Regulation of β-adrenoceptor-mediated relaxation of the rat aorta is modulated by endogenous ovarian hormones

2000 ◽  
Vol 98 (4) ◽  
pp. 381-387 ◽  
Author(s):  
María V. CONDE ◽  
Jesús MARÍN ◽  
Carmen FERNÁNDEZ-CRIADO ◽  
NGloria BALFAGÓ
Keyword(s):  
Thoracic Aorta ◽  
Ovarian Hormones ◽  
Rat Aorta ◽  
Nitric Oxide Donor ◽  
Ovx Rats ◽  
Adrenoceptor Agonist ◽  
Stimulatory G Protein ◽  
Female Wistar Rats ◽  
Rat Thoracic Aorta ◽  
Adrenoceptor Agonists

The aim of this study was to assess the influence of the endogenous status of ovarian hormones on the relaxation induced by the β-adrenoceptor agonists isoprenaline (isoproterenol) and dobutamine in thoracic aorta segments, precontracted with noradrenaline, from age-matched (13-week-old) virgin (oestrus) and ovariectomized (OVX) prepubertal female Wistar rats. Isoprenaline-induced relaxation was decreased in intact aortic segments from OVX rats compared with that in segments from oestrus rats. Relaxation was significantly reduced by endothelium removal, 1 µmol/l propranolol or 100 µmol/l NG-nitro-l-arginine methyl ester (l-NAME). The β1-adrenoceptor agonist dobutamine induced less relaxation in intact arteries from oestrus rats than did isoprenaline, and dobutamine-induced relaxation was markedly less in intact segments from OVX compared with oestrus rats. This dobutamine-induced relaxation was abolished by endothelium removal, and reduced by 1 µmol/l propranolol, 100 µmol/l l-NAME or 1 µmol/l yohimbine. Cholera toxin (an activator of the stimulatory G-protein Gs) caused relaxation in intact arteries from oestrus rats; this relaxation was decreased by both deprivation of ovarian hormones and endothelium removal. Forskolin (a direct activator of the catalytic subunit of adenylate cyclase) and sodium nitroprusside (a nitric oxide donor and cGMP-dependent vasodilator agonist) induced similar endothelium-independent relaxation in arteries from both oestrus and OVX rats. These results suggest that the relaxation elicited by endothelial β-adrenoceptor activation in the rat thoracic aorta is impaired by deprivation of female ovarian hormones; this impairment is caused, at least in part, by decreases in both the endothelial release of NO and Gs function.

scholarly journals Cilostazol enhances atorvastatin-induced vasodilation of female rat aorta during aging

2017 ◽  
Vol 104 (3) ◽  
pp. 226-234 ◽  
Author(s):  
KE Nurullahoğlu-Atalık ◽  
S Kutlu ◽  
H Solak ◽  
R Özen Koca
Keyword(s):  
Thoracic Aorta ◽  
Inhibitory Effect ◽  
Rat Aorta ◽  
Organ Bath ◽  
Female Rat ◽  
Response Curves ◽  
Adult Rat ◽  
Combined Application ◽  
Female Wistar Rats ◽  
Rat Thoracic Aorta

Statins have cholesterol-independent effects including an increased vascular nitric oxide activity and are commonly used by patients with cardiovascular disease. Such patients frequently have cardiovascular diseases, which may be treated with cilostazol, a platelet aggregation inhibitor. This study was designed to investigate whether combined use of cilostazol would increase the inhibitory effect of statin on vascular smooth muscle and how maturation would affect these responses. Female Wistar rats, aged 3–4 months (young) and 14–15 months (adult), were sacrificed by cervical dislocation and the thoracic aorta was dissected and cut into 3- to 4-mm-long rings. The rings were mounted under a resting tension of 1 g in a 20-ml organ bath filled with Krebs–Henseleit solution. Rings were precontracted with phenylephrine (10−6 M), and the presence of endothelium was confirmed with acetylcholine (10−6 M). Then, the concentration–response curves were obtained for atorvastatin alone (10−10 to 3 × 10−4 M; control) and in the presence of cilostazol (10−6 M) in young and adult rat aortas. This experimental protocol was also carried out in aorta rings, which had been pretreated with NG-nitro-l-arginine methyl ester (l-NAME, 10−4 M). Atorvastatin induced concentration-dependent relaxations in young and adult rat thoracic aorta rings precontracted with phenylephrine. The pIC50 value of atorvastatin was significantly decreased in adult rat aortas. In addition, pretreatment of aortas with cilostazol enhanced the potency of atorvastatin in both young and adult aortas. Incubation with l-NAME did not completely eliminate the relaxations to atorvastatin in the presence of cilostazol. These results suggest that combined application of cilostazol with atorvastatin was significantly more potent than atorvastatin alone. Combined drug therapy may be efficacious in delaying the occurrence of cardiovascular events.

