scholarly journals Vasorelaxant Effect Induced by the Essential Oil of Ocotea duckei Vattimo Leaves and Its Main Constituent, Trans-caryophyllene, in Rat Mesenteric Artery

Author(s):  
Tays Amanda Felisberto Gonçalves ◽  
Renildo Moura da Cunha ◽  
Dionatas Ulises de Oliveira Meneguetti ◽  
Marcio Roberto Viana Santos ◽  
José Maria Barbosa- Filho ◽  
...  

Aims: To evaluate the vasorelaxant effect induced by the essential oil of the leaves of O. duckei Vattimo (ODEO) and its main constituent, trans-caryophyllene, in rat superior mesenteric arteries. Methodology: Isolated rat superior mesenteric rings were suspended by cotton threads for isometric tension recordings in Tyrode’s solution at 37ºC, gassed with 95% O2 and 5% CO2 and different ODEO concentrations (0.1-300 μg/mL) or trans-caryophyllene (1-1000 μg/mL) were added cumulatively to the organ baths. Results: Vasorelaxant effect induced by the essential oil of Ocotea duckei leaves (ODEO) and its main constituent, trans-caryophyllene (60.54 %), was evaluated in this work. In intact isolated rat superior mesenteric rings ODEO (0.1-300 μg/mL, n=6) induced concentration-dependent relaxation of tonus induced by phenylephrine (10 µM) or K+-depolarizing solution (KCl 80 mM) (IC50=31±5, 5±0.4 µg/mL, respectively, n=6). The relaxations of phenylephrine-induced contractions were not significantly attenuated after removal of the vascular endothelium (IC50=25±5 µg/mL). ODEO antagonized the concentration-response curves to CaCl2 (10-6-3x10-2 M) and Bay K 8644 (10-10-3x10-6 M). Furthermore, in nominally without calcium solution, ODEO significantly inhibited, in a concentration-dependent manner, transient contractions induced by 10 µM phenylephrine or 20 µM caffeine. Trans-caryophyllene induced vasorelaxations, however, this effect was 18.6 times less potent when compared to ODEO-induced vasorelaxations. Conclusion: The relaxant effect induced by ODEO in rat superior mesenteric artery rings is endothelium-independent and seems to be related to both, inhibition of Ca2+ influx through L-type voltage-gated Ca2+-channels sensitive to dihydropyridines and inhibition of the calcium release from intracellular IP3-and caffeine-sensitive stores.

2012 ◽  
Vol 40 (02) ◽  
pp. 309-320 ◽  
Author(s):  
Li-Li Gong ◽  
Lian-Hua Fang ◽  
Hai-Lin Qin ◽  
Yang Lv ◽  
Guan-Hua Du

The aim of the present study was to evaluate the vasorelaxant effects of coptisine and its possible mechanisms in isolated rat aortic rings. Coptisine was evaluated on isolated rat aortic rings precontracted with norepinephrine (NE) and KCl. The mechanisms were evaluated in the presence or absence of specific pharmacological inhibitors. Coptisine (1 ~ 200 μM) relaxed NE (1 μM) or KCl (60 mM) induced sustained contraction with pEC50 values of 4.49 ± 0.48 and 4.85 ± 0.57 in a concentration dependent manner. Pretreatment with coptisine (10, 50 or 100 μM) also inhibited concentration-response curves to NE and KCl. The vasorelaxant effect of coptisine was attenuated significantly by endothelium removal, and incubation with Nω-nitro-L-arginine methyl ester (L-NAME, 100 μM), methylene blue (10 μM) and indomethacin (5 μM) partially reduced the vasorelaxant effect of coptisine. In endothelium-denuded rings, the vasorelaxant effect of coptisine was reduced significantly by 4-aminopyridine (4-AP, 100 μM), but not glibenclamide (10 μM) ortetraethylammonium (TEA, 5 mM). Coptisine also reduced NE-induced transient contraction in Ca2+ -free solution, and inhibited contraction induced by increasing external calcium in Ca2+ -free medium plus 60 mM KCl. It was concluded that coptisine induced both endothelium-dependent and -independent relaxation in rat aortic rings. The NO-cGMP mediated pathway may be involved in the endothelium-dependent relaxation and in the activation of voltage-dependent K+ channels, contributing in part to the endothelium-independent relaxation bycoptisine. Coptisine also blocks extracellular Ca2+ influx by interacting with both voltage- and receptor-operated Ca2+ channels.


2010 ◽  
Vol 65 (7-8) ◽  
pp. 451-457 ◽  
Author(s):  
Eurica Ribeiro ◽  
Fabíola F. Furtado ◽  
Vânia F. Noldin ◽  
Rogério Corrêa ◽  
Valtir Cechinel-Filho ◽  
...  

