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

Spontaneously hypertensive rats (SHR) manifest a hypothyroid state as evidenced by increased thyroid weight, an increased level of plasma thyroid-stimulating hormone (TSH) and a decreased level of plasma thyroxine (T4) and triiodothyronine (T3). In 18 patients with essential hypertension, plasma TSH, T4 and T3 concentrations were all within the normal range, but the T4 level was significantly lower than in the controls. Among 21 hypothyroid patients, 2 had essential hypertension. Administration of thyroid hormone brought the metabolic state to normal in SHR and in hypothyroid patients but failed to affect the blood pressure. It is suggested that abnormality of thyroid function is neither the cause nor the accentuating factor in the development of hypertension in SH rats and in man.
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PMID:Effect of normalization of hypometabolic state on blood pressure in spontaneously hypertensive rats and in patients with essential hypertension. 82 91

The study was aimed at the evaluation of treatment of hypothyroidism with L-thyroxine administration monitored by the determination of T3 and T4 concentrations. The investigations were carried out in a group of 57 patients with hypothyroidism including 37 patients with autoimmune etiology of hypothyroidism, 12 patients after strumectomy and 8 patients after treatment with 131J. The administration of L-thyroxine at a dose of 2 micrograms/kg/day effectively eradicated all symptoms of the disease and led to the normalization of blood serum T3 and T4 values in the majority of patients with autoimmune hypothyroidism. So the majority of women required the daily dose of L-thyroxine of 100-150 micrograms, and the majority of men 125-175 micrograms. Lower dosage of L-thyroxine (50-100 micrograms daily) was required to attain euthyroid state in some patients with postoperative or postradiation hypothyroidism. Monitoring of the therapy by the determination of blood serum T3 and T4 concentrations greatly facilitated the proper choice of the therapeutic dose of L-thyroxine as the return of the thyroid hormone concentrations to normal usually brought about the complete remission of symptoms of the disease. The exception from this rule was only in the case of patients with arterial hypertension and coronary disease in whom, because of the side-effects, lower dosage of L-thyroxine (usually 50 micrograms daily) must have been applied to attain the optimal improvement. The treatment with L-thyroxine caused much less side-effects as compared to the therapy using the dessicated thyroid preparations (Thyroideum).
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PMID:[Monitoring of treatment for hypothyroidism with L-thyroxine]. 134 65

Catecholamines stimulate thyroid hormone synthesis as well as release of thyroid hormone and cause immunologic disturbances that possibly contribute to the manifestations of Graves' disease. This has led to repeated speculations about the possible role of catecholamines in the initiation and maintenance of hyperthyroidism. We describe a patient with Graves' disease who was treated with antithyroid drugs for 2 years. After withdrawal of antithyroid drugs, the patient was in remission for 5 years. After the antithyroid drug treatment and the long remission, the probability of relapse of Graves' disease was very low. Nonetheless, a relapse did occur. Two years after subtotal thyroid resection, further investigation because of persistent hypertension revealed a pheochromocytoma. Retrospective anamnestic data suggest that this pheochromocytoma had been present 2 years before the patient's relapse of Graves' disease. This sequence of diseases has not been described previously. The low probability for a Graves' disease relapse in this patient and the association of this patient's relapse with the manifestation of a pheochromocytoma suggest a possible etiologic role of excess catecholamine production in the relapse of Graves' disease.
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PMID:Relapse of Graves' disease following development of a pheochromocytoma. 142 32

In this report we describe 26 pregnancies complicated by hypothyroidism cared for over 6.5 years at AIIMS, New Delhi. In 2 women hypothyroidism was diagnosed during pregnancy; others were diagnosed before pregnancy and continued to receive thyroxine replacement therapy throughout pregnancy. The thyroxine treatment needed readjustment in 7 (26.9%) pregnancies to maintain euthyroidism. Maternal complications included anaemia (23.0%), pregnancy induced hypertension (26.9%), postpartum haemorrhage (7.7%), intrauterine growth retardation (15.4%), postdatism (30.8%), and deficient lactation (19.2%). Perinatal mortality was 3.9%. No case of stillbirth occurred probably because of intensive fetal monitoring and timely termination of pregnancies on evidence of intrauterine fetal compromise. One neonatal death occurred due to fetal thyrotoxicosis. In these cases close surveillance during pregnancy is needed to maintain optimum thyroid hormone concentration, and intensive fetal monitoring is required to achieve a good perinatal outcome.
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PMID:Hypothyroidism complicating pregnancy. 144 36

