Influence of the Thyroid Hormone on the Effector Systems of the Mammalian Heart

Hoffmann, Francisco; Hoffmann, Elena J.; Talesnik, J

doi:10.1152/ajplegacy.1947.148.3.689

Cited by 25 publications

(11 citation statements)

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“…Indeed, several early studies suggested that hypothyroidism does reduce the responsiveness of the heart to catecholamine stimulation (7)(8)(9). Recent reports, however, have failed to confirm these findings.…”

Section: Resultsmentioning

confidence: 99%

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Decreased myocardial adenyl cyclase activity in hypothyroidism

Levey¹,

Skelton²,

Epstein³

1969

J. Clin. Invest.

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A B S T R A C T It has been suggested that hypothyroidism may alter the responsiveness of the heart to sympathetic stimulation. To define more precisely the interrelationship between hypothyroidism and catecholamine responsiveness we: (a) studied the effects of norepinephrine and fluoride on the activation of adenyl cyclase in the particulate fraction of heart homogenates from euthyroid and hypothyroid cats; and (b) assessed the contractile response of isolated right ventricular papillary muscles from the same cats to increasing concentrations of norepinephrine. It was found that maximal accumulation of cyclic 3',5'-adenosine monophosphate (3',5'-AMP) was significantly lower at peak norepinephrine concentrations in the hypothyroid (284 ±5 pmoles) than in the euthyroid group (326 ±10 pmoles) (P < 0.02). However, the Km for norepinephrine was similar in both groups (1-2 X 10' moles/liter), and there was no apparent change in the threshold concentration. Fluoride-mediated increases in Cyclic 3',5'-AMP accumulation were also significantly lower in the hypothyroid (585 +25 pmoles) as compared to the euthyroid group (790 ±20 pmoles) (P < 0.02). In contrast, norepinephrine produced a similar augmentation of contractility in isolated papillary muscles from the hypothyroid and euthyroid cats. It thus appears that although the hypothyroid state is associated with a decrease in the total amount of myocardial adenyl cyclase per milligram of tissue capable of being activated by norepinephrine or fluoride, there is no change in the sensitivity of the enzyme to norepinephrine stimulation. Moreover, the finding that the inotropic response to norepinephrine is unaltered in hypothyroidism is compatible with the hypothesis that only a fraction of the total intracellular cyclic 3',5'-AMP produced by norepinephrine activation of adenyl cyclase is required to elicit the inotropic response.

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Section: Resultsmentioning

confidence: 99%

“…The data from early studies on the effects of hypothyroidism on the heart also suggested that sensitivity to the physiologic effects of sympathetic stimulation was depressed (7)(8)(9). However, these studies generally lacked adequate control groups and statistical analysis.…”

Section: Introductionmentioning

confidence: 99%

Decreased myocardial adenyl cyclase activity in hypothyroidism

Levey¹,

Skelton²,

Epstein³

1969

J. Clin. Invest.

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“…Impairment of myocardial energy production due to altered enzyme function may have been a factor involved in the failure of an adequate cardiac output response to exercise (31)(32)(33)(34)(35). The action of thyroxin on myocardial function may well be mediated by sensitization of the myocardium to sympathetic nerve stimulation and to sympathomimetic amines (36)(37)(38)(39)(40). An increased concentration of catechol amines has also been demonstrated in the myocardia of thyrotoxic dogs (41).…”

Section: Discussionmentioning

confidence: 99%

A Correlation of Clinical and Hemodynamic Studies in Patients With Hyperthyroidism With and Without Congestive Heart Failure *

Graettinger¹,

Muenster²,

Selverstone³

et al. 1959

J. Clin. Invest.

127

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“…Our findings lead us to suggest that the decreased cardiac responses to vagal stimulation in hyperthyroid animals (Cairoli & Crout, 1967;Hoffmann et al, 1947) may be explained by postjunctional changes in the response to acetylcholine occurring at the receptor level. It remains to be established whether thyroxine treatment acts directly upon cardiac muscarinic receptors, as it does upon cardiac adrenoceptors (Tsai & Chen, 1978;Chang & Kunos, 1981), or indirectly by altering cardiovascular dynamics.…”

Section: Discussionmentioning

confidence: 71%

“…Similarly there have been reports of changes in the numbers of muscarinic receptor binding sites in rat myocardial membranes in altered thyroid state (Sharma & Banerjee, 1977;Robberecht, Waelbroeck, Claeys, Nguyen Huu, Chatelain & Christophe, 1982). However, studies of the influence of altered thyroid state upon responses mediated by cardiac muscarinic receptors in this species have been concerned with the effects of vagal stimulation upon heart rate in vivo (Hoffmann, Hoffmann & Talesnik, 1947;Cairoli & Crout, 1967;Frazer & Hess, 1969).…”

Section: Introductionmentioning

confidence: 99%

The effects of altered thyroid state upon responses mediated by atrial muscarinic receptors in the rat

Ishac

Pennefather

1983

British J Pharmacology

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1Untreated rats, and rats treated with methimazole (0.05% w/v in drinking water) or thyroxine (1 mg/kg, s.c., three times weekly) for 4 -6 weeks to induce hypo-and hyperthyroidism respectively, were used to study the influence of thyroid hormone upon negative chronotropic and inotropic responses mediated by cardiac muscarinic receptors, and upon the affinity of these receptors for atropine. 2 Negative chronotropic effects of methacholine were investigated by establishing partial concentration-response curves for isolated preparations of right atria. Methacholine was least potent in tissues from thyroxine-treated rats. 3 Isolated left atria paced at 3 Hz, and spontaneously beating right atria, were used in studies of the negative inotropic effects of methacholine. This agonist was least potent in atria from the thyroxinetreated rats in which it also produced the smallest maximal responses. 4 The negative inotropic effects of carbachol were examined on left atria paced at 3, 5 and 5.8 Hz to approximate the basal contraction rates of isolated right atria from methimazole-treated, untreated control and thyroxine-treated rats, respectively. At each of these frequencies, carbachol was most potent in atria from methimazole-treated rats, and least potent in atria from thyroxine-treated rats. Maximal responses were smallest in the latter group.5 pA2 values for atropine with methacholine as the agonist were obtained by the method of Arunlakshana & Schild (1959) for spontaneously beating right atria (negative chronotropic and inotropic effects) and left atria paced at 3 Hz (negative inotropic effects). Slopes of Schild plots did not differ from minus one in tissues from each of the experimental groups; pA2 values were similar, indicating that thyroid status is without effect upon the affinity of this antagonist for muscarinic receptors mediating both negative inotropic and chronotropic effects. 6 The results are discussed in the light of reports that hypothyroidism increases, and hyperthyroidism decreases the numbers of high affinity muscarinic receptor binding sites in the rat myocardium.

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Influence of the Thyroid Hormone on the Effector Systems of the Mammalian Heart

Cited by 25 publications

References 0 publications

Decreased myocardial adenyl cyclase activity in hypothyroidism

Decreased myocardial adenyl cyclase activity in hypothyroidism

A Correlation of Clinical and Hemodynamic Studies in Patients With Hyperthyroidism With and Without Congestive Heart Failure *

The effects of altered thyroid state upon responses mediated by atrial muscarinic receptors in the rat

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