AIMTo investigate the mechanisms of vasodilatation of plant-derived estrogen biochanin A.

METHODSIsolated aortic ring preparations from Sprague-Dawley rats were suspended in individual organ baths. The tension was measured isometrically.

RESULTSBiochanin A at the range of 10(-9)-10(-4) mol/L provoked concentration-dependent and endothelium-independent relaxation of the rings constricted by phenylephrine (10(-5) mol/L). Biochanin A caused concentration-dependent relaxation of denuded rings precontracted with KCl (6 x 10(-2) mol/L). Glibenclamide (3 x 10(-6) mol/L), a selective inhibitor of ATP-sensitive potassium channels, and tetraethylammonium (5 x 10(-3) mol/L), a Ca2+ -activated K+ channel inhibitor, significantly attenuated the relaxation induced by biochanin A. The vasoconstriction induced by phenylephrine was decreased by biochanin A in Ca2+ -free medium.

CONCLUSIONThe endothelium-independent relaxation of thoracic aorta induced by biochanin A might be mediated by ATP-sensitive K+ channels, Ca2+ -activated K+ channels and intracellular Ca2+ release from sarcoplasmic reticulum.

Animals ; Aorta, Thoracic ; drug effects ; physiology ; Genistein ; pharmacology ; In Vitro Techniques ; KATP Channels ; metabolism ; Male ; Muscle, Smooth, Vascular ; drug effects ; physiology ; Rats ; Rats, Sprague-Dawley ; Vasodilation ; drug effects

OBJECTIVETo 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.

METHODSA 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.

RESULTSCompared 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).

CONCLUSIONDietary 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.

Animals ; Aorta ; drug effects ; metabolism ; physiology ; Capsaicin ; pharmacology ; Diet, High-Fat ; adverse effects ; Endothelium, Vascular ; metabolism ; physiology ; Male ; Mice ; Mice, Inbred C57BL ; TRPV Cation Channels ; drug effects ; Vasodilation ; drug effects ; physiology ; rho-Associated Kinases ; metabolism ; rhoA GTP-Binding Protein ; metabolism

OBJECTIVETo investigate the effect of betulinic acid (BA) on relaxation in isolated rat aortic rings and its antioxidant property on oxidative stress of blood vessels.

METHODSAortic rings were isolated and BA was cumulatively added into organ bath. Isometric tension of endothelium intact or endothelium denuded thoracic aortic rings previously contracted by phenylephrine (PE) was recorded. Then aortic rings were randomly divided into normal control group, BA control group, H(2)O(2) group and BA+H(2)O(2) group, after being previously contracted by PE, isometric tension of endothelium-dependent relaxation induced by Ach was recorded.

RESULTExposure of intact endothelium rings previously contracted by PE to BA at the concentrations of 10(-7) mol/L-10(-4) mol/L evoked a significant concentration dependent relaxation, which was inhibited by pretreatment with N omega-nitro-L-arginine methyl ester (L-NAME, 10(-4)mol/L), but not by indometacin (10(-5)mol/L). The pD2 value of BA was 5.24 ± 0.04, and the EC(50)value was 2.45 x 10(-6)mol/L. Exposure of endothelium denuded rings previously contracted by PE to BA did not affect the relaxation in isolated aortic rings. ACh induced a dose-dependent relaxation that was weakened by pretreatment with H(2)O(2) (5 10(-4) mol/L) for 15 min. The EC(50) of BA markedly attenuated the inhibition of relaxation induced by H(2)O(2).

CONCLUSIONBA can evoke a concentration-dependent relaxation in aortic rings previously contracted by PE, which may be mediated by NO. And the decrease of endothelium-dependent relaxation in rat aortic rings exposed to H(2)O(2) can be markedly attenuated by BA, which may be mediated by reducing oxidative stress and maintaining the activity of NO in aortic rings.

Animals ; Aorta ; drug effects ; metabolism ; physiology ; Endothelium, Vascular ; drug effects ; metabolism ; physiology ; Hydrogen Peroxide ; pharmacology ; In Vitro Techniques ; Nitric Oxide ; metabolism ; Oxidative Stress ; drug effects ; Rats ; Rats, Sprague-Dawley ; Triterpenes ; pharmacology ; Vasodilation ; drug effects ; Vasodilator Agents ; pharmacology

OBJECTIVETo investigate the effect of gastrodin in relaxing isolated thoracic aorta rings in rats and discuss its possible mechanism.