Centrally administered thyrotropin-releasing hormone exerts a well documented hypertensive effect. In this study, the possible physiological role of thyrotropin-releasing hormone in the central cardiovascular regulation was evaluated in spontaneously hypertensive rats receiving long-term (8-14 days) intracerebroventricular infusion of a heterologous antiserum to thyrotropin-releasing hormone. The effect of this passive immunization on the blood pressure was monitored from conscious animals by the tail-cuff method. Thyrotropin-releasing hormone antiserum significantly decreased the systolic arterial pressure in adult rats with established hypertension. No alterations in serum thyroid hormone status were observed indicating that the antihypertensive effect of immunological blockade of thyrotropin-releasing hormone was not due to changes in the serum thyroid hormone levels. These results provide evidence for a role of endogenous brain thyrotropin-releasing hormone in the maintenance of hypertension in spontaneously hypertensive rats.
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PMID:Intracerebroventricular immunization with TRH-antiserum lowers blood pressure in spontaneously hypertensive rats. 159 55

To test conditions under which thyroid hormone might be deleterious to bone, we studied a group of 58 patients who had undergone thyroidectomy because of thyroid cancer 1 to 21 years previously and were treated with steady doses of exogenous thyroid hormone. Vertebral bone density (BMD Z-score) was significantly reduced and biochemical indices of bone resorption (urinary hydroxyproline and plasma tartrate-resistant acid phosphatase activity) and of osteoblastic activity (plasma osteocalcin and bone isoenzyme of serum alkaline phosphatase) as well as the calculated prevalence of bone resorption relative to osteoblastic activity (HBP) were significantly increased in thyroid hormone-treated post-menopausal women but not in men and premenopausal women. The HBP as well as the biochemical indices of bone remodeling were significantly negatively correlated with serum TSH levels. In treated patients, BMD Z-score was significantly dependent on the HBP, menopausal state, duration of treatment and serum TSH levels. In conclusion, the further increase in bone resorption by thyroid hormone is predisposed by menopausal changes in bone turnover. The simultaneous evaluation of biochemical indices of bone resorption and formation improves the assessment of bone loss in patients treated with thyroid hormone in a suppressive dose.
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PMID:Biochemical assessment of bone loss in patients on long-term thyroid hormone treatment. 162 31

Diabetes impairs cardiac performance more extensively in hypertensive rats than it does in nonhypertensive strains. A "low thyroid state" may contribute to the adverse cardiovascular effects of diabetes in spontaneously hypertensive rats (SHR). We tested this hypothesis by comparing the effects of thyroid hormone with those of insulin treatment on cardiac performance of diabetic SHR. Diabetes was induced with streptozotocin (45 mg/kg). Subsets of diabetic rats were treated with either insulin (10-20 units/kg/day) or triiodothyronine (8-10 micrograms/kg/day). Heart rate and systolic arterial pressure were obtained at weekly intervals. After 8 weeks, cardiac function was assessed using an isolated working heart preparation. Diabetes reduced arterial pressure and heart rate in vivo and markedly depressed cardiac performance under volume and pressure loading conditions ex vivo, confirming previous observations. As expected, insulin treatment prevented the bradycardia and depressor effect in vivo and the impairment of cardiac performance ex vivo caused by diabetes. The triiodothyronine treatment duplicated the effects of insulin on the hemodynamic measurements in vivo, and corrected nearly all depressed indexes of performance of diabetic SHR hearts ex vivo. Both treatment regimens successfully reduced 8-week mortality when compared with the untreated diabetic group. The results support the hypothesis that a low thyroid state may contribute to the cardiovascular dysfunction in diabetic SHR. Left ventricular hypertrophy may be an important factor in this phenomenon.
Hypertension 1990 Jun
PMID:Insulin, thyroid hormone, and heart function of diabetic spontaneously hypertensive rat. 214 Aug 15

