Raw data for NOS-dependent modulation of plasma-induced vasoconstrictionThis table contains raw vascular tension measurements from aortic rings stimulated with plasma from ECM or uninfected mice in the presence or absence of the NOS inhibitor L-NAME. Tension data are presented as variation from basal tension values. Data include measurements obtained under KH buffer conditions and during plasma concentration–response experiments.Table 5. Raw data for calcium channel-dependent plasma-induced vasoconstrictionThis table contains raw vascular tension measurements from aortic rings stimulated with plasma from ECM or control mice during pharmacological inhibition of calcium signaling using nifedipine and EGTA. Tension data are presented as variation from basal tension values. Data include sequential measurements from individual experimental replicates.Table 6. Raw data for sex-independent 5-HT₂A-mediated plasma-induced vasoconstrictionThis table contains raw vascular tension measurements from male and female aortic rings stimulated with plasma from ECM or uninfected mice in the presence or absence of the 5-HT₂A receptor antagonist ketanserin following NOS inhibition with L-NAME. Tension data are presented as variation from basal tension values. Data include concentration–response values and individual biological replicates.Table 7. Raw data for vascular reactivity of aortic rings from ECM mice stimulated with plasmaThis table contains raw vascular tension measurements from aortic rings obtained from ECM and uninfected mice stimulated with serotonin (5-HT), acetylcholine (ACh), plasma from ECM or control animals, and L-NAME. Tension data are presented as variation from basal tension values. Data include concentration–response values and individual biological replicates.Table 8. Raw data for polarized vasoconstrictive responses to plasma and serotoninThis table contains raw internal diameter measurements of isolated 3rd order mesenteric arterioles following luminal or abluminal application of plasma or serotonin (5-HT). Diameter data are presented as percentage change from basal diameter values. Data include individual vessel responses and measurements obtained after acetylcholine (ACh) stimulation.