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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroid hormone has a broad effect on cardiovascular system. 3,3',5-triiodo-l-thyronine (T3), a biologically active form of thyroid hormone, increases cardiac contractility. T3 causes arterial relaxation and reduction of systemic vascular resistance, resulting in an increase in cardiac output. However, the molecular mechanisms of vascular relaxation by T3 are incompletely characterized. We studied the effect of T3 on the angiotensin (Ang) II type 1 receptor (AT1R) expression in vascular smooth muscle cells. T3 dose-dependently decreased expression levels of AT1R mRNA, with a peak at 6 hours of stimulation. Binding assay using [125I]Sar1-Ile8-Ang II revealed that AT1R number was decreased by stimulation with T3 without changing the affinity to Ang II. T3 reduced calcium response of vascular smooth muscle cells to Ang II by 26%. AT1R promoter activity measured by luciferase assay was reduced by 50% after 9 hours of T3 administration. mRNA stability was also decreased by T3. Real-time quantitative reverse transcription-polymerase chain reaction and Western blot analysis revealed that AT1R mRNA and protein were downregulated in the aorta of T3-treated rats. These results suggest that T3 downregulates AT1R expression both at transcriptional and posttranscriptional levels, and attenuates biological function of Ang II. Our results suggest that downregulation of AT1R gene expression may play an important role for T3-induced vascular relaxation.
Hypertension 2003 Mar
PMID:Downregulation of vascular angiotensin II type 1 receptor by thyroid hormone. 1262 65

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 (n=8 each) of male Wistar rats were used: a control group; 3 groups that were treated with thyroxine (50 microg/d), Nw-nitro-L-arginine methyl ester (L-NAME; subpressor dose, 1.5 mg x kg(-1) d(-1)), or thyroxine plus L-NAME; and another 4 similarly treated groups that received losartan (20 mg x kg(-1) x d(-1)) 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 thyroxine+L-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 thyroxine+L-NAME hypertension.
Hypertension 2003 Aug
PMID:Increased pressor sensitivity to chronic nitric oxide deficiency in hyperthyroid rats. 1282 1

Eight cases of myxedema with interesting features are presented. Hypertension is common in myxedema and usually persists when the myxedema is treated. Two patients are reported in whom the hypertension improved with the treatment of the myxedema. Other cases presented with ascites, psychosis, recurrent coma with marked hyponatremia and hypochloremia, ataxia, muscular hypertrophy and myotonia. In each patient the abnormalities were corrected by administration of thyroid hormone. In most instances the mechanism whereby symptoms are produced is poorly understood.
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PMID:UNUSUAL MANIFESTATIONS OF MYXEDEMA. 1430 5

The effects of NaCl, glucose, and thyroid hormone on the production of superoxide (O2*-) within the renal medulla of Sprague-Dawley rats were examined. Responses of intracellular superoxide [O2*-]i in isolated medullary thick ascending limbs (mTALs) were studied using real-time fluorescent microscopy with measurement of the dehydroethidium (DHE) to ethidium (Eth) conversion ratio (Eth/DHE ratio unit). The results demonstrated that elevations of extracellular NaCl (from 152 to 252 mmol/L), D-glucose (from 5 to 25 mmol/L), and triiodo-thyronine (T3; 10 micromol/L) significantly increased [O2*-]i levels. Preincubation with superoxide scavenger 4,5-dihydroxy-1,3-benzene-disulfonic acid (1 mmol/L) significantly inhibited these responses. Stimulation with equamolar amounts of choline chloride or L-glucose failed to increase [O2*]i, indicating that these O2*- responses were not determined by changes in osmolality. The responses to NaCl, D-glucose, and T3 were abolished by pretreatment with the Na+/K+-ATPase pump inhibitor ouabain (4 mmol/L) and with Na+/H+ -exchanger inhibitor dimethylamiloride (100 micromol/L). We conclude that elevations of extracellular NaCl, D-glucose, or T3 levels can activate both the Na+/K+-ATPase pump and Na+/H+ exchanger in mTAL, which, in turn, is associated with increased intracellular concentrations of superoxide.
Hypertension 2004 Feb
PMID:Renal oxidative stress in medullary thick ascending limbs produced by elevated NaCl and glucose. 1471 54