The vasorelaxant response of N-p-nitrophenylmaleimide (4-NO2-NPM) was evaluated. The mesenteric rings (1 - 2 mm i.d.) were suspended by cotton thread for isometric tension recordings in a Tyrode’s solution at 37 °C and gassed with a mixture of 95% O2 and 5% CO2, under a resting tension of 0.75 g. 4-NO2-NPM induced relaxation in mesenteric rings pre-contracted with phenylephrine (Phe; 10 μM, pD2 = 6.7 ± 0.3) or KCl (80 mM, pD2 = 3.9 ± 0.2). This effect was significantly attenuated after removal of the vascular endothelium, NG-nitro L-arginine methyl ester (L-NAME; 100 μM), atropine (1 μM), indomethacin (10 μM), L-NAME + indomethacin or 1H-[1,2,3]oxadiazolo[4,3-α]quinoxalin-1-one (ODQ; 10 μM). LArginine (1 mM) reversed the inhibitory effect of L-NAME. In endothelium-intact preparations pre-incubated with 20 mM KCl, tetraethylammonium bromide (TEA; 1 mM) or glibenclamide (Glib; 10 μM), the vasorelaxant effect was significantly attenuated when compared to controls (endothelium intact). In denuded rings, separate incubation with 20 mM KCl, TEA or Glib did not change the relaxation when compared with that obtained in denuded rings. 4-NO2-NPM inhibited in a concentration-dependent and non-competitive manner the concentration-response curves induced by CaCl2. In calcium-free medium, the transient contractions induced by Phe (10 μM) or caffeine (20 mM) were inhibited. The relaxant effect induced by 4-NO2 -NPM appeared to be due to endothelial muscarinic receptors activation, NO and prostacyclin release and KATP and BKCa (Ca2+-activated K+ channels) endotheliumdependent activation. Inhibition of the Ca2+ influx and inhibition of the Ca2+ release from intracellular IP3- and caffeine-sensitive stores are also involved in the vasorelaxation


2005 ◽  
Vol 289 (5) ◽  
pp. H2234-H2243 ◽  
Author(s):  
Takayuki Matsumoto ◽  
Kentaro Wakabayashi ◽  
Tsuneo Kobayashi ◽  
Katsuo Kamata

To assess the functional change in adenylyl cyclases (AC) associated with the diabetic state, we investigated AC-mediated relaxations and cAMP production in mesenteric arteries from rats with streptozotocin (STZ)-induced diabetes. The relaxations induced by the water-soluble forskolin (FSK) analog NKH477, which is a putative AC5 activator, but not by the β-adrenoceptor agonist isoproterenol (Iso) and the AC activator FSK, were reduced in intact diabetic mesenteric artery. In diabetic rats, however, Iso-, FSK-, and NKH477-induced relaxations were attenuated in the presence of inhibitors of nitric oxide synthase and cyclooxygenase. To exclude the influence of phosphodiesterase (PDE), we also examined the relaxations induced by several AC activators in the presence of 3-isobutyl-1-methylxanthine (IBMX; a PDE inhibitor). Under these conditions, the relaxation induced by Iso was greatly impaired in STZ-diabetic rats. This Iso-induced relaxation was significantly attenuated by pretreatment with SQ-22536, an AC inhibitor, in mesenteric rings from age-matched controls but not in those from STZ-diabetic rats. Under the same conditions, the relaxations induced by FSK or NKH477 were impaired in STZ-diabetic rats. Neither FSK- nor A-23187 (a Ca2+ ionophore)-induced cAMP production was significantly different between diabetics and controls. However, cAMP production induced by Iso or NKH477 was significantly impaired in diabetic mesenteric arteries. Expression of mRNAs and proteins for AC5/6 was lower in diabetic mesenteric arteries than in controls. These results suggest that AC-mediated relaxation is impaired in the STZ-diabetic rat mesenteric artery, perhaps reflecting a reduction in AC5/6 activity.


2005 ◽  
Vol 289 (5) ◽  
pp. H1923-H1932 ◽  
Author(s):  
Daniel Martí ◽  
Raquel Miquel ◽  
Khalid Ziani ◽  
Regina Gisbert ◽  
M. Dolores Ivorra ◽  
...  

