The Direct Vasomotor Effect of Thyroid Hormones on Rat Skeletal Muscle Resistance Arteries

Park, Kyung W.; Dai, Haibin; Ojamaa, Kaie; Lowenstein, Edward; Klein, Irwin; Sellke, Frank W.

doi:10.1097/00000539-199710000-00005

Cited by 71 publications

(45 citation statements)

References 26 publications

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“…Our preliminary experiment showed that T 3 was devoid of effects in preparations in which the Ach-induced relaxation was less than 50%; therefore, we applied the protocol of T 3 administration only to C57BL/6 mice. In agreement with the results previously reported in rat skeletal muscle resistance arteries [7], T 3 is effective in our present work at all concentrations used (10 -9 to 10 -7 M ). This result indicates that the mesenteric arteries are a target site for T 3 , where it regulates physiological vascular tone.…”

Section: Discussionsupporting

confidence: 94%

“…The disruption of TRα in this background significantly blunted the mesenteric response to Ach. This result contrasts with that obtained in the tail artery of TRα-mutant mice [4], but is in agreement with the fact that TH has been shown to stimulate NO production via both endothelium-dependent [7] and endothelium-independent mechanisms [30]. In addition, the responses to SNP, AII and PE were also all blunted in TRα 0/0 C57 mice.…”

Section: Discussionsupporting

confidence: 61%

“…This effect may be mediated by releasing relaxing factors from vascular endothelial cells [7] and/or via a direct effect on VSMC [30,32]. Our preliminary experiment showed that T 3 was devoid of effects in preparations in which the Ach-induced relaxation was less than 50%; therefore, we applied the protocol of T 3 administration only to C57BL/6 mice.…”

Section: Discussionmentioning

confidence: 99%

“…These observations suggest a relaxing action of TH in peripheral arteries. Indeed, a vasodilatation has been observed when 3,3′5-triiodo- L -thyronine sodium salt (T 3 ) or thyroxine (T 4 ) was administrated in rat skeletal muscle resistance arteries, with T 3 having a greater effect than T 4 [7]. Besides this direct vasomotor effect, TH are also involved in normal vascular smooth muscle cell (VSMC) proliferation [8], an action that may modulate vascular reactivity.…”

Section: Introductionmentioning

confidence: 99%

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Vascular Function of the Mesenteric Artery Isolated from Thyroid Hormone Receptor-E Knockout Mice

Liu

Canaple²,

Gauthier³

et al. 2014

J Vasc Res

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Objective: This study evaluated the consequences of thyroid hormone receptor-E (TRE) disruption on vascular reactivity. Methods: The activity of superior mesenteric arteries isolated from TRE knockout mice generated in the SV129 background (TRE^0/0SV) or in a pure C57BL/6 background (TRE^0/0C57) was compared to that of their corresponding wild-type strains (SV129 or C57BL/6 mice). Results: The wild-type SV129 mice exhibited an impaired acetylcholine (Ach)-induced mesenteric artery relaxationcompared to C57BL/6 mice, associated with greater responses to angiotensin II (AII) and phenylephrine (PE). The disruption of TRE decreased the vascular response to sodium nitroprusside and PE in both the SV129 and C57BL/6 genetic backgrounds.Responses to Ach and AII were also blunted, but only in TRE^0/0C57 mice. The administration of 3,3′5-triiodo-L-thyronine sodium salt (T₃) elicited a vasodilatation in C57BL/6 mice even at the lowest concentration (10^-9M); a maximal relaxation of more than 50% was observed with the concentrations between 10^-9 and 10^-8M. However, the response to T₃ was nearly absent in TRE^0/0C57 mice. Conclusion: TRE is essential for the control of vascular tone, particularly in thyroid hormone-mediated relaxation. The difference in response to Ach observed between the two wild-type mice should be taken into account for interpreting the vascular responses of genetically engineered mice. i 2014 S. Karger AG, Basel

