The effect of hyperthyroidism on capillarity and oxidative capacity in rat soleus and gastrocnemius muscles.

Capó, L A; Sillau, A. H.

doi:10.1113/jphysiol.1983.sp014835

Cited by 53 publications

(30 citation statements)

References 40 publications

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“…These observations are in agreement with previous studies in other vascular beds (Capo & Sillau 1983. However, at the microvascular level, the increased numerical density of CD31-positive capillaries in the heart and kidney of both hyperthyroid and hypothyroid animals does not conform to the usual differential pattern in these disorders.…”

Section: Discussionsupporting

confidence: 83%

“…Greater capillarity was observed in soleus and gastrocnemius muscles of hyperthyroid rats vs controls (Capo & Sillau 1983), and TH analogues were found to generate new arterial buds and increase the number of vessels per muscle fibre in a rabbit model of hind-limb ischaemia (El Eter et al 2007). It has also been reported that TH provides an important support for the neovascularisation required by tumour masses (Yalcin et al 2010).…”

Section: Introductionmentioning

confidence: 99%

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Influence of thyroid state on cardiac and renal capillary density and glomerular morphology in rats

Rodríguez-Gómez

Banegas

Wangensteen

et al. 2012

Journal of Endocrinology

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The purpose was to analyse the cardiac and renal capillary density and glomerular morphology resulting from a chronic excess or deficiency of thyroid hormones (THs) in rats. We performed histopathological, morphometrical and immunohistochemical analyses in hypothyroid and hyperthyroid rats to evaluate the density of mesenteric, renal and cardiac vessels at 4 weeks after induction of thyroid disorders. The main angiogenic factors in plasma, heart and kidney were measured as possible mediators of vascular changes. Mesenteric vessel branching was augmented and decreased in hyper-and hypothyroid rats respectively. The numerical density of CD31-positive capillaries was higher in left and right ventricles and in cortical and medullary kidney from both hyper-and hypothyroid rats vs controls. Numbers of podocytes and glomeruli per square millimetre were similar among groups. Glomerular area and percentage mesangium were greater in the hyperthyroid vs control or hypothyroid groups. No morphological renal lesions were observed in any group. Vascularisation of the mesenteric bed is related to TH levels, but an increased capillarity was observed in heart and kidney in both thyroid disorders. This increase may be produced by higher tissue levels of angiogenic factors in hypothyroid rats, whereas haemodynamic factors would predominate in hyperthyroid rats. Our results also indicate that the renal dysfunctions of thyroid disorders are not related to cortical or medullary microvascular rarefaction and that the proteinuria of hyperthyroidism is not secondary to a podocyte deficit. Finally, TH or its analogues may be useful to increase capillarity in renal diseases associated with microvascular rarefaction.

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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Influence of thyroid state on cardiac and renal capillary density and glomerular morphology in rats

Rodríguez-Gómez

Banegas

Wangensteen

et al. 2012

Journal of Endocrinology

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“…An increased capillary density was reported in hyperthyroid rats and human subjects. 7,8 Data obtained in rat aortic rings suggest that TH exerts part of its vascular effects through an endothelium-mediated mechanism. 9 In contrast, other in vitro data suggest that the smooth muscle cell, rather than the endothelium, is the main target of TH.…”

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confidence: 99%

“…The mechanisms underlying this hemodynamic pattern are, to a large extent, still unclear. 7,8,10,11 In particular, no attempt has previously been made to clarify the impact of chronic TH elevation on vascular reactivity in humans. The present study provides evidence that endothelial NO production plays a central role in the abnormal vascular tone in hyperthyroid patients.…”

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confidence: 99%

Impact of Hyperthyroidism and Its Correction on Vascular Reactivity in Humans

Napoli

Biondi²,

Guardasole³

et al. 2001

Circulation

171

108

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Background — Although thyroid hormone (TH) exerts relevant effects on the cardiovascular system, it is unknown whether TH also regulates vascular reactivity in humans. Methods and Results — We studied 8 patients with hyperthyroidism, basally (H) and 6 months after euthyroidism was restored by methimazole (EU). Thirteen healthy subjects served as control subjects (C). We measured forearm blood flow (FBF) by strain-gauge plethysmography during intrabrachial graded infusion of acetylcholine, sodium nitroprusside (SNP), norepinephrine, and L-NMMA (inhibitor of NO synthesis). Basal FBF (in mL · dL −1 · min −1 ) was markedly higher in H than in C (5.8±1.2 and 1.9±0.1, respectively; P <0.001) and was close to normal in EU (2.6±0.3, P <0.01 versus H). During acetylcholine infusion, FBF increased much more in H (+33±5) than in C (+14±3, P <0.01 versus H) and in EU (+20±5, P =0.01 versus H and P =NS versus C). In contrast, the response to SNP infusion was comparable in the patients and control subjects. During norepinephrine infusion, the fall in FBF was much more pronounced in H (−6±1) than in C (−0.7±0.3, P <0.005 versus H) and in EU (−1.5±0.3, P <0.01 versus H). Finally, inhibition of NO synthesis by L-NMMA decreased FBF by 2.8±0.6, 0.61±0.7, and 1.4±0.3 in H, C, and EU, respectively (H versus C and EU, P <0.05). Conclusions — In hyperthyroidism, (1) the marked basal vasodilation is largely accounted for by excessive endothelial NO production, (2) vascular reactivity is exaggerated because of enhanced sensitivity of the endothelial component, (3) the vasoconstrictory response to norepinephrine is potentiated, and (4) this abnormal vascular profile is corrected when euthyroidism is restored by medical therapy. The data demonstrate that vascular endothelium is a specific target of TH.