The mRNA levels for the three α1-adrenoceptor subtypes, α1A, α1B, and α1D, were quantified by real-time RT-PCR in arteries from Wistar rats. The α1D-adrenoceptor was prominent in both aorta (79.0%) and mesenteric artery (68.7%), α1A predominated in tail (61.7%) and small mesenteric artery (73.3%), and both α1A- and α1D-subtypes were expressed at similar levels in iliac artery. The mRNA levels of the α1B-subtype were a minority in all vessels (1.7–11.1%). Concentration-response curves of contraction in response to phenylephrine or relaxation in response to α1-adrenoceptor antagonists on maximal sustained contraction induced by phenylephrine were constructed from control vessels and vessels pretreated with 100 μmol/l chloroethylclonidine (CEC) for 30 min. The significant decrease in the phenylephrine potency observed after CEC treatment together with the inhibitory potency displayed by 8-{2-[4-(2-methoxyphenyl)-1-piperazinyl]-8-azaspiro ( 4 , 5 ) decane-7-dionedihydrochloride} (BMY-7378, an α1D-adrenoceptor antagonist) confirm the relevant role of α1D-adrenoceptors in aorta and iliac and proximal mesenteric arteries. The potency of 5-methylurapidil (an α1A-adrenoceptor antagonist) and the changes in the potency of both BMY-7378 and 5-methylurapidil after CEC treatment provided evidence of a mixed population of α1A- and α1D-adrenoceptors in iliac and distal mesenteric arteries. The low potency of prazosin (pIC50 < 9) as well as the high 5-methylurapidil potency in tail and small mesenteric arteries suggest the main role of α1A/α1L-adrenoceptors with minor participation of the α1D-subtype. The mRNA levels and CEC treatment corroborated this pattern and confirmed that the α1L-adrenoceptor could be a functional isoform of the α1A-subtype.


2013 ◽  
Vol 48 (4-5) ◽  
pp. 709-716 ◽  
Author(s):  
Leylliane de Fátima Leal Interaminense ◽  
Fernanda Elizabethe dos Ramos-Alves ◽  
Rodrigo José Bezerra de Siqueira ◽  
Fabiano Elias Xavier ◽  
Gloria Pinto Duarte ◽  
...  

1993 ◽  
Vol 265 (6) ◽  
pp. H2137-H2141 ◽  
Author(s):  
M. Nakashima ◽  
P. M. Vanhoutte

The present study was designed to determine whether endothelin (ET) induces endothelium-dependent hyperpolarization in the isolated rat mesenteric artery and, if so, to identify the receptor subtype involved. Main superior mesenteric arteries of Wistar-Kyoto and spontaneously hypertensive rats were used for the measurement of electrical responses of smooth muscle cells, using glass microelectrode. In tissues with endothelium of both strains, ET-1 (10(-8) M) caused an initial transient hyperpolarization followed by a sustained depolarization. In tissues without endothelium, only depolarization was observed. ET-3 (10(-8) M) produced transient hyperpolarizations only in preparations with endothelium. There was no significant difference in maximal amplitude of hyperpolarization between the two strains. BQ-123 (selective ETA-receptor antagonist) blocked the depolarization to ET-1 but did not inhibit hyperpolarizing responses to either isopeptide. IRL-1620 (specific ETB-receptor agonist) produced transient membrane hyperpolarizations in tissues with endothelium. The hyperpolarizations induced by ET were not affected by NG-nitro-L-arginine. These data suggest that both ET-1 and ET-3 can cause endothelium-dependent hyperpolarization in the rat mesenteric artery and that the endothelial receptor involved may belong to ETB subtype.


2014 ◽  
Vol 28 (12) ◽  
pp. 923-927 ◽  
Author(s):  
Daniel Dias Rufino Arcanjo ◽  
Joaquim Soares da Costa-Júnior ◽  
Lucas Henrique Porfírio Moura ◽  
Alexandre Barros Falcão Ferraz ◽  
Raíssa Rebés Rossatto ◽  
...  

2016 ◽  
pp. S391-S399 ◽  
Author(s):  
J. TÖRÖK ◽  
A. ZEMANČÍKOVÁ ◽  
Z. KOCIANOVÁ

The inhibitory action of perivascular adipose tissue (PVAT) in modulation of arterial contraction has been recently recognized and contrasted with the prohypertensive effect of obesity in humans. In this study we demonstrated that PVAT might have opposing effect on sympatho-adrenergic contractions in different rat conduit arteries. In superior mesenteric artery isolated from normotensive Wistar-Kyoto rats (WKY), PVAT exhibited inhibitory influence on the contractions to exogenous noradrenaline as well as to endogenous noradrenaline released from arterial sympathetic nerves during transmural electrical stimulation or after application of tyramine. In contrast, the abdominal aorta with intact PVAT responded with larger contractions to transmural electrical stimulation and tyramine when compared to the aorta after removing PVAT; the responses to noradrenaline were similar in both. This indicates that PVAT may contain additional sources of endogenous noradrenaline which could be responsible for the main difference in the modulatory effect of PVAT on adrenergic contractions between abdominal aortas and superior mesenteric arteries. In spontaneously hypertensive rats (SHR), the anticontractile effect of PVAT in mesenteric arteries was reduced, and the removal of PVAT completely eliminated the difference in the dose-response curves to exogenous noradrenaline between SHR and WKY. These results suggest that in mesenteric artery isolated from SHR, the impaired anticontractile influence of PVAT might significantly contribute to its increased sensitivity to adrenergic stimuli.


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