Thyroid hormones may alter red blood cell (RBC) sodium content and transport. The functional importance of lithium-sodium (Li-Na) countertransport in regulating sodium (Na) transport in vascular smooth muscle and kidney by Na-H countertransport and the potential effect of thyroid hormone on these processes led us to study Li-Na countertransport and other sodium transporters in RBCs of patients with thyroid dysfunction. Patients with untreated hypothyroidism (10) and hyperthyroidism (10) were studied, along with normal subjects (10). The mean value for Li-Na countertransport was significantly higher in the hypothyroid group [0.46 +/- 0.08 (+/- SE) mmol/L cell.h; P less than 0.05] and lower in the hyperthyroid group (0.15 +/- 0.04 mmol/L cell.h; P less than 0.05) compared to that in the normal subjects (0.25 +/- 0.03 mmol/L cell.h). When all groups were combined, significant negative correlations were found between Li-Na countertransport and serum T4 (r = -0.48; P less than 0.01), free T4 index (r = -0.42; P less than 0.05), and serum T3 (r = -0.38; P less than 0.05). Li-Na countertransport was positively correlated with serum triglyceride (r = 0.57; P less than 0.01), but not with serum cholesterol levels (r = 0.28; P = NS). The values became normal in subsets of the hypothyroid (n = 5) and hyperthyroid groups (n = 5) during treatment. We found a bidirectional effect of thyroid status on RBC Li-Na countertransport, which was reversible when serum thyroid hormone levels became normal. Changes in Li-Na countertransport, a pathway of Na-H exchange, may influence renal sodium handling and vascular tone in patients with thyroid disease and contribute to abnormalities such as hypertension that occur in patients with hypothyroidism.
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PMID:Reversible alteration of red cell lithium-sodium countertransport in patients with thyroid disease. 291 49

The isolated perfused working heart was used to study hypertensive diabetes-induced alterations in cardiac function at 6 and 12 wk after diabetes was induced. At 6 wk after diabetes induction, cardiac performance was depressed in the diabetic animals. However, there was no difference in cardiac function between normotensive Wistar and spontaneously hypertensive (SHR) diabetic rats. Wistar-Kyoto (WKY) rats were also included as normotensive controls in our 12-wk study. Hearts from 12-wk SHR and Wistar diabetic animals exhibited a depressed left ventricular developed pressure and positive and negative dP/dt when compared with control animals. However, this depression was not seen in the WKY diabetic animals. In addition, quantitation of various parameters of heart function revealed highly significant differences between SHR diabetic animals and all other groups associated with an increased mortality. Serum lipids were elevated in SHR and Wistar and were unaffected in WKY diabetic rats. Furthermore, thyroid hormone levels were not depressed in WKY diabetic rats as seen in the other two diabetic groups. This normal lipid metabolism and thyroid status could, in part, explain the lack of cardiac dysfunction in these animals. The data provide further evidence that the combination of hypertension and diabetes mellitus produces greater myocardial dysfunction than with either disease alone and is associated with a significant mortality.
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PMID:Cardiac function in spontaneously hypertensive diabetic rats. 294 94

Hypothyroidism has been known to be associated, at times, with diastolic hypertension. We have found in 40 thyrotoxic patients that the induction of hypothyroidism by radioiodine therapy significantly increased diastolic blood pressure, raising it above 90 mm Hg in 16 (40%) of the patients. Restoration of euthyroidism with thyroxine administration significantly reduced the systolic and diastolic blood pressures in these patients, with a fall in diastolic pressure below 90 mm Hg in nine of 16 patients. The prevalence of hypothyroidism was determined by measurements of serum thyroxine and thyrotropin concentrations in 688 consecutive hypertensive patients, referred for evaluation and therapy of their hypertension. Hypothyroidism was found in 25 (3.6%) of the patients. Restoration of normal serum thyroxine and thyrotropin levels with thyroid hormone replacement therapy lowered diastolic blood pressure to levels below 90 mm Hg in 32% of these patients who could be followed up after withdrawal of all antihypertensive drug therapy when euthyroidism had been restored (i.e., 1.2% of the 688 patients). It is concluded that diastolic hypertension resulting from hypothyroidism is a relatively common disorder, present in 1.2% of our referred hypertensive patients, that should be sought and treated.
Hypertension 1988 Jan
PMID:Effects of thyroid function on blood pressure. Recognition of hypothyroid hypertension. 333 42


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