ABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of dietary capsaicin in activating transient receptor potential vanilloid 1 (TRPV1) and thus influencing the vascular dysfunction mediated by high-fat diet and the potential mechanisms.</p><p><b>METHODS</b>A total of 80 male C57BL/6J mice aged 10 weeks were equally divided into four groups, in which the mice were fed with normal diet (ND), normal diet plus capsaicin (NC), high-fat diet (HD), or high-fat diet plus capsaicin (HC) for 20 weeks. Tail-cuff blood pressure (BP), vascular function of mice aortic rings, expressions of voltage-gated potassium-channel Kv1.4, RhoA and Rho kinase in aorta were examined.</p><p><b>RESULTS</b>Compared with ND group, both nitroglycerin [(18.9 +/- 13)% vs. 100%, P < 0.01] and acetylcholine [(26 +/- 12)% vs. 100%, P < 0.01] induced vasorelaxation of aortic rings were significantly reduced in HD group. Both endothelium dependent and independent aortic rings vasorelaxation in HC group were significantly improved compared with that in HD group [acetylcholine: (69 +/- 15)%; nitroglycerin: (46.5 +/- 6)%, P < 0.05], but still reduced compared with that in ND group (P < 0.05, P < 0.01). High fat diet induced the expression of RhoA and Rho kinase. Dietary capsaicin down-regulated the expression of RhoA and Rho kinase but up-regulated the expression of Kv1.4 in aorta in mice fed with normal or high fat diet (all P < 0.05).</p><p><b>CONCLUSION</b>Dietary capsaicin can ameliorate vasorelaxation dysfunction mediated by high-fat diet. The potential mechanisms may be related with TRPV1 activation, which in turn stimulates potassium channel and inhibits RhoA and Rho kinase in the vasculature.</p>
Subject(s)
Animals , Male , Mice , Aorta , Metabolism , Physiology , Capsaicin , Pharmacology , Diet, High-Fat , Endothelium, Vascular , Metabolism , Physiology , Mice, Inbred C57BL , TRPV Cation Channels , Vasodilation , Physiology , rho-Associated Kinases , Metabolism , rhoA GTP-Binding Protein , MetabolismABSTRACT
<p><b>AIM</b>To investigate the influence of L-arginine (NO donors, L-Arg) on spontaneous contractions of ileum in mice and study the effects of activation of beta-adrenoceptor on NO-induced inhibition in spontaneous contractions of ileum.</p><p><b>METHODS</b>The method of spontaneous contractions recording was used to investigate the effect of L-NNA, ODQ, Isoprenaline( beta-adrenoceptor agonist) and Propranolol (beta-adrenoceptor antagonist) on NO-induced inhibition in spontaneous contractions of ileum.</p><p><b>RESULTS</b>(1) L-Arg inhibited the spontaneous contractions of ileum and had concentration-response relationship. (2) L-NNA (3 x 10(-4) mol/L), ODQ (3 x 10(-6) mol/L) relieved the inhibitory effect of L-Arg in ileum . (3) Propronalol (3 x 10(-6) mol/L) decreased significantly the inhibitory effect of L-Arg. (4) Iso (1 x 10(-7) mol/L) increased the inhibitory effect of L-Arg. After Iso (1 x 10(-7) mol/L) and Propronalol (3 x 10(-6) mol/L) being coapplied, the inhibitory effect of L-Arg was not changed.</p><p><b>CONCLUSION</b>NOS catalyzed L-Arg and produced NO. NO exerted its inhibitory effect by the cGMP pathway, the activation of beta-adrenoceptor was partly involved in NO-induced relaxation in ileum.</p>
Subject(s)
Animals , Mice , Arginine , Pharmacology , Ileum , Physiology , Mice, Inbred Strains , Muscle Contraction , Physiology , Nitric Oxide , Receptors, Adrenergic, beta , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the renin-angiotensin system (RAS) in mesenteric adipose tissues and effect of angiotensin II on adipocyte differentiation.</p><p><b>METHODS</b>Thirty normal 8-week-old male Wistar rats were divided into groups on normal diet and high-fat diet. The rats on high-fat diet for 24 weeks developed the metabolic syndrome respectively. The mRNA and protein expression of mesenteric adipose tissue were measured by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Lipid drop in 3T3-L1 preadipocytes and mature adipocytes were observed using oil-red O staining. The fluorescence microscope was used to detect cytosolic-free calcium in 3T3-L1 preadipocytes and mature adipocytes.</p><p><b>RESULTS</b>The expressions of angiotensinogen, angiotensin converting enzyme, angiotensin II receptor type 1 in mesenteric adipose tissue were significantly increased in rats with metabolic syndrome compared with those in rats on normal diet (P <0. 05, P <0. 01). After administration of angiotensin II , no lipid droplet in 3T3 -L1 preadipocytes and adipocytes were observed, however, intensive lipid droplet in adipocyte was found after administration of captopril and candesartan. Angiotensin II increased the intracellular-free calcium concentration in preadipocytes (P < 0. 01 ) , which was blocked by captopril and candesartan; in contrast, angiotensin II effect was blunt in mature adipocyte. Captopril and candesartan partially recovered the angiotensin II -mediated increase of cytosolic-free calcium.</p><p><b>CONCLUSION</b>RAS in the mesenteric adipose tissues is active in rats with metabolic syndrome, and antagonization of RAS can recover the lipogenesis of adipocyte.</p>