Parameters from the maximum response (<i>R_max</i>) and agonist concentration that produced 50% of the maximum response (<i>EC₅₀</i>) for the ACh concentration-response curve in aortic rings from male and female rats in an intact endothelium (Control) and incubated with tetraethylammonium (TEA), aminopyridine (4-AP), iberiotoxin (IbTX), charybdotoxin (ChTX) and apamin.

<p>Results are expressed as the mean ± SEM; maximal effect (<i>R_max</i>); -log one-half <i>R_max (pEC₅₀</i>); male and female intact endothelium (Control); tetraethylammonium (TEA); 4-aminopyridine(4-AP); iberiotoxin (IbTX); charybdotoxin (ChTX); apamin; and <i>N</i>^G-nitro-L-arginine methyl ester (L-NAME). *P<0.05 (<i>pEC₅₀</i> of female <i>vs.</i> male rats) and †P<0.05 (<i>R_max</i> of female <i>vs.</i> male rats). Results are expressed as the mean ± S.E.M. Differences were analyzed using Student’s <i>t</i>-test, and P<0.05 was considered significant.</p><p>Parameters from the maximum response (<i>R_max</i>) and agonist concentration that produced 50% of the maximum response (<i>EC₅₀</i>) for the ACh concentration-response curve in aortic rings from male and female rats in an intact endothelium (Control) and incubated with tetraethylammonium (TEA), aminopyridine (4-AP), iberiotoxin (IbTX), charybdotoxin (ChTX) and apamin.</p

Acetylcholine (ACh) concentration-response curve for the aortic rings from male and female rats.

<p>Endothelium intact (Control) and 4-aminopyridine (4-AP 5 mM) curves (A); Difference of the area under curve (dAUC) control and 4-AP (B); Control and iberiotoxin (IbTX 30 nM) curves (C); dAUC control and IbTX (D); Control and apamin (0.5 µM) curves (E); dAUC control and apamin (F) and Control and charybdotoxin (ChTX 0.1 µM) curves (G); dAUC control and ChTX (H). <i>R_max</i> *P<0.05, male vs. female 4-AP, IbTX, Apamin and ChTX incubations. *P<0.05, dAUC male vs. female. Student’s <i>t</i>-test. Number of animals used is indicated in parentheses.</p

Effect of losartan (10 µM) (A, B) and enalapril (10 µM) (C, D) on the concentration-response curves to phenylephrine in endothelium-intact aortic segments from untreated (CT) and lead-treated rats (Pb⁺²).

<p>Densitometry analyses of the western blots for receptors AT₁ (E) and AT₂ (F) in aortas from untreated (CT) and lead-treated rats (Pb⁺²). Representative blots are also shown.*P<0.05 by Student's <i>t-</i>test. Number of animals used is indicated in parentheses.</p

Angiotensin converting enzyme (ACE) activity (nmol His-Leu/min) in plasma; correlation between systolic arterial blood pressure and ACE activity (nmol His-Leu/min) in plasma of control and lead-treated rats (r = 0.787, P<0.05).

<p>*P<0.05 by Student's <i>t-</i>test. Number of animals used is indicated in parentheses.</p

The effects of seven-day exposure to lead acetate on the concentration-response curves to phenylephrine (A), acetylcholine (B) and sodium nitroprusside (NSP; C) treatment in aortic rings.

<p>*P<0.05 by Student's <i>t-</i>test. Number of animals used is indicated in parentheses.</p

Superoxide anion production in papillary muscle of SHAM, Ovariectomized (OVX), Ovariectomized plus carvedilol (OVX+CAR) at 60 days postsurgery.

<p>The values are expressed as the means ± S.E.M. * Significantly different from SHAM and # from OVX (<i>p</i><0.05) using one-way ANOVA and Tukey post hoc test.</p

Effects of aminoguanidine, TEA, losartan and enalapril on the vascular responses to phenylephrine (R_max and pD₂) in aortas from untreated and lead-treated rats.

<p>Results are expressed as mean ± SEM of the number of animals shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0017117#pone-0017117-g003" target="_blank">Figs. 3</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0017117#pone-0017117-g005" target="_blank">5</a> ; R_max, maximal effect (expressed as a percentage of the maximal response induced by 75 mM KCl); pD₂, −log one-half R_max; AG; aminoguanidine, TEA; tetraethylammonium, losartan, enalapril. P<0.05 <i>vs.</i> untreated control rats (^#) and lead-treated control rats (*).</p

The effects of endothelium removal (E⁻) (A, B) and <i>N</i>^G-nitro-L-arginine methyl ester (L-NAME, 100 µM) (D, E) on the concentration-response curve for phenylephrine treatment in aortic rings from untreated (CT) and lead-treated rats (Pb⁺²).

<p>The inset shows differences in area under the concentration-response curves (dAUC) in endothelium–denuded and intact segments (C) and in the presence and absence of L-NAME (F). Densitometry analyses of western blots for endothelial nitric oxide synthase (eNOS) and phosphorylated endothelial nitric oxide synthase (p-eNOS) protein expression in aortas from untreated (CT) and lead-treated rats (Pb⁺²) (G). Representative blots are also shown. *P<0.05 by Student's <i>t-</i>test. Number of animals used is indicated in parentheses.</p

Potassium-induced relaxation in aortic rings from untreated (CT) and lead-treated (Pb⁺²) rats previously incubated in a K⁺-free medium and contracted with phenylephrine before and after incubation with 100 µM ouabain (A).

<p>Densitometry analyses of the western blots for the alpha-1 subunit (B) and alpha-2 subunit (C) in aortas from untreated (CT) and lead-treated rats (Pb⁺²). Representative blots are also shown. *P<0.05 (CT <i>vs.</i> Pb⁺²) by Student's <i>t-</i>test or two-way ANOVA followed by a Bonferroni test. ^#P<0.05 (CT OUA <i>vs.</i> Pb⁺² OUA) by two-way ANOVA followed by a Bonferroni test. Number of animals used is indicated in parentheses.</p

Left ventricular collagen content.

<p>The data is expressed as the mean ± S.E.M. * <i>p</i><0.05 vs. SHAM rats. # <i>p</i><0.05 vs. OVX rats using one-way ANOVA and Tukey post hoc test. Number of animals in indicated in parenthesis.</p