Biochemical and physiologic effects of thyroid hormone on cardiac performance

Morkin, Eugene; Flink, Irwin L.; Goldman, Steven

doi:10.1016/0033-0620(83)90004-x

Cited by 227 publications

(104 citation statements)

References 185 publications

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“…It is therefore possible that increased cardiac output, a feature of human hyperthyroidism (Martin et al 1991) and animal models of the disease (cf. Morkin et al 1983), led to increased eNOS expression in HYPER via a chronic increase in shear stress on the aortic endothelium.…”

Section: Capacity For No Formationmentioning

confidence: 99%

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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Section: Capacity For No Formationmentioning

confidence: 99%

Thyroid status and nitric oxide in rat arterial vessels

McAllister¹,

Albarracin²,

Price³

et al. 2005

Journal of Endocrinology

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“…Cardiac performance is significantly altered, with an increase in heart rate and in the force and velocity of contraction, with concomitant hypertrophy (Morkin et al 1983). The nature of many of these adaptations has been clarified by measuring the mechanical, electrophysiological, and biochemical properties of hyperthyroid hearts.…”

Section: Introductionmentioning

confidence: 99%

Hyperthyroidism selectively modified a transient potassium current in rabbit ventricular and atrial myocytes.

Shimoni

Banno

Clark

1992

The Journal of Physiology

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SUMMARY1. Transient outward potassium currents (It) were compared in single cardiac myocytes obtained from normal and hyperthyroid rabbits. Currents were recorded using the suction electrode whole-cell voltage clamp technique.2. In ventricular myocytes from hyperthyroid animals (at 22 TC and a stimulation rate of 0-2 Hz), It was 4-to 5-fold larger than in normal myocytes, in a potential range of -20 to + 60 mV. As in normal myocytes, It in hyperthyroid myocytes was calcium insensitive, and was more than 90 % suppressed by 2 mm 4-aminopyridine.3. The increase in It was observed over a wide range of stimulation rates, even at rates sufficiently slow to enable complete reactivation of the It channels. However, there was a major change in the rate dependence of It in hyperthyroid myocytes, with significant It current still present at rates (e.g. 1-2 Hz) at which it is normally completely suppressed.4. The augmentation of It in the hyperthyroid myocytes could not be accounted for by changes in the voltage dependence or the kinetics of channel activation or inactivation. There was no change in the reversal potential of It, implying no change in the selectivity of the channel.5. Single-channel activity was recorded using the cell-attached mode of recording. In myocytes from hyperthyroid rabbit we observed the following: (a) active patches (often containing two channels) were obtained more frequently in comparison to control; (b) the unitary conductance of the channel was the same; (c) single-channel openings persisted at high stimulation rates.6. In contrast to hyperthyroid ventricular cells, It in atrial cells from the same hearts was not substantially changed.7. The rate dependence of It in atrial cells was also unaffected by hyperthyroidism, in contrast to the large changes observed in ventricular cells. Thus, in atrial cells from hyperthyroid hearts the current was totally suppressed at rates of 1-2 Hz, as in euthyroid conditions.

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“…Both naturally occurring and experimental hyperthyroidism are associated with predictable changes on the heart and cardiovascular system (1)(2)(3). Previous studies have shown that administration of excess thyroid hormone leads to increased synthesis of RNA, increased protein synthesis, and the development of cardiac hypertrophy (4,5).…”

Section: Introductionmentioning

confidence: 99%

Effects of thyroid hormone on cardiac size and myosin content of the heterotopically transplanted rat heart.

Klein¹,

Hong²

1986

J. Clin. Invest.

165

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Infrarenal heterotopic cardiac isografts maintain structural and functional integrity. We have used this transplantation model to further explore the mechanisms of thyroid hormone-induced cardiac hypertrophy. Thyroid hormone administration, 1-thyroxine (T4) 10 Mg/animal per d, led to a significant 30% increase in total heart weight and a 40% increase in the myosin content of the in situ heart when compared with control. In contrast, T4 treatment was without effect on the heart weight, protein content, rate of protein synthesis, or calculated myosin content of the heterotopic, nonworking heart. Heterotopic hearts demonstrated a significant decrease in the percentage of the VI myosin isoenzyme from 95% to 61%. This shift occurred in euthyroid animals but was prevented by T4 treatment. These results suggest that thyroxine-induced cardiac hypertrophy is mediated indirectly via changes in cardiac work. Myosin isoenzyme expression can be altered by changes in work load but is still responsive to increased levels of thyroid hormone.

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Biochemical and physiologic effects of thyroid hormone on cardiac performance

Cited by 227 publications

References 185 publications

Thyroid status and nitric oxide in rat arterial vessels

Thyroid status and nitric oxide in rat arterial vessels

Hyperthyroidism selectively modified a transient potassium current in rabbit ventricular and atrial myocytes.

Effects of thyroid hormone on cardiac size and myosin content of the heterotopically transplanted rat heart.

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