Endothelium-Dependent and Endothelium-lndependent Vasodilation in Hyperthyroid and Hypothyroid Rats

Vargas, Félix; Fernández-Rivas, Antonio; Garcı́a-Estañ, Joaquı́n; Rio, C. Garcia Del

doi:10.1159/000139340

Cited by 40 publications

(33 citation statements)

References 16 publications

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“…These data are consistent with the increased and decreased responsiveness to acetylcholine, the endothelium-dependent vasodilator, in perfused kidneys and isolated aortas from hyperthyroid and hypothyroid rats respectively (5). Our data in the hypothyroid group contrast with the increased staining of endothelial NOS using immunohistochemical techniques in the aortic endothelium of hypothyroid rats (30).…”

Section: Discussionsupporting

confidence: 88%

“…Hyperthyroidism manifests a hyperdynamic circulation with increased cardiac output, increased heart rate and decreased peripheral resistance, whereas the hypothyroid state is associated with low cardiac output, bradycardia and raised peripheral resistance (2 -4). Hyperthyroidism increases the responsiveness of resistance vessels to the endothelium-dependent vasodilator, acetylcholine, whereas methimazole-induced hypothyroidism attenuates the endothelium-dependent response (5). Thyroid dysfunctions also affect cardiac and renal weight as well as renal sodium handling (2,6,7).…”

Section: Introductionmentioning

confidence: 99%

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Nitric oxide synthase activity in hyperthyroid and hypothyroid rats

Quesada

Sainz

Wangensteen

et al. 2002

European Journal of Endocrinology

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Objective: Thyroid disorders are accompanied by important changes in haemodynamic and cardiac functions and renal sodium handling. Since nitric oxide (NO) plays a crucial role in regulating vascular tone and renal sodium excretion, the present paper was designed to determine whether changes in the activity of NO synthase (NOS) participate in the cardiovascular and renal manifestations of thyroid disorders. Methods: We measured NOS activity in the heart (left and right ventricles), vessels (aorta and cava) and kidney (cortex and medulla) of euthyroid, hyperthyroid and hypothyroid rats after 6 weeks of treatment. NOS activity was determined by measuring the conversion of L-Results: NOS activity was higher in all tissues from hyperthyroid rats when compared with controls, except in the right ventricle. In the hypothyroid group, NOS activity showed a more heterogeneous pattern, with significant increases in both ventricles but significant reduction in the aorta, while in the vena cava, renal cortex and medulla the enzyme activity also tended to be higher, but significance was not reached. Conclusions: These data indicated that NOS activity was upregulated in tissues primarily related to blood pressure control in hyperthyroid rats, suggesting that an increased NO production may contribute to the hyperdynamic circulation in hyperthyroidism and may have a protective homeostatic effect in the target organs of the hypertension that accompanies this endocrine disease. The aortic and renal findings in hypothyroid rats suggested a possible role for NOS in the increased peripheral resistance and the normal pressure -diuresis -natriuresis response of these hypotensive animals, although hypothyroidism produced a heterogeneous tissue response in NOS activity.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Nitric oxide synthase activity in hyperthyroid and hypothyroid rats

Quesada

Sainz

Wangensteen

et al. 2002

European Journal of Endocrinology

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“…Further, these findings are consistent with earlier findings concerning vascular function. We (Delp et al 1995, McAllister et al 2000 and others (Vargas et al 1995) have found endothelium-dependent dilation of rat vasculature to be blunted in hypothyroidism; conversely, we (McAllister et al 1998(McAllister et al , 2000 and others (Scivoletto et al 1986, Vargas et al 1995, Honda et al 2000 have observed augmented endothelium-dependent vasodilation in the hyperthyroid state. Since a primary mediator of endothelium-dependent dilation in vasculature of the rat is NO (Delp et al 1993), our findings collectively suggest that alterations in endothelium-dependent vasodilation with changes in thyroid status are, in part, accounted for by an altered capacity for NO formation.…”

Section: Capacity For No Formationmentioning

confidence: 48%

“…Endothelium-independent vasodilation has generally been reported to be normal in both the hypothyroid (Delp et al 1995, McAllister et al 2000 and hyperthyroid states (McAllister et al 1998(McAllister et al , 2000, although exceptions have been reported (Vargas et al 1995, Honda et al 2000. Collectively, these findings suggest that thyroid status primarily affects the vascular endothelium.…”