METHODIsotonic tension of isolated thoracic aortic rings in rats with norepineprine (NE) and KCl was recorded to observe the vasodilatory effect of gastrodin and the influence of various drugs on it.

RESULTGastrodin had the effect in relaxing thoracic aortas with or without endothelium, and there was no significant difference. NG-nitro-L-argininemethylester (L-NAME, 1 x 10(-4) mol x L(-1)), methylene blue (MB, 1 x 10(-5) mol x L(-1)), indomethacin (INDO, 1 x 10(-5) mol x L(-1)) had no effect on the vasodilation action of gastrodin on thoracic aortas precontracted by NE. 4-aminopyrimide (4-AP, 1 x 10(-4) mol x L(-1)), tetrathylamonium (TEA, 1 x 10(-3) mol x L(-1)), BaCl2 (1 x 10(-4) mol x L(-1)) and glibenclamide (Gli, 1 x 10(-5) mol x L(-1)) could inhibit gastrodin's effect in relaxing thoracic aorta rings. In the absence of Ca2+, pre-incubated gastrodin showed a notable inhibitory effect in relaxing NE contraction.

CONCLUSIONGastrodin shows a dose-dependent and endothelium-independent effect in relaxing rat isolated thoracic aorta rings. The mechanism is related to K+ channel, inhibition of release of Ca+ stored in endoplasmic reticulum of vascular smooth muscle cells and inflow of external calcium Ca2+.

Animals ; Aorta, Thoracic ; drug effects ; physiology ; Benzyl Alcohols ; pharmacology ; Calcium ; metabolism ; Endothelium, Vascular ; physiology ; Glucosides ; pharmacology ; In Vitro Techniques ; Male ; Norepinephrine ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Vasodilation ; drug effects

OBJECTIVETo study the effect of gastrodin on isolated thoracic aorta rings of rats and to investigate the potential mechanism.

METHODSA perfusion model of isolated thoracic aorta rings of rats was applied. The effect of cumulative gastrodin (5, 50, 100,150, 200, and 250 μmol/L) on endothelium-intact aorta rings was investigated. The same procedure was applied to observe the effect of gastrodin on endothelium-intact/denuded aorta rings pre-contracted with 10(-6) mol/L phenylephrine hydrochloride (PE). The aorta rings incubated by 200 mmol/L gastrodin in the Ca(2+)-free (K-H) solution was contracted by using PE. The effect of 200 mmol/L gastrodin on endothelium-denuded aorta rings pre-contracted with 60 mmol/L KCl was also observed.

RESULTSCompared with the denuded gastrodin group, the intact gastrodin group could significantly relax the PE-contracted aorta rings (P<0.01). In Ca(2+)-free (K-H) solution KHS, the PE-induced contraction rate of aorta rings pre-incubated by gastrodin was 6.5%±0.7%, which was significantly less than the control group (11.8%±0.9%,P<0.01). However, after 3 mmol/L CaCl2 was added, the Ca(2+)-induced contraction in the gastrodin group (51.7%±2.4%) was similar to that in the control group (49.8%±2.8%). The contractile rate of rings in the KCl-contracted gastrodin group (96.3%±0.6%) was not significantly different from that in the control group (96.8%±1.2%).

CONCLUSIONSGastrodin has the effect of vasorelaxation on isolated thoracic aorta rings of rats. The mechanism of the vasorelaxation of gastrodin may mainly work through the inhibition of inositol 1, 4, 5-trisphosphosphate receptor on the sarcoplasmic reticulum of the arterial smooth muscle, which leads to the reduction of the Ca(2+) released from the sarcoplasmic reticulum.

Animals ; Aorta, Thoracic ; drug effects ; physiology ; Benzyl Alcohols ; pharmacology ; Calcium ; metabolism ; Endothelium, Vascular ; physiology ; Female ; Glucosides ; pharmacology ; In Vitro Techniques ; Male ; Phenylephrine ; pharmacology ; Rats ; Rats, Wistar ; Vasodilation ; drug effects

OBJECTIVECrassostrea gigas oyster extract has been reported to have antioxidant, antihypertensive and lipid-lowering properties that may be useful for treating cardiovascular diseases. This study aimed to evaluate the effect of C. gigas oyster extract on cardiovascular function in tissues from healthy rats.