Subclinical thyroid disease is defined by an abnormally high (subclinical hypothyroidism) or low (subclinical hyperthyroidism) serum thyrotropin (TSH) with peripheral thyroid hormone concentrations within the laboratory reference ranges. Such abnormalities in thyroid function tests are very common in the population and have been extensively dealt with in textbooks and reviews. Subclinical hypothyroidism is common especially in elderly women. There is no clear evidence to date that subclinical hypothyroidism causes clinical hearth disease. However, mild thyroid gland failure, evidenced solely by elevation of the serum TSH concentration, may be associated with increased morbidity, particularly for cardiovascular disease and subtly decreased myocardial contractility. In subclinical hypothyroidism both cardiac structures and function remain normal at rest, but impaired ventricular function as well as cardiovascular and respiratory adaptation to effort may became unmasked during exercise. These changes are reversible when euthyroidism is restored. Subclinical hypothyroidism does result in small increase in low density lipoprotein cholesterol and a decrease in high density lipoprotein, changes that enhance the risk for development of atherossclerosis and coronary artery disease. Because undetected subclinical hypothyroidism during pregnancy may adversely affect the neuropsychological development and survival of the fetus and be associated with hypertension and toxemia, screening pregnant women has been advocated. In addition, data suggesting that subclinical hypothyroidism is associated with ovulatory dysfunction and infertility may make screening worthwhile in this population as well. The combination of an undetectable serum thyrotropin concentration, as measured by an assay with a threshold of detection that is 0.1 mU per liter or less, and normal serum triiodothyronine and thyroxine concentrations (usually at the upper end of the normal range) is known as subclinical hyperthyroidism. This condition reflects the facts that before clinical features of thyrotoxicosis are apparent, the thyrotrophs usually respond to minor increments in thyroid hormone concentrations, which remain within the normal range, by switching off the production and secretion of thyrotropin. In the absence of clinical signs of thyroid disease, and even after additional investigations such as isotope uptake and imaging and measurement of the thyrotropin receptor antibody concentration, it may be difficult to decide whether the pattern seen on thyroid function tests is a consequence of nonthyroidal illness and concomitant medication, underlyling thyroid autonomous function or the initial phase of thyroiditis. Routine screening for thyroid disease with thyroid function tests is not recommended for asymptomatic children or adults. This recommendation does not mean that clinicians should not monitor thyroid function in patients with a previous history of thyroid disease. There is insufficient evidence to recommend for or against screening for thyroid disease with thyroid function tests in high-risk patients, including elderly persons, postpartum women, and persons with Down syndrome, but recommendations may be made on other grounds, such as the higher prevalence of disease and the increased likelihood that symptoms of thyroid disease will be overlooked in these patients. If screening is performed, the preferred test is measurement of thyroid-stimulating hormone (TSH) using a sensitive immunometric or similar assay, because of its superior sensitivity and specificity.
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PMID:[Subclinical thyroid disease--should we treat, should we screen for it?]. 1511 90

Overt and subclinical hypothyroidism are associated with increased systemic vascular resistance and hypertension. We examined the relationship between thyroid function and blood pressure homeostasis in euthyroid individuals. A total of 284 subjects (68% hypertensive) consumed high- (200 mmol) and low- (10 mmol) sodium diets, and their blood pressure responses were assessed as percentage change in the mean arterial pressure (MAP). p-Aminohippuric acid clearance was used to estimate effective renal plasma flow. Renal vascular resistance (RVR) was calculated as MAP divided by effective renal plasma flow. Serum free T(4) index (FTI) was lower (P < 0.0001) and TSH was higher (P = 0.046) in hypertensive compared with normotensive subjects independent of other baseline characteristics. FTI (beta = -1.51, P < 0.0001), baseline MAP, and race independently predicted MAP salt sensitivity. The FTI relationship with salt sensitivity adjusted for baseline MAP and race was similar among normotensive (beta = -1.42, P = 0.008) and hypertensive subjects (beta = -1.66, P = 0.0001). FTI correlated negatively with high- (P = 0.0001) and low- (P = 0.008) salt RVR, whereas TSH correlated positively with high- (P = 0.016) and low- (P = 0.012) salt RVR independent of age, gender, race, and body mass index. We have found that FTI is lower and TSH is higher in hypertensive compared with normotensive euthyroid subjects and that FTI independently predicts blood pressure salt sensitivity. These data show that the influence of thyroid function on blood pressure homeostasis extends into euthyroid range and likely reflects the action of thyroid hormone on peripheral vasculature.
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PMID:Thyroid function and blood pressure homeostasis in euthyroid subjects. 1524 Jun 31