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“…This is thought to be a consequence of T3-mediated relaxation of vascular smooth muscle cells, leading to general arteriolar vasodilatation (17,19). Reduced vascular resistance may also be secondary to increased vascularity and/or alterations in the vascular control mechanisms favoring enhanced vasodilatation (26), such as increased muscular capillary vessel number (4,5) and heightened local release of vasodilators in peripheral tissue (3,22). Therefore, thyroid hormone-induced decreases in peripheral vascular resistance may underlie the lower diastolic blood pressures observed in TXϩR fetuses.…”

Section: Discussionmentioning

confidence: 99%

Thyroid hormone replacement normalizes renal renin and angiotensin receptor expression in thyroidectomized fetal sheep

Chen¹,

Carey²,

Valego³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Chen K, Carey LC, Valego NK, Rose JC. Thyroid hormone replacement normalizes renal renin and angiotensin receptor expression in thyroidectomized fetal sheep. Am J Physiol Regul Integr Comp Physiol 293: R701-R706, 2007. First published June 13, 2007; doi:10.1152/ajpregu.00232.2007.-Previous studies have suggested that thyroid hormone influences maturation of the renin-angiotensin system (RAS) and cardiovascular function in the late-gestation fetal sheep. To further examine the importance of thyroid hormone in this regard, we used the technique of thyroidectomy (TX) to remove endogenous thyroid hormone from the circulation and then replaced it with physiological amounts of exogenous thyroxine. We hypothesized that the previously observed changes in RAS activity and cardiovascular function associated with TX would be normalized. TX was performed at 120 days of gestational age (dGA), and control fetuses were sham operated. After 3 days of recovery, TX fetuses were continuously intravenously infused with thyroxine until delivery by cesarean section close to term (around 138 dGA). Immediately before necropsy, fetuses were infused with isoproterenol, and the hemodynamic responses were noted. Thyroid hormone replacement normalized not only plasma triiodothyronine (T3) and thyroxine (T4) levels but also the TX-induced decreases in renal renin mRNA and renal renin content. Renal ANG II subtype receptor expression levels were also normalized for both mRNA and protein. Decreased basal heat rate and systolic blood pressure associated with TX returned to normal following replacement; however, changes in mean blood pressure and isoproterenol-induced changes in mean blood pressure were not altered. These findings demonstrate that replacement of thyroid hormone in hypothyroid sheep fetuses can restore renal ANG II receptor and renin expression and secretion to normal. fetus; ANG I and II receptors; thyroidectomy; ovine COMPONENTS OF THE RENIN ANGIOTENSIN system (RAS) undergo maturational changes during fetal life. These changes appear to be important for regulating aspects of fetal development. Although the precise mechanisms mediating the changes in RAS expression are not completely understood, thyroid hormone, the levels of which increase dramatically close to term, is thought to be important in this regard. Findings from our recent studies lend support to this idea (6). We noted that fetal sheep thyroidectomized (TX) at 120 days of gestation (dGA, where term is around 145 dGA) did not show the expected increases in renal renin mRNA, renal active renin levels, and kidney ANG II receptor (AT1 and AT2) mRNA and protein expression close to term (6,8).Thyroid hormone is also thought to influence development of the cardiovascular system, particularly that pertaining to cardiac contractility and output, arterial relaxation, and systemic vascular resistance (14). Unsurprisingly, we found that TX sheep fetuses presented with altered cardiovascular function, namely decreased basal heart rate and blood pressure, and responsiveness to ...

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The effect of hyperthyroidism on capillarity and oxidative capacity in rat soleus and gastrocnemius muscles.

Cited by 53 publications

References 40 publications

Influence of thyroid state on cardiac and renal capillary density and glomerular morphology in rats

Influence of thyroid state on cardiac and renal capillary density and glomerular morphology in rats

Impact of Hyperthyroidism and Its Correction on Vascular Reactivity in Humans

Thyroid hormone replacement normalizes renal renin and angiotensin receptor expression in thyroidectomized fetal sheep

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