METHODSSingle-cell microelectrode and isolated thoracic aortic organ bath studies were performed on tissues from 8-week-old healthy Wistar rats, using varying concentrations of C. gigas oyster extract. To elucidate a mechanism of action for the oyster's vasoactive properties, concentration response curves were carried out in the presence of a calcium channel inhibitior (verapamil), a nitric oxide synthase inhibitor (N(G)-nitro-L-arginine methyl ester), a potassium channel inhibitor (4-aminopyridine), in addition to the α-adrenoceptor inhibitor prazosin.

RESULTSOyster solution at 7 500 mg/mL inhibited noradrenaline-induced contraction in isolated aortic rings. Cardiac electrophysiology results showed that neither concentration of oyster solution was able to significantly reduce action potential duration at all phases of repolarisation in left ventricular papillary muscles from healthy animals.

CONCLUSIONWhen administered to healthy vascular tissue, C. gigas oyster extract inhibits contraction induced by noradrenaline. This effect is likely to be mediated through α-adrenoceptor inhibition, and to a lesser extent, calcium modulating activity.

Action Potentials ; drug effects ; Adrenergic alpha-Antagonists ; pharmacology ; Animals ; Aorta, Thoracic ; drug effects ; physiology ; Calcium ; metabolism ; Crassostrea ; Heart ; drug effects ; physiology ; Male ; Norepinephrine ; antagonists & inhibitors ; pharmacology ; Rats ; Rats, Wistar ; Vasoconstriction ; drug effects

OBJECTIVETo investigate the vasorelaxation effect of crocetin (CCT) and its mechanism.

METHODSIsolated aortic rings from Sprague-Dawley rats were mounted in the organ bath system. The tension of the aorta was recorded.

RESULTCCT significantly provoked concentration-dependent relaxation in both endothelium-intact and-denuded aortic rings pre-constricted by phenylephrine (10⁻⁵ mol/L), and the vasorelaxation in endothelium-intact aortic rings was stronger than that in endothelium-denuded ones. CCT had no significant effects on aortic rings pre-constricted with KCl (6 × 10⁻² mol/L). Pretreatment with eith L-NAME (10⁻⁴ mol/L), an inhibitor of nitric oxide synthase (NOS), or indomethacin (10⁻⁵ mol/L), an inhibitor of cyclooxygenase, for 30 min significantly attenuated the relaxation of endothelium-intact aortic rings induced by CCT. Besides, both tetraethylammonium (a Ca²(+)-activated K(+) channel inhibitor, 5 × 10⁻³ mol/L) and 4-aminopyridine (a voltage-sensitive K(+) channel inhibitor, 10⁻³ mol/L), but not the ATP-sensitive K(+) channel inhibitor glibenclamide (3 × 10⁻⁶ mol/L), significantly attenuated CCT-induced relaxation in endothelium-denuded aortic rings.

CONCLUSIONCCT had partial endothelium-dependent relaxation in rat aortas, which may be mediated by activating the endothelial NOS-NO and cyclooxygenase-prostacyclin pathways. The endothelium-independent relaxation in rat aortas induced by CCT may be mediated by Ca²(+)-activated K(+) channels and voltage-sensitive K(+) channels.

Animals ; Aorta, Thoracic ; drug effects ; metabolism ; physiology ; Carotenoids ; pharmacology ; Endothelium, Vascular ; drug effects ; metabolism ; In Vitro Techniques ; Male ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Phenylephrine ; pharmacology ; Potassium Channel Blockers ; metabolism ; Rats ; Rats, Sprague-Dawley ; Vasodilation ; drug effects ; Vasodilator Agents ; pharmacology

AIMTo investigate the action of anions and anion channel blockers in the regulation of vascular contraction induced by norepinephrine (NE).

METHODSNE-induced contraction was observed in rat aorta by using routine blood vascular perfusion in vitro.