The cardiovascular risk in patients with hypothyroidism is related to an increased risk of functional cardiovascular abnormalities and to an increased risk of atherosclerosis. The pattern of cardiovascular abnormalities is similar in subclinical and overt hypothyroidism, suggesting that a lesser degree of thyroid hormone deficiency may also affect the cardiovascular system. Hypothyroid patients, even those with subclinical hypothyroidism, have impaired endothelial function, normal/depressed systolic function, left ventricular diastolic dysfunction at rest, and systolic and diastolic dysfunction on effort, which may result in poor physical exercise capacity. There is also a tendency to increase diastolic blood pressure as a result of increased systemic vascular resistance. All these abnormalities regress with L-T4 replacement therapy. An increased risk for atherosclerosis is supported by autopsy and epidemiological studies in patients with thyroid hormone deficiency. The "traditional" risk factors are hypertension in conjunction with an atherogenic lipid profile; the latter is more often observed in patients with TSH >10 mU/L. More recently, C-reactive protein, homocysteine, increased arterial stiffness, endothelial dysfunction, and altered coagulation parameters have been recognized as risk factors for atherosclerosis in patients with thyroid hormone deficiency. This constellation of reversible cardiovascular abnormalities in patient with TSH levels <10 mU/L indicate that the benefits of treatment of mild thyroid failure with appropriate doses of L-thyroxine outweigh the risk.
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PMID:Hypothyroidism as a risk factor for cardiovascular disease. 1524 98

In this study three problems concerning interactions between thyroid and cardiovascular system are discussed. Cardiac arrhythmias, congestive heart failure, pleural effusion, hyperlipidaemia, arterial hypertension may be consequences of thyroid disorders leading to inappropriate hormone secretion. During such illnesses as heart failure, myocardial infarction and in patients undergoing coronary artery bypass surgery profound changes may occur in thyroid hormone metabolism known as sick euthyroid syndrome. Treatment with amiodarone may lead to changes in thyroid tests results and to development of hypothyroidism or thyrotoxicosis.
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PMID:[Thyroid and cardiovascular disorders]. 1551 16

Cushing's syndrome is characterized by endogenously increased production of glucocorticoids. The activity of immune system is regulated mainly by two systems in the body. Glucocorticoids and NF-kappaB counteract the effects of each other on the immune system. It has been reported that immune response is exaggerated after the amelioration of Cushing's syndrome. We report a rare case of exacerbation of Graves' disease after unilateral adrenalectomy for Cusing's syndrome. A 50-yr-obese woman with hypertension, dyslipidemia, impaired glucose tolerance and insulin resistance wasadmitted to outpatients clinic of endocrinology. The results of evaluation of glucocorticoids metabolism and adrenal magnetic resonance imaging revealed the Cusing's syndrome. We also assessed thyroid function tests because of the diagnosis of goiter and thyroid hormone replacement in her medical history, and the presence of exophthalmia and tachycardia in examination. Althoug TSH level was detected at the lower border of normal range, free T4 and free T3 were in normal range and autoantibody of thyroidal peroxidase and thyroglobulin was higer than normal reference range. An operation was performed and a mass was removed from her left adrenal gland. The pathologic examination confirmed adrenal adenoma. She was re-admitted to the outpatient clinic 9 months after with complaints of palpitation, malaise and weight loss. Tests carried out to determine the thyroid function revealed Graves' disease. We prescribed propylthiouracil and beta-blocker treatment.
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PMID:Exacerbations of Graves' disease after unilateral adrenalectomy for Cushing's syndrome. 1571 57

The association of renal disease and autoimmune thyroid disorders has been reported previously. Renal findings associated with autoimmune thyroiditis present more commonly as proteinuria ranging from mild to nephrotic levels. We report here two adolescent girls with hyperthyroidism associated with transient proteinuria correlated with thyroid hormone levels. They had positive antithyroid peroxidase and antithyroglobulin antibodies. Ultrasonographic and scintigraphic findings of the thyroid gland were consistent with Graves' disease in both. Their renal functions were normal except proteinuria (daily protein excretion of 13.5 mg/m2/h in patient 1 and 11 mg/m2/h in patient 2). When they became euthyroid on antithyroid treatment, proteinuria decreased without associated hematuria and/or hypertension. In conclusion, patients with autoimmune thyroid disease should be assessed for the possibility of proteinuria and the etiological investigation of proteinuria should include evaluation of thyroid functions.
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PMID:Autoimmune thyroiditis with associated proteinuria: report of two patients. 1581 12


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