Nitric oxide synthase activity in hyperthyroid and hypothyroid rats

Quesada, Andrés; Sainz, Juan; Wangensteen, Rosemary; Rodríguez-Gómez, Isabel; Vargas, Félix; Osuna, Antonio

doi:10.1530/eje.0.1470117

Cited by 91 publications

(75 citation statements)

References 34 publications

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“…Our findings for aortic NOS activity in different thyroid states resemble those reported by Quesada et al (2002). Further, these findings are consistent with earlier findings concerning vascular function.…”

Section: Capacity For No Formationsupporting

confidence: 93%

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 Formationsupporting

confidence: 93%

Thyroid status and nitric oxide in rat arterial vessels

McAllister¹,

Albarracin²,

Price³

et al. 2005

Journal of Endocrinology

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“…Various mechanisms or sets of mechanisms might participate in the increased sensitivity to partial NOS blockade in hyperthyroid rats. This study and several reports [13][14][15] provide evidence that the hyperdynamic circulation of hyperthyroidism is accompanied by increased NO production. Anemia 25 and cirrhosis of the liver 26 are also associated with hyperdynamic circulation and increased NO production, and cirrhotic rats also show an increased pressor responsiveness to NO blockade.…”

Section: Discussionsupporting

confidence: 82%

“…13 Fernández et al 14 demonstrated that hyperthyroidism leads to a significant and reversible enhancement in rat liver NOS activity. More recently, our group reported 15 that NOS activity is upregulated in tissues primarily related to BP control in hyperthyroid rats. Our finding suggested that increased NO production might contribute to the hyperdynamic circulation in hyperthyroidism and might have a protective homeostatic effect on the increased BP that accompanies this endocrine disease.…”

mentioning

confidence: 94%

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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“…These results are similar to findings of previous studies in SHHF rats (5). The exact mechanism of the increase in hypertension in this model is not known and could be caused by any individual factor or combination of factors, including increased body weight, leptin resistance, increased salt sensitivity, increased levels of Ang II, or reduced levels of bradykinin and NO (3,16,24,27,36,37,39).…”

Section: Discussionsupporting

confidence: 91%

Effects of long-term captopril andl-arginine treatment on ventilation and blood pressure in obese male SHHF rats

Schlenker

Kost

Likness

2004

Journal of Applied Physiology

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Schlenker, E. H., C. K. Kost, Jr., and M. M. Likness. Effects of long-term captopril and L-arginine treatment on ventilation and blood pressure in obese male SHHF rats. J Appl Physiol 97: 1032-1039, 2004. First published May 14, 2004 10.1152/japplphysiol.00255.2004We investigated the effects of captopril (Cap) and L-arginine (Arg) on hypertension and cardiopulmonary function. Our hypothesis was that Cap therapy or Arg will improve cardiopulmonary risk factors for hypertension and hypoventilation in the obese spontaneously hypertensive heart failure rat, which is characterized by hypertension, obesity, and disorders of lipid and carbohydrate metabolism. For the first study, one group of rats received Cap in drinking water, and a second group received deionized water (DI). For the second study, rats were further subdivided. Some Cap-treated rats continued on this treatment, and the other half were now given DI to determine whether there would be residual effects of Cap treatment. A subgroup of rats who had received DI was then given Arg, whereas the rest remained on DI. In the first study, Cap-treated rats exhibited decreases in systolic and diastolic blood pressures, frequency of breathing, and minute ventilation, but ventilatory control was maintained. In contrast, blood pressures and relative ventilation to metabolism were higher in the DI-treated group. Removal of Cap increased blood pressure and decreased tidal volume while these rats maintained frequency. Although Arg-treated rats did not exhibit a decrease of blood pressure, ventilation was maintained in this group by preserving tidal volume. Thus Cap and Arg affected ventilation through different mechanisms independent of blood pressure.spontaneously hypertensive heart failure rat; hypertension; metabolic syndrome X; ventilatory equivalent; frequency OBESITY, DIABETES, AND HYPERTENSION are major risk factors for cardiopulmonary and renal disease (1,7,9,18,41). The concurrence of these risk factors is also known as the metabolic syndrome X (8, 49). In addition to metabolic and cardiovascular complications, individuals with metabolic syndrome X can also present with hypoventilation during sleep and obstructive sleep apnea (8, 47).Hypertension and congestive heart failure originate from the activation of multiple neuroendocrine systems, including the renin-angiotensin (Ang), endothelin, and atrial natriuretic peptide systems (13, 23-25, 41, 51). One in four adults develops hypertension and is at increased risk of stroke, coronary disease, congestive heart failure, and end-stage renal disease (2). Ang-converting enzyme (ACE) inhibitors are regarded as the first line of hypertensive therapy in diabetic patients due to their protective effects on the cardiovascular and renal systems (23,27,45). Ideally, treatment of hypertension would normalize blood pressure early in the disease, thus decreasing the incidence of cardiovascular-associated morbidity and mortality. Another agent that has been shown to decrease blood pressure is L-arginine (Arg) (50), a substrate ...

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Nitric oxide synthase activity in hyperthyroid and hypothyroid rats

Cited by 91 publications

References 34 publications

Thyroid status and nitric oxide in rat arterial vessels

Thyroid status and nitric oxide in rat arterial vessels

Increased Pressor Sensitivity to Chronic Nitric Oxide Deficiency in Hyperthyroid Rats

Effects of long-term captopril andl-arginine treatment on ventilation and blood pressure in obese male SHHF rats

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