Abstract
It has been previously demonstrated that inflammation in adipose tissue may be implicated in vascular dysfunction (Circulation 2009; 119(12):1661–1670). In particular, adipocytes secrete adiponectin, a physiological modulator of local vascular tone through an increased nitric oxide bioavailability. This capacity is lost in obesity by the development of adipocyte hypertrophy, leading to hypoxia, inflammation, and oxidative stress. Aim of the study was to investigate the feasibility a pharmacological modulation of the concerned effect in an animal model (Wistar-Kyoto normotensive rats: WKY). Materials and Methods: We investigated 25 WKY of 12 weeks of age. Mesenteric small resistance arteries were dissected and mounted on a wire myograph, according to Mulvany-Halpern technique (internal diameter about 200 μm). A concentration-response to norepinephrine (NE, from 10–9 to 10–5 Mol/l) was evaluated in the following conditions: 1) in vessels with intact prerivascular fat tissue (WF); 2) in vessels in which perivascular fat tissue was removed (NoF); 3) in WF vessels kept in hypoxic condition (no oxygen supply) (WF + Hyp); 4) in NoF vessels kept in hypoxic condition (NoF + Hyp); 5) in WF + Hyp vessels incubated with telmisartan 10–2 Mol/l for 3 hour (WF + Hyp + Telm); 6) in WF + Hyp vessels incubated with captopril 10–2 Mol/l for 3 hour (WF + Hyp + Capt). Results are summarized in the figure (active media stress: KPa, mean of two vessels for each rat).A significantly greater reactivity to NE was observed in NoF vessels compared with WF vessels (ANOVA p = 0.003 between curves), confirming previous observations. This increased reactivity is similar to that observed in WF + Hyp (ANOVA p = NS between, NoF and WF + Hyp), therefore hypoxia seems to abolish the anti-vasoconstrictor effects of perivascular fat. Captopril was able to completely prevent the effect of hypoxia (ANOVA p < 0.05 between WF + Hyp and WF + Hyp + Capt), while telmisartan had a very modest effect. In conclusion, the ACE inihibitor captopril, but not the angiotensin-receptor blocker telmisartan, seems to be able to restore the anti-contractile effects of perivascular fat tissue lost after hypoxia, possibly through an increased bradykinin activity.
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