β-Adrenoceptor-mediated vascular relaxation in spontaneously hypertensive rats

Mallem, Yassine; Holopherne, Delphine; Reculeau, Olivier; Coz, Olivier Le; Desfontis, Jean‐Claude; Gogny, Marc

doi:10.1016/j.autneu.2005.01.003

Cited by 18 publications

(18 citation statements)

References 21 publications

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“…β 3 ‐ and low‐affinity‐state β 1 ‐adrenoceptors co‐exist with classical β 1 ‐ and β 2 ‐adrenoceptors in rat thoracic aorta and could be involved in the isoprenaline‐induced nadolol‐insensitive effect. The hypothesis is supported by previous experiments showing, by using selective antagonists, that β 3 ‐ or low‐affinity‐state β 1 ‐adrenoceptors (or both) can also play a role in the isoprenaline‐induced relaxation in rat thoracic aorta 9,11 …”

Section: Discussionsupporting

confidence: 54%

“…Moreover, analysis of variance has been designed for the analysis of linear data and is not accurate for nonlinear data. In our previous work, CCRC data analysis consisted of an estimation of the E m , n, pD 2 values for each CCRC by nonlinear regressions according to Hill's equation using a least square estimator [9] . For each parameter and for each treatment group, the mean of the individual values previously computed was considered as an estimation of the population parameter value.…”

Section: Discussionmentioning

confidence: 99%

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Nonlinear mixed effects models applied to cumulative concentration–response curves

Thorin

Mallem

Noireaud

et al. 2010

Journal of Pharmacy and Pharmacology

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Nonlinear mixed effects models applied to cumulative concentration–response curves

Thorin

Mallem

Noireaud

et al. 2010

Journal of Pharmacy and Pharmacology

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“…After the equilibrium period, aortic rings were contracted with phenylephrine (10 µmol/L), followed by exposure to acetylcholine (ACh; 10 µmol/L) to test the integrity of the endothelium. The presence of an intact endothelium was confirmed by the observation of ACh‐induced relaxation > 60% 14 . In some experiments, the endothelium was removed mechanically by gently rubbing the internal surface of the vessel.…”

Section: Methodsmentioning

confidence: 97%

Comparative Effects of Tramadol on Vascular Reactivity in Normotensive and Spontaneously Hypertensive Rats

Raimundo

Pontes

Antunes

et al. 2008

Clin Exp Pharma Physio

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The aim of the present study was to determine the effects of tramadol on vascular reactivity in aortic rings from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Aortic rings, with or without endothelium, were obtained from male WKY rats and SHR (15-20 weeks old) and prepared for isometric tension recording. Aortic rings were precontracted with phenylephrine (10 micromol/L) or 40 mmol/L KCl and then exposed to cumulative concentrations of tramadol (0.1-1 mmol/L). Tramadol produced a concentration-dependent relaxation of precontracted aortic rings from WKY rats and SHR, which was not dependent on functional endothelium. Vascular relaxation was significantly greater in rings from SHR than WKY rats. The concentration of tramadol necessary to produce a 50% reduction of the maximal contraction to phenylephrine (IC(50)) in rings with and without endothelium from SHR was 0.47 +/- 0.08 and 0.44 +/- 0.03 mmol/L, respectively (P = 0.76). Tramadol attenuated the contracture elicited by Ca2+ in depolarized tissue, suggesting that it may inhibit L-type Ca2+ channels. However, pretreatment with nicardipine (1 micromol/L) prevented the relaxation induced by tramadol in aortic rings from WKY rats and partially reduced its inhibitory effect in aortic rings from SHR. 6. Pretreatment of endothelium-denuded aorta with glybenclamide (3 micromol/L), 4-aminopyridine (3 mmol/L), tetraethylammonium (3 mmol/L) and naloxone (100 micromol/L) did not affect tramadol-induced vasodilation of aortic rings from either WKY rats or SHR. Intravenous administration of tramadol (10 mg/kg) to conscious SHR significantly reduced both systolic and diastolic blood pressure from 171.4 +/- 5.3 to 129.3 +/- 5.3 (P = 0.002) and from 125.0 +/- 6.5 to 57.8 +/- 8.9 mmHg (P = 0.003), respectively.