Androgen-receptor defect abolishes sex differences in nitric oxide and reactivity to vasopressin in rat aorta

2001 ◽  
Vol 91 (6) ◽  
pp. 2602-2610 ◽  
Author(s):  
John N. Stallone ◽  
Ronald L. Salisbury ◽  
Clifford T. Fulton
Keyword(s):  
Nitric Oxide ◽  
Androgen Receptor ◽  
Methyl Ester ◽  
Thoracic Aorta ◽  
Vascular Reactivity ◽  
Rat Aorta ◽  
Maximal Response ◽  
Maximal Contraction ◽  
Rat Thoracic Aorta ◽  
Recessive Defect

Contractions of rat thoracic aorta to vasopressin (VP) are threefold higher in females (F) than in males (M), primarily because nitric oxide (NO) attenuation of contraction is greater in M. To determine the role of the androgen receptor (AR) in this mechanism, vascular reactivity to VP was examined in thoracic aorta of the testicular-feminized male (Tfm) rat, which has an X-linked, recessive defect in AR function in affected M. Maximal contraction of normal aortas to VP was fourfold higher in F (4,128 ± 291 mg/mg ring wt) than in M (971 ± 133 mg); maximal response of Tfm (3,967 ± 253 mg) was similar to that of normal F. N G-nitro-l-arginine methyl ester increased maximal response to VP threefold in M but had no effect in F or Tfm. In contrast, maximal contraction of normal aortas to phenylephrine was 43% higher in M (4,011 ± 179 mg) than in F (2,809 ± 78 mg); maximal response of Tfm (2,716 ± 126 mg) was similar to that of normal F. N G-nitro-l-arginine methyl ester increased maximal response to phenylephrine by >50% in F and Tfm but had no effect in M. Maximal contractile response to 80 mM KCl did not differ among M, F, or Tfm. Thus androgens and normal vascular AR function are important in the greater NO-mediated attenuation of reactivity to VP in M than in F rat aorta, which may involve specific modulation of endothelial VP signal transduction pathways and NO release by androgens. These data also establish the importance of the Tfm rat as a model to study the effects of androgens on cardiovascular function.

scholarly journals Comparative Contractile Effects of Halothane and Sevoflurane in Rat Aorta

2000 ◽  
Vol 92 (1) ◽  
pp. 219-219 ◽  
Author(s):  
Vu Huu Vinh ◽  
Taijiro Enoki ◽  
Shinichi Hirata ◽  
Hiroshi Toda ◽  
Masahiro Kakuyama ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Thoracic Aorta ◽  
Volatile Anesthetic ◽  
Rat Aorta ◽  
Isometric Tension ◽  
Dependent Manner ◽  
Anesthetic Agents ◽  
Rat Thoracic Aorta ◽  
Dose Dependent ◽  
Ca2 Channels

Background Volatile anesthetic agents have been shown to have contractile effects in vascular tissues during specific conditions. This study compared contractile effects of halothane and sevoflurane in rat aorta treated with verapamil. This study also tried to elucidate the mechanism of the contraction. Methods Endothelium-denuded rat thoracic aorta was used for recording of isometric tension and measurement of influx of 45Ca2+. All experiments were performed in the presence of verapamil. In recording of tension, rings were precontracted with a submaximum dose of phenylephrine, followed by exposure to halothane or sevoflurane. For measurement of influx of 45Ca2+, rat aortic strips were exposed to phenylephrine and then to additional halothane or sevoflurane. Influx of Ca2+ was estimated by incubating the strips in 45Ca2+-labeled solution for 2 min. Results Halothane (0.5-4.0%) induced contraction in a dose-dependent manner, whereas sevoflurane (1-4%) had no effect on tension. Influx of 45Ca2+ was strongly enhanced by halothane at 1% and 2%, but only slightly at 4%, and was not affected by 1-4% sevoflurane. SK&F 96365, a blocker of voltage-independent Ca2+ channels, abolished contraction and influx of 45Ca2+ by 1% halothane. Depletion of Ca2+ from the sarcoplasmic reticulum with ryanodine or thapsigargin reduced the contraction induced by halothane at 4% but not that at 1% and 2%. Conclusion Halothane is suggested to cause contraction by enhancing influx of Ca2+ via voltage-independent Ca2+ channels at concentrations up to 2% and by inducing release of Ca2+ at 4%. Sevoflurane (1-4%) is devoid of these contractile effects.