Section: Introductionmentioning

confidence: 89%

“…When vasomotor responses were determined for euthyroid and hypothyroid rats, endothelium-dependent dilation was also found to be blunted in isolated aortae (Delp et al 1995, McAllister et al 2000 and isolated perfused kidneys (Vargas et al 1995) in the hypothyroid state. Paradoxically, given that exercise tolerance is reduced, hyperthyroidism is associated with enhanced muscle blood flow during exercise (Frey 1967, McAllister et al 1995c) and augmented endotheliumdependent vasodilation (Scivoletto et al 1986, Vargas et al 1995, McAllister et al 1998, Honda et al 2000. Thus, in both thyroid disease states, alterations in endothelium-dependent vasodilation are consistent with patterns of blood flow to exercising skeletal muscle.…”

Section: Introductionmentioning

confidence: 94%

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Thyroid status and nitric oxide in rat arterial vessels

McAllister¹,

Albarracin²,

Price³

et al. 2005

Journal of Endocrinology

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Thyroid disease has profound effects on cardiovascular function. Hypo-and hyperthyroidism, for example, are associated with reduced and increased maximal endothelium-dependent vasodilation respectively. We therefore hypothesized that the capacity for vascular nitric oxide (NO) formation is decreased in hypothyroidism and increased in hyperthyroidism. To test this hypothesis, rats were made hypothyroid (HYPO) with propylthiouracil or hyperthyroid (HYPER) with triiodothyronine over 3-4 months. Compared with euthyroid control rats (EUT), HYPO exhibited blunted growth and lower citrate synthase activity in the soleus muscle; HYPER exhibited left ventricular hypertrophy and higher citrate synthase activity in the soleus muscle (P<0·05 for all effects). The capacity for NO formation was determined in aortic extracts by formation of [ . Expression of endothelial and neural isoforms of NOS was modulated by thyroid status in a parallel fashion. Capacity for responding to NO was also determined via measuring cGMP concentration in aortae incubated with sodium nitroprusside. Stimulated cGMP formation was also modulated by thyroid status (EUT, 73·0 20·2 pmol/mg protein; HYPO, 152·4 48·7; HYPER, 10·4 2·6; P<0·05, HYPER vs HYPO). These data indicate that thyroid status alters capacities for both formation of and responding to NO. The former finding may contribute to previous findings concerning vascular function in thyroid disease states.

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Nongenomic signaling pathways triggered by thyroid hormones and their metabolite 3‐iodothyronamine on the cardiovascular system

Axelband

Dias

Ferrão

et al. 2010

Journal Cellular Physiology

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Thyroid hormones play a wide range of important physiological activities in almost all organism. As changes in these hormones levels-observed in hypothyroidism and hyperthyroidism-promote serious derangements of the cardiovascular system, it is important to know their mechanisms of action. Although the classic genomic actions which are dependent on interaction with nuclear receptors to modulate cardiac myocytes genes expression, there is growing evidence about T(3) and T(4)-triggered nongenomic pathways, resulted from their binding to plasma membrane, cytoplasm, or mitocondrial receptors that leads to a rapidly regulation of cardiac functions. Interestingly both actions converge to amplify thyroid hormone effects on cardiovascular system. T(3) and T(4) nongenomic actions modify inotropic and chronotropic effects, cardiac action potential duration, cardiac growth, and myocyte shape by protein translation through protein kinases-dependent signaling cascades, which include PKA, PKC, PI3K, and MAPK, and changes on ion channels and pumps activity. In respect to the decreased systemic vascular resistance seen in hyperthyroidism, T(3) appears to activate NOS or ATP-sensitive K(+) channels. In addition, a novel biologically active T(4)-derived metabolite has been described, 3-iodothyronamine, T(1)AM, which also acts through membrane receptors to mediate nongenomic cardiac effects. This metabolite influences the physiological manifestations of thyroid hormone actions by inducing opposite effects from those stimulated by T(3) and T(4), such as negative inotropic and chronotropic effects. Therefore, beyond genomic and nongenomic effects of thyroid hormones, it is crucial for there to be an equilibrium between T(3) or T(4) and T(1)AM levels for maintaining cardiac homeostasis.

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Endothelium-Dependent and Endothelium-lndependent Vasodilation in Hyperthyroid and Hypothyroid Rats

Cited by 40 publications

References 16 publications

Nitric oxide synthase activity in hyperthyroid and hypothyroid rats

Nitric oxide synthase activity in hyperthyroid and hypothyroid rats

Thyroid status and nitric oxide in rat arterial vessels

Nongenomic signaling pathways triggered by thyroid hormones and their metabolite 3‐iodothyronamine on the cardiovascular system

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