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“…Because the TP mice had been maintained in our animal facility with KO 3 KO matings, WT C57BL/6 mice served as Ctrls (TP‐Ctrl mice). Pertussis toxin (PTX) was administered intraperitoneally in some of the animals for 5 d prior to the experiments at a dosage of 50 μg/kg body weight to inhibit G i proteins (26, 27).…”

Section: Methodsmentioning

confidence: 99%

LPA ₁ receptor–mediated thromboxane A ₂ release is responsible for lysophosphatidic acid‐induced vascular smooth muscle contraction

et al. 2017

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Lysophosphatidic acid (LPA) has been recognized recently as an endothelium-dependent vasodilator, but several lines of evidence indicate that it may also stimulate vascular smooth muscle cells (VSMCs), thereby contributing to vasoregulation and remodeling. In the present study, mRNA expression of all 6 LPA receptor genes was detected in murine aortic VSMCs, with the highest levels of LPA, LPA, LPA, and LPA In endothelium-denuded thoracic aorta (TA) and abdominal aorta (AA) segments, 1-oleoyl-LPA and the LPA agonist VPC31143 induced dose-dependent vasoconstriction. VPC31143-induced AA contraction was sensitive to pertussis toxin (PTX), the LPA antagonist Ki16425, and genetic deletion of LPA but not that of LPA or inhibition of LPA, by diacylglycerol pyrophosphate. Surprisingly, vasoconstriction was also diminished in vessels lacking cyclooxygenase-1 [COX1 knockout (KO)] or the thromboxane prostanoid (TP) receptor (TP KO). VPC31143 increased thromboxane A (TXA) release from TA of wild-type, TP-KO, and LPA-KO mice but not from LPA-KO or COX1-KO mice, and PTX blocked this effect. Our findings indicate that LPA causes vasoconstriction in VSMCs, mediated by LPA-, G-, and COX1-dependent autocrine/paracrine TXA release and consequent TP activation. We propose that this new-found interaction between the LPA/LPA and TXA/TP pathways plays significant roles in vasoregulation, hemostasis, thrombosis, and vascular remodeling.-Dancs, P. T., Ruisanchez, E., Balogh, A., Panta, C. R., Miklós, Z., Nüsing, R. M., Aoki, J., Chun, J., Offermanns, S., Tigyi, G., Benyó, Z. LPA receptor-mediated thromboxane A release is responsible for lysophosphatidic acid-induced vascular smooth muscle contraction.

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β-Adrenoceptor-mediated vascular relaxation in spontaneously hypertensive rats

Cited by 18 publications

References 21 publications

Nonlinear mixed effects models applied to cumulative concentration–response curves

Nonlinear mixed effects models applied to cumulative concentration–response curves

Comparative Effects of Tramadol on Vascular Reactivity in Normotensive and Spontaneously Hypertensive Rats

LPA ₁ receptor–mediated thromboxane A ₂ release is responsible for lysophosphatidic acid‐induced vascular smooth muscle contraction

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β-Adrenoceptor-mediated vascular relaxation in spontaneously hypertensive rats

Cited by 18 publications

References 21 publications

Nonlinear mixed effects models applied to cumulative concentration–response curves

Nonlinear mixed effects models applied to cumulative concentration–response curves

Comparative Effects of Tramadol on Vascular Reactivity in Normotensive and Spontaneously Hypertensive Rats

LPA 1 receptor–mediated thromboxane A 2 release is responsible for lysophosphatidic acid‐induced vascular smooth muscle contraction

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LPA ₁ receptor–mediated thromboxane A ₂ release is responsible for lysophosphatidic acid‐induced vascular smooth muscle contraction