RESULTSThe anion channel blockers niflumic acid (NFA) and 5-nitro-2-(3-phenoxylpropylamino)-benzoic acid (NPPB) produced inhibitory effects on NE-evoked contractions in the aorta. NE-induced contraction was not significantly changed after the extracellular Na+ was replaced by choline, in contrast, the vascular was relaxed when the extracellular Cl- was replaced by glutamate. Moreover, the vasoconstriction induced by NE was further enhanced with the replacement of the extracellular Cl- by Br-, which was still sensitive to either NFA or NPPB.

CONCLUSIONSAnion channels play an important role in the regulation of blood vascular tone, which may be responsible for the salt-sensitivity hypertension.

Animals ; Anions ; metabolism ; Aorta ; drug effects ; physiology ; In Vitro Techniques ; Ion Channels ; antagonists & inhibitors ; Male ; Muscle Contraction ; drug effects ; physiology ; Muscle, Smooth, Vascular ; drug effects ; physiology ; Norepinephrine ; pharmacology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo examine the effect of puerarin on high glucose-induced decrease in contraction of isolated rat aortic rings, and to elucidate its underlying mechanism.

METHODSThe thoracic aortic rings with or without endothelium of male Sprague-Dawley rats were mounted on a bath system. Isometric contractions of aortic rings were measured. The activity of heme oxygenase-1 (HO-1) was also measured.

RESULTS(1) After incubation with 44 mmol/L of glucose (high glucose) for 4 h, the vascular contraction responses to phenylephrine (PE) decreased in an endothelium-dependent manner, when compared with the control group (containing 11 mmol/L of glucose). (2) After coincubation with puerarin ( 10(-10) - 10(-8) mol/L) and high glucose, the decrease in contraction responses to PE of arteries was partly inhibited in a dose-dependent manner. (3) After incubation with puerarin for 4 h, the HO-1 activity of thoracic aorta increased; ZnPP, an inhibitor of HO-1, abrogated the protection effect of puerarin.

CONCLUSIONPuerarin could prevent the high glucose-induced decrease in contraction responses to PE in intact aortic rings. The mechanism might be involved in the activation of HO-1.

Animals ; Aorta, Thoracic ; drug effects ; physiology ; Glucose ; pharmacology ; Heme Oxygenase (Decyclizing) ; metabolism ; In Vitro Techniques ; Isoflavones ; pharmacology ; Male ; Rats ; Rats, Sprague-Dawley ; Vasoconstriction ; drug effects ; Vasodilator Agents ; pharmacology

OBJECTIVETo study the effects of iptakalim (IPT) on pressure-overload induced cardiac remodeling in rats, and investigate correlation between this protection effects and plasma PGI2 content.

METHODThe pressure-overload induced cardiac remodeling model was induced by abdominal aorta constriction for 6 weeks, and the rats were divided into 5 groups repectively: (1) sham group, (2) control group, (3) IPT 3 mg/kg group (IPT 3), (4) indomethacin 2 mg/kg group (Indo 2), (5) indomethacin 2 mg/kg + IPT 3 mg/kg group (Indo 2 + IPT 3). RM6000 eight channel physiological recorder was used to record haemodynamics index, heart weight was weighed and the cardiac remodeling index was calculated, HE stain and Masson's stain were employed to perform histological analysis, colorimetric method was used to detect the hydroxyproline content in cardiac tissue, radioimmunological method was used to measure the plasma PGI2 content.

RESULTSAfter 42 days of aortic banding, the hyperdynamic circulation state, cardiac remodeling and decreased plasma PGI2 content were observed in the model group compared with those in the sham group, which were effectively reserved by treatment with IPT 3 mg/kg. Single-use indomethacin led to further deterioration of this pathophysiological changes, however, combination administration of IPT 3 mg/kg prevented these from worsening characteristic by ameliorating hyperdynamic circulation state and cardiac remodeling, augmnent plasma PGI2 content.

CONCLUSIONIPT can significantly reverse abdominal aorta binding/pressure-overload induced cardiac remodeling, its mechanism may contribute to binding K(ATP) channel in endothelial cells, ameliorating endothelium cells function, augmenting PGI2 synthesis and secretion.

Animals ; Aorta, Abdominal ; surgery ; Constriction ; Endothelium, Vascular ; metabolism ; physiology ; Epoprostenol ; blood ; Hypertension ; blood ; physiopathology ; KATP Channels ; drug effects ; Male ; Propylamines ; pharmacology ; Rats ; Ventricular Remodeling ; drug effects