scholarly journals Sulfur dioxide relaxes rat aorta by endothelium-dependent and -independent mechanisms

2009 ◽  
pp. 521-527 ◽  
Author(s):  
Y-K Wang ◽  
A-J Ren ◽  
X-Q Yang ◽  
L-G Wang ◽  
W-F Rong ◽  
...  
Keyword(s):  
Sulfur Dioxide ◽  
Thoracic Aorta ◽  
Vascular Tissue ◽  
Rat Aorta ◽  
Isometric Tension ◽  
Organ Bath ◽  
Kca Channels ◽  
Voltage Dependent ◽  
Rat Thoracic Aorta ◽  
High Doses

This study aimed to investigate the vasoactivity of sulfur dioxide (SO2), a novel gas identified from vascular tissue, in rat thoracic aorta. The thoracic aorta was isolated, cut into rings, and mounted in organ-bath chambers. After equilibrium, the rings were gradually stretched to a resting tension. Isometric tension was recorded under the treatments with vasoconstrictors, SO2 derivatives, and various drugs as pharmacological interventions. In endothelium-intact aortic rings constricted by 1 μM phenylephrine (PE), SO2 derivatives (0.5 – 8 mM) caused a dosedependent relaxation. Endothelium removal and a NOS inhibitor L-NAME reduced the relaxation to low doses of SO2 derivatives, but not that to relatively high doses (≥ 2 mM). In endotheliumdenuded rings, SO2 derivatives attenuated vasoconstriction induced by high K+ (60 mM) or CaCl2 (0.01-10 mM). The relaxation to SO2 derivatives in PE-constricted rings without endothelium was significantly inhibited by blockers of ATPsensitive K+ (KATP) and Ca2+-activated K+ (KCa) channels, but not by those of voltage-dependent K+ channels, Na+-K+-ATPase or Na+-Ca2+ exchanger. SO2 relaxed vessel tone via endotheliumdependent mechanisms associated with NOS activation, and via endothelium-independent mechanisms dependent on the inhibition of voltage-gated Ca2+ channels, and the opening of KATP and KCa channels.

scholarly journals Stimulation of inorganic-phosphate incorporation into phosphatidylinositol in rat thoracic aorta mediated through V1-vasopressin receptors

1981 ◽  
Vol 194 (1) ◽  
pp. 167-172 ◽  
Author(s):  
A P Takhar ◽  
C J Kirk
Keyword(s):  
Thoracic Aorta ◽  
Rat Hepatocytes ◽  
Rat Aorta ◽  
Vasopressin Receptors ◽  
Rat Thoracic Aorta ◽  
Relative Potencies ◽  
Phosphate Incorporation ◽  
Vasopressin Analogues ◽  
Stimulation Of

Vasopressin stimulates the incorporation of [32P]Pi into phosphatidylinositol but not into other phospholipids in rat thoracic aorta strips. The relative abilities of three vasopressin analogues to stimulate phosphatidylinositol labelling in rat aorta are similar to their relative pressor potencies in vivo and to their relative potencies in stimulating the metabolism of rat hepatocytes, but very different from their relative antidiuretic potencies. The vasopressor antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid),8-arginine]vasopressin competitively inhibits [Arg8]vasopressin-stimulated phosphatidylinositol labelling in rat aorta with a pA2 of 8.1. It is concluded that the Ca2+-mobilizing vasopressin receptors (V1-receptors) of the rat aorta stimulate phosphatidylinositol metabolism, probably by enhancing phosphatidylinositol breakdown.

Abstract 624: Resolvin E1 Inhibits Thromboxane-Induced Contraction of Rat Aorta and Human Pulmonary Artery

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Melanie Jannaway ◽  
Christopher Torrens ◽  
Jane A Warner ◽  
Anthony P Sampson
Keyword(s):  
Pulmonary Artery ◽  
Thoracic Aorta ◽  
Response Curve ◽  
Rat Aorta ◽  
Omega 3 ◽  
Omega 6 ◽  
Rat Thoracic Aorta ◽  
Human Pulmonary Artery ◽  
Induced Aggregation

