1. Endogenous antimicrobial peptide LL-37 induces human vasodilatation†
I. Berkestedt, A. Nelson, M. Bodelsson 
British Journal of Anaesthesia 
Volume 100, Issue 6, Pages (June 2008)
DOI: /bja/aen074
Copyright © 2008 British Journal of Anaesthesia Terms and Conditions

2. Fig 1
Representative recorder tracings illustrating the effect of LL-37 on isolated human omental artery (a) and vein segments (b and c) precontracted with ET-1 (ET). Log molar concentrations are indicated. LL-37 induced no or only weak relaxations in the artery segments (a). In vein segments with intact endothelium, LL-37 induced a relaxation (b), while no or only weak relaxations were induced in endothelium-denuded segments (c). The experiments shown were performed on segments with a comparatively fast response to LL-37 enabling full concentration–response experiments to be performed.
British Journal of Anaesthesia  , DOI: ( /bja/aen074)
Copyright © 2008 British Journal of Anaesthesia Terms and Conditions

3. Fig 2
Endothelium dependency of the relaxation induced by LL-37 in isolated human omental vein segments precontracted by a submaximal concentration of ET-1. The LL-37-induced relaxation was markedly reduced after removal of the endothelium (*, two-way repeated measurement anova for the factors LL-37 concentration and endothelium removal followed by Dunnett's post hoc test). Values are means+sem, n=5.
British Journal of Anaesthesia  , DOI: ( /bja/aen074)
Copyright © 2008 British Journal of Anaesthesia Terms and Conditions

4. Fig 3
Relaxation induced by LL-37 in isolated segments of human omental vein precontracted by a submaximal concentration of ET-1 in the absence or presence of the nitric oxide synthase inhibitor, Nω-nitro-l-arginine methyl ester (l-NAME, 0.3 mM), potassium chloride (30 mM), or both to inhibit hyperpolarization. l-NAME inhibited the LL-37-induced relaxation by about 30% whereas KCl nearly abolished the LL-37-induced relaxation. Values are means+sem, n=8–11. Asterisk indicates statistically significant difference from control (two-way repeated measurement anova for the factors LL-37 concentration and l-NAME, KCl or both treatment followed by Dunnett's post hoc test).
British Journal of Anaesthesia  , DOI: ( /bja/aen074)
Copyright © 2008 British Journal of Anaesthesia Terms and Conditions

5. Fig 4
Relaxation induced by the ALX agonist, WKYMVm (WKY; n=6) or LL-37 (n=5) in isolated segments of human omental vein precontracted by a submaximal concentration of ET-1 in the absence or presence of the selective ALX antagonist WRWWWW (WRW4; 10 μM). WRW4 inhibited the relaxation in response to both WKY and LL-37 (*, two-way repeated measurement anova for the factors WKY or LL-37 concentration and WRW4 treatment followed by Dunnett's post hoc test). Values are means±sem.
British Journal of Anaesthesia  , DOI: ( /bja/aen074)
Copyright © 2008 British Journal of Anaesthesia Terms and Conditions

6. Fig 5
Representative recorder tracings illustrating the effect of LL-37 and substance P (SP, 100 nM) on isolated human omental vein segments precontracted with ET-1 (ET) in the presence (a) or absence (b) of the ALX antagonist WRWWWW (WRW4). Log molar concentrations are indicated. LL-37 induced a relaxation in the control segment (b), whereas no relaxation was induced in the presence of WRW4 (a). SP, however, induced a similar relaxation in the presence and absence of WRW4.
British Journal of Anaesthesia  , DOI: ( /bja/aen074)
Copyright © 2008 British Journal of Anaesthesia Terms and Conditions

7. Fig 6
Representative agarose gel of RT–PCR products generated from RNA isolated from a vein segment with (+) or without (−) endothelium. Removal of the endothelium reduced the amount of the ALX transcript. The RT–PCR product using the primers for glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and a size marker scribed in base pairs (bp) are also shown.
British Journal of Anaesthesia  , DOI: ( /bja/aen074)
Copyright © 2008 British Journal of Anaesthesia Terms and Conditions