Animals ; Aorta, Thoracic ; physiology ; Dopamine ; pharmacology ; Hydrogen-Ion Concentration ; In Vitro Techniques ; Rats ; Vasoconstriction ; drug effects

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

Anesthetics, Intravenous ; pharmacology ; Animals ; Aorta, Thoracic ; drug effects ; physiology ; Endothelium, Vascular ; physiology ; Female ; In Vitro Techniques ; Male ; Norepinephrine ; pharmacology ; Potassium Channels ; physiology ; Propofol ; pharmacology ; Rabbits ; Vasodilation ; drug effects

AIMTo examine the effect of HO-1 inducer hemin on hydrogen peroxide (H2O2) caused decrease in contraction of isolated rat aortic rings, and to elucidate the underlying mechanism.

METHODSThe thoracic aortic rings with endothelium of male Sprague-Dawley rats were mounted on a bath system. Isometric contractions of aortic rings were measured.

RESULTS(1) After intraperitoneal injection of HO-1 inducer hemin, HO-1 activity of thoracic aorta and COHb concentration in rat blood enhanced. And it also prevented the decrease in contraction responses to PE which pretreatment of arteries with 300 micromol/L H2O2. (2) Pretreatment of ATP-sensitive potassium channel inhibitor glibenclamide, but not GC inhibitor methylene blue, could partly abolish the protection of hemin in arteries with H2O2 exposure. (3) Hemin could not influence the shift of concentration-response curve to [Ca2+]o in arteries with H2O2 exposure. (4) In Ca(2+) -free K-H solution, exposure of H2O2 reduced caffeine and PE-induced constriction in the rat aortic rings. After pretreatment of hemin, could prevent the decrease in contraction responses to caffeine and PE.

CONCLUSIONIncrease in HO-1 activity could prevent the H2O2 induced decrease in contraction responses to PE in intact aortic rings. The mechanism might be involved in activation of ATP-sensitive potassium channel and mobilization of intracellular calcium stores, but had no relationship with the GC pathway.

Animals ; Aorta, Thoracic ; drug effects ; physiology ; Endothelium, Vascular ; Heme Oxygenase-1 ; pharmacology ; Hydrogen Peroxide ; adverse effects ; KATP Channels ; drug effects ; Male ; Rats ; Rats, Sprague-Dawley ; Vasoconstriction ; drug effects

Retinoic acids may inhibit vascular smooth muscle cell proliferation, but may promote endothelial cell proliferation in cell culture. However, little data are available about the effects of all-trans-retinoic acid (ATRA) on endothelial regeneration and functional recovery in an experimental model of vascular injury. Accordingly, we investigated whether ATRA may attenuate neointima formation and accelerate endothelial regeneration with functional recovery in balloon-injured rat aorta. Twelve-week-old male Sprague-Dawley rats underwent endothelial denudation of the thoracic aorta by balloon injury. Fourteen rats were fed a standard rat pellet diet. Another 14 rats were fed ATRA (1.5 mg/day) for 2 weeks. The animals were killed on day 14 for organ chamber study and morphometric analysis. Rats in the ATRA group had a significantly improved acetylcholine-induced relaxation response than those in control group. However, endothelial independent response was not significantly different between the two groups. The extent of reendothelialization was markedly superior in the ATRA group compared with control group (p>0.05). Furthermore, neointima area and the ratio of neointima to medial area were significantly less in ATRA group than in control group (p>0.05). In conclusion, ATRA may accelerate endothelial regeneration with functional recovery, and attenuate neointima formation in balloon-injured rat aorta.
Acetylcholine/pharmacology ; Animal ; Aorta, Thoracic/physiology ; Aorta, Thoracic/injuries ; Aorta, Thoracic/drug effects* ; Balloon Dilatation/adverse effects ; Endothelium, Vascular/physiology ; Endothelium, Vascular/drug effects ; Male ; Muscle Relaxation/physiology ; Muscle Relaxation/drug effects ; Muscle, Smooth, Vascular/physiology ; Muscle, Smooth, Vascular/drug effects ; Rats ; Rats, Sprague-Dawley ; Regeneration/physiology ; Regeneration/drug effects ; Tretinoin/pharmacology* ; Tunica Intima/physiology ; Tunica Intima/pathology* ; Tunica Intima/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

OBJECTIVETo investigate the vascular effect of acute and chronic treatment of interferon-alpha (IFN-alpha) in rat aortic rings.

METHODSIsolated thoracic aortic rings were mounted on the organ bath and the tension of the vessel was recorded.

RESULTSIFN-alpha(10, 100, 1,000 and 10,000 U/ml) caused concentration -dependent relaxation of endothelium-intact aorta rings preconstricted with phenylephrine (PE,10(-6)mol/L), to(90.1+/-0.91)%, (65.1+/-5.21)%, (39.5+/-8.22)% and (35.3+/-8.27)% of pre-drug control, respectively. Removal of the endothelium inhibited the relaxation by IFN-alpha. The vasorelaxant effect of IFN-alpha (100 U/ml ) was attenuated by pretreatment with L-NAME (10(-4)mol/L), methylene blue (10(-5)mol/L) or AMG (10(-4)mol/L), to (97.2+/-5.34)%, (95.1+/-6.25)% and (93.7+/-8.82)% of the control, respectively. Pretreatment with IFN-alpha (1,000,000 U/d, i.p.) for five days markedly inhibited the endothelium-dependent relaxation of the aortic rings to acetylcholine. But the endothelium-dependent relaxation to acetylcholine was not changed by pretreatment of IFN-alpha (10,000 U/ml) with the isolated aorta rings for 2 h.

CONCLUSIONThe vasorelaxation induced by IFN-alpha in rat aorta rings is endothelium-dependent and is possibly mediated by inducible nitric oxide synthase. Chronic treatment of IFN-alpha may impair the endothelium or NO-sGC pathway.

Acetylcholine ; pharmacology ; Animals ; Aorta, Thoracic ; drug effects ; physiology ; Endothelium, Vascular ; physiology ; Guanylate Cyclase ; physiology ; Interferon-alpha ; pharmacology ; Male ; Nitric Oxide ; physiology ; Nitric Oxide Synthase ; physiology ; Nitric Oxide Synthase Type II ; Phenylephrine ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Vasodilation ; drug effects

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

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