Thromboxane is a vasoactive omega-6-derived lipid implicated in hypertension. Omega-3 fatty acid derivatives including resolvin (Rv) E1 have important roles in the resolution of inflammation, but their ability to mediate vasomotor activity is unknown. We assessed whether RvE1 modulates contraction of rat thoracic aorta and human pulmonary artery (HPA) in vitro. Rats were culled by CO2 inhalation and cervical dislocation, and the thoracic aorta was removed. HPA were obtained with informed consent from lung tissue of surgical patients at Southampton General Hospital. Segments of aorta or HPA were incubated in DMEM-F12 with or without RvE1 (10 nM, 100 nM or 300 nM) for 1 or 24 hours, and then mounted on a wire myograph. Mounted segments were bathed at 37[[Unable to Display Character: ]]C in Kreb’s buffer, gassed (95%/5% O2/CO2) and set to 1.5 g of baseline tension. Functional integrity was confirmed by a contractile response to 125 mM KPSS. After washing to restore baseline tension, a cumulative concentration-response curve was defined to the stable thromboxane A2 mimetic U46619 (1 nM - 1 μM). Contractions are expressed as percent of KPSS response and differences determined by two-way ANOVA and by pairwise comparisons. In rat aorta, treatment with RvE1 (10 nM) significantly shifted the U46619 curve rightwards, increasing the EC50 value 13-fold from 0.13 μM to 1.75 μM after 1 hour (n=5), and 4-fold from 0.093 μM to 0.41 μM after 24 hours (n=5). In contrast, 300 nM RvE1 caused no significant change in EC50 (1 hour 0.11 μM; 24 hours 0.097 μM, n=5). In HPA segments, RvE1 (10 nM, 1 hour) increased the U46619 EC50 value 7-fold from 0.0079 μM to 0.054 μM (n=3), with a preliminary experiment suggesting a similar outcome after 24 hours. Higher concentrations of RvE1 had no significant effect, suggesting the relaxant action of RVE1 has a bell-shaped response curve. In preliminary experiments, RvE1 inhibited U-46619 contractions of bronchiolar airways from the same human donors. Resolvin E1 is known for its immunomodulatory actions on leukocytes and also inhibits U46619-induced aggregation of platelets, but our results are the first evidence that this pro-resolution mediator can also inhibit contractions of intact vasculature from rat and human lung induced by a thromboxane mimetic.

Contraction of rat thoracic aorta strips induced by phorbol 12-myristate 13-acetate

1987 ◽  
Vol 252 (2) ◽  
pp. C244-C247 ◽  
Author(s):  
H. Itoh ◽  
K. Lederis
Keyword(s):  
Thoracic Aorta ◽  
Smooth Muscle Contraction ◽  
Progressive Increase ◽  
Rat Aorta ◽  
Base Line ◽  
Complete Relaxation ◽  
Adventitial Layer ◽  
Rat Thoracic Aorta ◽  
Lower Maximum ◽  
Repeated Applications

Phorbol 12-myristate 13-acetate (PMA) induced a slow and progressive increase in tension of rat thoracic aorta strips in the presence of extracellular Ca2+. Complete relaxation could not be obtained in Ca2+-free buffer containing 1 mM ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid (EGTA) and 10(-7) M PMA. In the absence of extracellular Ca2+, PMA (10(-7) M) induced a small but sustained contraction which was not altered by the addition of another 2 mM EGTA and 3 X 10(-5) M verapamil. Papaverine (10(-4) M) relaxed the PMA-induced contraction to the base line, but phentolamine (10(-5) M), cyproheptadine (10(-5) M), atropine (10(-5) M) and tetrodotoxine (10(-6) M) did not change the contraction. Ca2+-depleted muscle strips, prepared by four repeated applications of 10(-7) M norepinephrine in Ca2+-free buffer, were contracted by 10(-7) M PMA, but at a lower maximum tension than nontreated strips. The action of PMA on rat aorta strips in Ca2+-free buffer did not require the presence of the adventitial layer or endothelial cells. These results suggest that PMA may induce activation of protein kinase C and smooth muscle contraction in the absence of extracellular Ca2+, without an increase in myoplasmic Ca2+.

scholarly journals Mixed β 3 -adrenoceptor agonist and α 1 -adrenoceptor antagonist properties of nebivolol in rat thoracic aorta

2006 ◽  
Vol 147 (7) ◽  
pp. 699-706 ◽  
Author(s):  
Bertrand Rozec ◽  
Thuy Tran Quang ◽  
Jacques Noireaud ◽  
Chantal Gauthier
Keyword(s):  
Thoracic Aorta ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Rat Thoracic Aorta
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