Urinary excretion of digoxin-like immunoreactive factor and arginine-vasopressin in hyper- and hypo-thyroid rats

Vargas, Félix; Baz, M. J.; Luna, Juan de Dios; Andrade, J.; Haro, Juan

doi:10.1042/cs0810471

Cited by 22 publications

(25 citation statements)

References 20 publications

(16 reference statements)

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“…Medullary NO plays a major role in the renal regulation of sodium and water excretion and therefore in the control of arterial blood pressure (8,9). The normal values in medullary NOS activity in our hypothyroid rats indicate that the medulla has an adequate capacity to synthesize NO, which is consistent with the normal sodium handling of hypothyroid rats under normal conditions and after several challenges (6,7). The high NOS activity in the renal cortex of hyperthyroid rats may be secondary to the hyperdynamic circulation of these animals, because cortical NOS activity is mainly produced by constitutive endothelial NOS (33).…”

Section: Discussionsupporting

confidence: 54%

“…Hyperthyroidism increases the responsiveness of resistance vessels to the endothelium-dependent vasodilator, acetylcholine, whereas methimazole-induced hypothyroidism attenuates the endothelium-dependent response (5). Thyroid dysfunctions also affect cardiac and renal weight as well as renal sodium handling (2,6,7). Thus, hyperthyroidism occurs with a reduced sodium excretion after a saline load (7) and a blunted pressure -diuresis -natriuresis (PDN) response (6, 7) whereas, in hypothyroidism, a normal sodium excretion (7) or a tendency to sodium loss (2) have been reported.…”

Section: Introductionmentioning

confidence: 99%

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Nitric oxide synthase activity in hyperthyroid and hypothyroid rats

Quesada

Sainz

Wangensteen

et al. 2002

European Journal of Endocrinology

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Objective: Thyroid disorders are accompanied by important changes in haemodynamic and cardiac functions and renal sodium handling. Since nitric oxide (NO) plays a crucial role in regulating vascular tone and renal sodium excretion, the present paper was designed to determine whether changes in the activity of NO synthase (NOS) participate in the cardiovascular and renal manifestations of thyroid disorders. Methods: We measured NOS activity in the heart (left and right ventricles), vessels (aorta and cava) and kidney (cortex and medulla) of euthyroid, hyperthyroid and hypothyroid rats after 6 weeks of treatment. NOS activity was determined by measuring the conversion of L-Results: NOS activity was higher in all tissues from hyperthyroid rats when compared with controls, except in the right ventricle. In the hypothyroid group, NOS activity showed a more heterogeneous pattern, with significant increases in both ventricles but significant reduction in the aorta, while in the vena cava, renal cortex and medulla the enzyme activity also tended to be higher, but significance was not reached. Conclusions: These data indicated that NOS activity was upregulated in tissues primarily related to blood pressure control in hyperthyroid rats, suggesting that an increased NO production may contribute to the hyperdynamic circulation in hyperthyroidism and may have a protective homeostatic effect in the target organs of the hypertension that accompanies this endocrine disease. The aortic and renal findings in hypothyroid rats suggested a possible role for NOS in the increased peripheral resistance and the normal pressure -diuresis -natriuresis response of these hypotensive animals, although hypothyroidism produced a heterogeneous tissue response in NOS activity.

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Section: Discussionsupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Nitric oxide synthase activity in hyperthyroid and hypothyroid rats

Quesada

Sainz

Wangensteen

et al. 2002

European Journal of Endocrinology

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“…30 This mechanism might increase peripheral resistance and therefore increase BP. Moreover, hyperthyroidism affects renal sodium handling in rats, 2,5,6 reduces sodium excretion after a saline load, 5 and blunts the pressure-diuresisnatriuresis response. 6 These antinatriuretic effects might be aggravated by NO deficiency 9,10 and contribute to producing a displacement to the right in the set point of the pressurediuresis-natriuresis relation, as indicated by the normal sodium excretion with increased BP in the T 4 ϩL-NAMEtreated group.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] Animal studies have reported a dose-and time-related increase in arterial pressure 5,6 and have shown that the hyperthyroid state affects cardiac and renal weight and reduces renal sodium excretion. 2,5,6 It is well known that nitric oxide (NO) plays a major role in the regulation of vascular tone, 7 renal sodium excretion, 8,9 and therefore, of arterial blood pressure (BP). 10 Both acute and chronic administration of NO synthase (NOS) inhibitors increase systemic arterial BP.…”

mentioning

confidence: 99%

Increased Pressor Sensitivity to Chronic Nitric Oxide Deficiency in Hyperthyroid Rats

