Effects of thyroid status on atrial natriuretic peptide release from isolated rat atria

Wong, Norman L.M.; Huang, D. T. K.; Guo, Ningning; Wong, Eric; Hu, D. C. K.

doi:10.1152/ajpendo.1989.256.1.e64

Cited by 15 publications

(9 citation statements)

References 12 publications

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“…The blood was taken into a prcehilled EDTA tube. To determine ANF secretion rate the right atrium was rapidly removed and superfused in a modi fied Langendorff apparatus as described before [10]. The atria were superfused with Tyrode solution at 0.5 ml/min for 60 min.…”

Section: Methodsmentioning

confidence: 99%

Changes in Atrial Natriuretic Factor Processing and Secretion with Age

Kao

Wong²,

Wong³

1992

Cardiology

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The effect of age on atrial natriuretic factor (ANF) metabolism in the rat was studied. Plasma ANF levels rose with age. A positive correlation was found between age and plasma ANF levels. Molecular forms of ANF were also examined. α-ANF and γ-ANF were present in the circulation. The ratio of γ-ANF/α-ANF increased with age. The atria were isolated and perfused to determine the ANF secretion rate. The spontaneous release of ANF decreased with age. The released ANF mainly consisted of α-ANF with a small amount of γ-ANF. The ratio of γ-ANF/α-ANF in the effluent increased with age. ANF concentrations in the atria varied with age, but the molecular forms did not. γ-ANF was the main form found in the atria. These results suggest that ANF secretion as well as post-transcriptional processing is altered with age.

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Section: Methodsmentioning

confidence: 99%

Changes in Atrial Natriuretic Factor Processing and Secretion with Age

Kao

Wong²,

Wong³

1992

Cardiology

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“…Hyperthyroidism causes an increase in atrial natriuretic peptide (ANP) secretion and a decreased release occurs in hypothyroid humans (143) and rats (144,145). Moreover, it has been reported that, in cultured rat atrial myocytes, T 3 stimulates both synthesis and release of ANP (146,147).…”

Section: Other Vasoactive Hormonesmentioning

confidence: 99%

Vascular and renal function in experimental thyroid disorders

Moreno²,

et al. 2006

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This review focuses on the effects of thyroid hormones in vascular and renal systems. Special emphasis is given to the mechanisms by which thyroid hormones affect the regulation of body fluids, vascular resistance and, ultimately, blood pressure. Vascular function is markedly affected by thyroid hormones that produce changes in vascular reactivity and endothelial function in hyper-and hypothyroidism. The hypothyroid state is accompanied by a marked decrease in sensitivity to vasoconstrictors, especially to sympathetic agonists, alteration that may play a role in the reduced blood pressure of hypothyroid rats, as well as in the preventive effects of hypothyroidism on experimental hypertension. Moreover, in hypothyroid rats, the endothelium-dependent and nitric oxide donors vasodilation is reduced. Conversely, the vessels from hyperthyroid rats showed an increased endothelium-dependent responsiveness that may be secondary to the shear-stress induced by the hyperdynamic circulation, and that may contribute to the reduced vascular resistance characteristic of this disease. Thyroid hormones also have important effects in the kidney, affecting renal growth, renal haemodynamics, and salt and water metabolism. In hyperthyroidism, there is a resetting of the pressure-natriuresis relationship related to hyperactivity of the renin-angiotensin system, which contributes to the arterial hypertension associated with this endocrine disease. Moreover, thyroid hormones affect the development and/or maintenance of various forms of arterial hypertension. This review also describes recent advances in our understanding of thyroid hormone action on nitric oxide and oxidative stress in the regulation of cardiovascular and renal function and in the long-term control of blood pressure.

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“…Various studies have suggested the involvement of AT1 receptors in the expression of sodium appetite behavior using central administration of antagonists specific for these receptors (10)(11)(12). These alterations were revealed concomitantly with the observation of low genetic expression and reduced basal and stimulated release of atrial natriuretic peptide in hypothyroidism (9,13,14) together with the decreased capacity of proximal tubular sodium reabsorption (15). Literature data have led to the conclusion that the sodium appetite of hypothyroid rats is unique because it occurs in the presence of reduced plasma levels of both aldosterone and angiotensin II (3,(5)(6)(7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Effect of chronic oral administration of a low dose of captopril on sodium appetite of hypothyroid rats: Influence of aldosterone treatment

Ventura

Olivares

Passos

et al. 2001

Braz J Med Biol Res

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Rats rendered hypothyroid by treatment with methimazole develop an exaggerated sodium appetite. We investigated here the capacity of hypothyroid rats (N = 12 for each group) to respond to a low dose of captopril added to the ration, a paradigm which induces an increase in angiotensin II synthesis in cerebral areas that regulate sodium appetite by increasing the availability of circulating angiotensin I. In addition, we determined the influence of aldosterone in hypothyroid rats during the expression of spontaneous sodium appetite and after captopril treatment. Captopril significantly increased (P<0.05) the daily intake of 1.8% NaCl (in ml/100 g body weight) in hypothyroid rats after 36 days of methimazole administration (day 36: 9.2 ± 0.7 vs day 32: 2.8 ± 0.6 ml, on the 4th day after captopril treatment). After the discontinuation of captopril treatment, daily 1.8% NaCl intake reached values ranging from 10.0 ± 0.9 to 13.9 ± 1.0 ml, 48 to 60 days after treatment with methimazole. Aldosterone treatment significantly reduced (P<0.05) saline intake before (7.3 ± 1.6 vs day 0, 14.4 ± 1.3 ml) and after captopril treatment. Our results demonstrate that, although hypothyroid rats develop a deficiency in the production of all components of the renin-angiotensin-aldosterone system, their capacity to synthesize angiotensin II at the cerebral level is preserved. The partial reversal of daily 1.8% NaCl intake during aldosterone treatment suggests that sodium retention reduces both spontaneous and captopril-induced salt appetite. Key wordsPrevious studies have shown a reduction in NaCl aversion in hypothyroid rats with urinary sodium loss and an increase in sodium appetite in different experimental models (1-4). However, controversies still exist regarding the physiological mechanism responsible for sodium appetite, since genetic expression, synthesis and release of the components of the renin-angiotensin-aldosterone system are reduced in hypothyroidism (3,(5)(6)(7)(8)(9). Moreover, angiotensin II receptor density is altered in hypothyroidism. An increase in

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Effects of thyroid status on atrial natriuretic peptide release from isolated rat atria

Cited by 15 publications

References 12 publications

Changes in Atrial Natriuretic Factor Processing and Secretion with Age

Changes in Atrial Natriuretic Factor Processing and Secretion with Age

Vascular and renal function in experimental thyroid disorders

Effect of chronic oral administration of a low dose of captopril on sodium appetite of hypothyroid rats: Influence of aldosterone treatment

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