Catecholamine sensitivity in hyperthyroidism and hypothyroidism.

McDevitt, DG; Riddell, J. G.; Hadden,; Da, Montgomery

doi:10.1111/j.1365-2125.1978.tb00855.x

Cited by 41 publications

(8 citation statements)

References 10 publications

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“…Many of the clinical manifestations of this disease resemble the effects of stimulation of the sympathetic nervous system, but the reasons for this have never been satisfactorily explained. Increased sensitivity to catecholamines has been said to occur in hyperthyroidism, but catecholamine concentrationresponse curves have not been found to alter in patients when they were hyperthyroid compared to when they were euthyroid (Aoki, Wilson & Theilin, 1972;McDevitt, Riddell, Hadden & Montgomery, 1978). Another possible explanation involves alterations in protein binding: if the fraction of catecholamines bound to plasma proteins was substantially reduced (and, conversely, the free fraction increased) then an apparent increase in sensitivity to catecholamines might be seen.…”

Section: Resultsmentioning

confidence: 99%

Plasma protein binding of propranolol and isoprenaline in hyperthyroidism and hypothyroidism.

Kelly¹,

McDevitt²

1978

Brit J Clinical Pharma

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1The possibility that thyroid disease might result in alterations in the plasma protein binding of drugs has been investigated by studying the binding of propranolol and isoprenaline in patients with hyperthyroidism and hypothyroidism. 2 Plasma protein binding of propranolol and isoprenaline has been measured in seven hyperthyroid patients and ten hypothyroid patients. Plasma binding was estimated by equilibrium dialysis at 370C using tritiated propranolol and isoprenaline, both when the patients had thyroid dysfunction and again when they were euthyroid.

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Section: Resultsmentioning

confidence: 99%

Plasma protein binding of propranolol and isoprenaline in hyperthyroidism and hypothyroidism.

Kelly¹,

McDevitt²

1978

Brit J Clinical Pharma

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“…However, this hypothesis has been questioned on the basis that plasma catecholamine levels are normal and even low in hyperthyroid patients [2][3][4]. In addition, controversial data have been obtained with respect to cardiovascular sensitivity to catecholamines [10,11] or to the number of fl-adrenergic receptors present in hyperthyroidism [12]. Similarly, the observation that fl-adrenoceptor blockade induces a reduction in heart rate of equivalent magnitude in normal and hyperthyroid conditions does not suggest an increase in sympathetic activity in human hyperthyroidism [13][14][15].…”

Section: Discussionmentioning

confidence: 98%

Short-term variability of blood pressure and heart rate in hyperthyroidism

Girard

Hugues

Jeunne

et al. 1998

Clinical Autonomic Research

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The effect of hyperthyroidism on the short-term memory variability of blood pressure and heart rate was evaluated in 12 untreated hyperthyroid patients during thyrotoxicosis and after a 6 1/2 month treatment designed to achieve a stable euthyroid state. Beat-by-beat finger blood pressure was measured with a Finapres device. The pulse interval, from which pulse rate was derived, was obtained from the blood pressure signal. Due to the significant change in heart rhythm associated with thyrotoxicosis, both pulse interval (taken as a surrogate of heart period) and pulse rate (taken as a surrogate of heart rate) were computed. Power spectral analysis showed a reduction in the overall heart period variability in the supine position in the hyperthyroid compared to the euthyroid state. This effect was observed in the low-frequency (0.005-0.068 Hz), mid-frequency (0.068-0.127 Hz) and high-frequency (respiratory) domains as well, with a significant reduction of the modulus of these bands of 31%, 35% and 47%, respectively. The heart rate spectral modulus also exhibited a reduction of the high-frequency component (31%) in the supine position in the hyperthyroid subjects. These changes in heart rhythmicity corroborate a vagal deficit in hyperthyroidism. In addition, blood pressure spectral power exhibited a significant deficit in the orthostatism-induced mid-frequency systolic blood pressure rise in the hyperthyroid state (64%) compared with the euthyroid state. This observation may reflect a reduced vascular sympathetic activation with standing. The resulting vasodilatation could well contribute to normalize blood pressure in thyrotoxicosis in which cardiac output is increased.

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“…Earlier studies have suggested that an altered car¬ diovascular sensitivity to circulating catecholamines might exist in hyperthyroidism (Harrison 1964;Waldstein 1966) but more recent work has not confirmed this suggestion (Aoki et al 1967;Levey 1971;McDevitt et al 1978). The adenylate cyclase system is involved in the peripheral actions of catecholamines (Sutherland & Robison 1966;Broadus 1977) and following increased ß-adrener¬ gic stimulation plasma and urinary excretion of cAMP were raised (Ball et al 1972;Kunitada et al 1978).…”

mentioning

confidence: 87%

Effects of propranolol and atenolol on plasma and urinary cyclic adenosine 3′,5′-monophosphate in hyperthyroid patients

Nilsson

Andersson

Karlberg

1980

Acta Endocrinologica

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Supine and upright plasma concentrations and the urinary excretion of cyclic adenosine 3\ m=' \ , 5\ m=' \ \ x =r eq-\ monophosphate (cAMP) were studied in 26hyper t hyr oid patients before and during treatment for 3\p=n-\6 days and one month with a non-selective (propranolol, n = 13) or a selective \ g = b \ -l -a d r e n e r g i c antagonist (atenolol, n = 13). Before treatment supine and upright plasma concentrations of cAMP were elevated compared to healthy controls and compared to a re-investigation in the euthyroid state. Propranolol and atenolol both reduced supine and upright plasma cAMP and the reduction persisted during one month of treatment. In five untreated hyperthyroid patients no changes in plasma cAMP were observed between two different investigations. Turning to an upright posture was associated with an increase in plasma cAMP levels in 22 out of the 31 hyperthyroid patients (P < 0.05), while all 11 patients re-examined in the euthyroid state showed a rise in plasma cAMP in the upright position (P < 0.001). The 24 h urinary excretion of cAMP was unaltered during treatment with \g=b\-adrenergic antagonists. The data support earlier findings of stimulation of adrenergic receptor activity by thyroid hormone excess. In hyperthyroidism \g=b\-adrenergicantagonists decrease but do not normalize the activity of the adenylate cyclase system. This reducing effect may be of importance for the alleviation of hyperthyroid symptoms and signs during treatment with \g=b\-adrenergicantagonists.

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Catecholamine sensitivity in hyperthyroidism and hypothyroidism.

Cited by 41 publications

References 10 publications

Plasma protein binding of propranolol and isoprenaline in hyperthyroidism and hypothyroidism.

Plasma protein binding of propranolol and isoprenaline in hyperthyroidism and hypothyroidism.

Short-term variability of blood pressure and heart rate in hyperthyroidism

Effects of propranolol and atenolol on plasma and urinary cyclic adenosine 3′,5′-monophosphate in hyperthyroid patients

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