et al. 2003

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Abstract-We studied the effects of a possible interaction between partial nitric oxide deficiency and thyroid hormone excess on the long-term control of blood pressure (BP) and morphological and renal variables and examined the role of the renin-angiotensin system in the increased BP of this interaction. Eight groups (nϭ8 each) of male Wistar rats were used: a control group; 3 groups that were treated with thyroxine (50 g/d), N w -nitro-L-arginine methyl ester (L-NAME; subpressor dose, 1.5 mg · kg, or thyroxine plus L-NAME; and another 4 similarly treated groups that received losartan (20 mg · kg Ϫ1 · d Ϫ1) in their drinking fluid. All treatments were maintained for 3 weeks. The time course of tail systolic BP was recorded once a week. At the end of the experimental period, we measured mean arterial pressure in conscious rats and assessed the morphological, metabolic, plasma, and renal variables. Thyroxine produced a mild BP increase from the second week of treatment and an increase in plasma angiotensin II and plasma nitrates/nitrites by the end of the study. Simultaneous administration of thyroxine and a subpressor dose of L-NAME produced a marked BP increase that reached significance from the first week of treatment. Losartan produced normotension in thyroxine-treated rats and attenuated the BP elevation in thyroxineϩL-NAME-treated rats. Hyperthyroid rats showed relative renal and ventricular hypertrophy, absence of absolute left ventricular hypertrophy, and proteinuria. These alterations were not changed by losartan. We conclude that an impaired nitric oxide system might have a counterregulatory homeostatic role against the prohypertensive effects of thyroid hormone and that the renin-angiotensin system plays an important role in thyroxineϩL-NAME hypertension. Key Words: blood pressure Ⅲ hypertrophy, cardiac Ⅲ losartan Ⅲ nitric oxide Ⅲ hyperthyroidism T he hyperthyroid state is an endocrine disorder associated with important changes in hemodynamic, renal, and cardiac function. 1-3 Hyperthyroidism manifests a hyperdynamic circulation, with increased cardiac output, increased heart rate, and decreased peripheral resistance. 2-4 These characteristic cardiovascular manifestations of hyperthyroidism have been reproduced in rats by thyroid hormone treatment. [1][2][3] Animal studies have reported a dose-and time-related increase in arterial pressure 5,6 and have shown that the hyperthyroid state affects cardiac and renal weight and reduces renal sodium excretion. 2,5,6 It is well known that nitric oxide (NO) plays a major role in the regulation of vascular tone, 7 renal sodium excretion, 8,9 and therefore, of arterial blood pressure (BP). 10 Both acute and chronic administration of NO synthase (NOS) inhibitors increase systemic arterial BP. 11,12 Hyperthyroidism in rats increases the responsiveness of resistance vessels to the endothelium-dependent vasodilator acetylcholine. 13 Fernández et al 14 demonstrated that hyperthyroidism leads to a significant and reversible enhancement in rat liver NOS activity. More rec...

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“…Some authors have found high plasma AVP and postulate the role of this hormone in the development of hyponatremia of hypothyroidism (Skowsky & Kikuchi 1978, Laczi et al 1987. Others have found that plasma AVP is normal or even suppressed (Iwasaki et al 1990, Vargas et al 1991, Arnaout et al 1992, Ota et al 1994. Probably the discrepancies are due to the different characteristics of the individuals studied, principally the duration and severity of the hypothyroidism, which may cause an increase in plasma AVP by raising non-osmotic stimuli.…”

Section: Discussionmentioning

confidence: 90%

Water metabolism disturbances at different stages of primary thyroid failure

Villabona¹,

Rosel²,

Navarro³

et al. 2001

Journal of Endocrinology

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The aim of the present study was to study salt and water metabolism in thyroid deficiency.We performed an oral water loading test (OWL) and a hypertonic 5% saline infusion test (HSI) in 16 patients with overt primary hypothyroidism before replacement treatment (PRE group) and after, in eight patients with subclinical hypothyroidism (SUB group) and in 16 normal individuals (CG group).In the PRE group, a lower free water clearance was detected in the OWL (P<0·022), with lower plasma osmolality (OWL: P<0·005; HSI: P<0·001) and arginine vasopressin (AVP) (OWL: P<0·001; HSI: P<0·001) than the CG group, across both tests; they normalized with the replacement treatment. The same plasma abnormalities were detected in the SUB group with the HSI. Although the AVP and thirst thresholds did not differ between the groups, the lag between them was lower in the PRE (4·1 3·2 mOsm/kg) and SUB group (2·6 2·1 mOsm/ kg) than in the CG group (13·3 9·2 mOsm/kg) (P<0·05). There were no differences in atrial natriuretic hormone (ANH), plasma renin activity (PRA) and plasma aldosterone among the groups.These results indicate that plasma hypo-osmolality and low levels of AVP are present in primary hypothyroidism, and indeed are already present in the subclinical phase of the disease. An overlap between the thresholds of thirst and AVP seem to play a role in these abnormalities, but ANH, PRA and plasma aldosterone do not appear to contribute.

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Urinary excretion of digoxin-like immunoreactive factor and arginine-vasopressin in hyper- and hypo-thyroid rats

Cited by 22 publications

References 20 publications

Nitric oxide synthase activity in hyperthyroid and hypothyroid rats

Nitric oxide synthase activity in hyperthyroid and hypothyroid rats

Increased Pressor Sensitivity to Chronic Nitric Oxide Deficiency in Hyperthyroid Rats

Water metabolism disturbances at different stages of primary thyroid failure

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