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Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Vascular Function of the Mesenteric Artery Isolated from Thyroid Hormone Receptor-E Knockout Mice

Liu

Canaple²,

Gauthier³

et al. 2014

J Vasc Res

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“…For years, studies have suggested that T3 causes vascular relaxation exclusively via EC. However, compelling data support a rapid vasorelaxant effect of T3 also occurring via VSMC [11, 33]. Therefore, identification of vasodilatory mechanisms activated independently of endothelium by T3 is imperative.…”

Section: Discussionmentioning

confidence: 99%

Triiodothyronine Potentiates Vasorelaxation via PKG/VASP Signaling in Vascular Smooth Muscle Cells

Samuel

Zhang

Tang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Vascular relaxation caused by Triiodothyronine (T3) involves direct activation of endothelial cells (EC) and vascular smooth muscle cells (VSMC). Activation of protein kinase G (PKG) has risen as a novel contributor to the vasorelaxation mechanism triggered by numerous stimuli. We hypothesize that T3-induced vasorelaxation involves PKG/vasodilator-stimulated phosphoprotein (VASP) signaling pathway in VSMC. Methods: Human aortic endothelial cells (HAEC) and VSMC were treated with T3 for short (2 to 60 minutes) and long term (24 hours). Nitric oxide (NO) production was measured using DAF-FM. Expression of protein targets was determined using western blot. For functional studies, rat aortas were isolated and treated with T3 for 20 minutes and mounted in a wire myograph. Relaxation was measured by a concentration-dependent response to acetylcholine (ACh) and sodium nitroprusside (SNP). Results: Aortas stimulated with T3 exhibited augmented sensitivity to ACh and SNP-induced relaxation, endothelium-dependent and endothelium-independent responses, respectively. T3 directly increased vasorelaxation, which was abolished in the presence of a PKG inhibitor. T3 markedly induced phosphorylation of Akt, eNOS and consequently increased NO production in EC. Likewise, T3 induced phosphorylation of VASP at serine 239 via the PKG pathway in VSMC. Conclusion: Our findings have uncovered a PKG/VASP signaling pathway in VSMC as a key molecular mechanism underlying T3-induced vascular relaxation.

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Hyperthyroid heart disease

Fadel

Ellahham

Lindsay

et al. 2000

Clinical Cardiology

131

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Summary:The heart is an organ sensitive to the action of thyroid hormone, and measurable changes in cardiac performance are detected with small variations in thyroid hormone serum concentrations. Most patients with hyperthyroidism experience cardiovascular manifestations, and the most serious complications of hyperthyroidism occur as a result of cardiac involvement. Recent studies provide important insights into the molecular pathways that mediate the action of thyroid hormone on the heart and allow a better understanding of the mechanisms that underlie the hemodynamic and clinical manifestations of hyperthyroidism. Several cardiovascular conditions and drugs can interfere with thyroid hormone levels and may pose a difficulty in interpretation of laboratory data in patients with suspected thyroid heart disease. The focus of this report is a review of the current knowledge of thyroid hormone action on the heart and the clinical and hemodynamic laboratory findings as well as therapeutic management of patients with hyperthyroid heart disease.

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The Direct Vasomotor Effect of Thyroid Hormones on Rat Skeletal Muscle Resistance Arteries

Abstract: Thyroid hormones may have modest direct vasodilatory effects. This may partially account for the cardiovascular actions of the hormones in hyperthyroidism or when administered pharmacologically in cardiac surgery.

Cited by 71 publications

References 26 publications

Vascular Function of the Mesenteric Artery Isolated from Thyroid Hormone Receptor-E Knockout Mice

Vascular Function of the Mesenteric Artery Isolated from Thyroid Hormone Receptor-E Knockout Mice

Triiodothyronine Potentiates Vasorelaxation via PKG/VASP Signaling in Vascular Smooth Muscle Cells

Hyperthyroid heart disease

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