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

Pituitary cell reaggregates from 14-day-old and adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were cultured in serum-free, chemically defined medium supplemented with the thyroid hormone triiodothyronine and the glucocorticoid dexamethasone. After 1 wk in culture, aggregates were transferred into a perifusion system, and the effect of angiotensin II (ANG II) on prolactin (PRL) and growth hormone (GH) release was studied. In aggregates from adult SHR, ANG II displayed a significant and dose-dependent GH releasing activity, whereas a negligible effect or no effect was seen in aggregates from adult WKY. In contrast, no difference in the stimulation of PRL release by ANG II was found. To exclude the possibility that the enhanced GH responsiveness was secondary to longstanding hypertension, aggregates from animals in the prehypertensive stage were studied. Both the GH and PRL responses to ANG II were significantly higher in aggregates from 14-day-old SHR than in aggregates from 14-day-old WKY. These data indicate that abnormal GH and PRL responses to ANG II exist in pituitary cell aggregates from SHR long before hypertension develops. Because these differences were found in pituitary cells maintained in culture for 1 wk, they do not seem to be secondary to changes in brain regulation of pituitary function but rather are caused by factors intrinsic to the pituitary.
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PMID:Enhanced ANG II activity in anterior pituitary cell aggregates from hypertensive rats. 341 35

The pattern of age-induced changes in each endocrine system is unique. Both hormone levels and target organ responsivity are altered in the aging endocrine-cardiovascular system. Serum levels of vasopressor hormones both increase (norepinephrine) and decrease (renin, aldosterone). Target organ responses to beta-adrenergic stimulation in the heart and probably also in vascular smooth muscle decrease due to postreceptor changes. These effects contribute to the clinical problems of hypertension and orthostatic hypotension which characterize the elderly. Aging produces mild carbohydrate intolerance and a minimal increase in fasting serum glucose in healthy, nonobese individuals, primarily due to decreasing postreceptor responsiveness to insulin. Aging decreases the metabolism of thyroxine, including its conversion to triiodothyronine, but clinically significant alterations of thyroid hormone levels do not occur. Changes in the end-organ response to thyroid hormones, however, significantly alter the clinical presentation of thyroid diseases. Aging shifts the serum vasopressin-serum osmolality relationship toward higher serum vasopressin levels probably due to altered baroreceptor input, probably contributing to the tendency toward hyponatremia in the elderly. Aging slows the metabolism of cortisol, but glucocorticoid levels in the human are essentially unaltered by age. However, recent data indicate that delta-5 adrenal steroids decrease markedly in both men and women. Nodules in the anterior pituitary, the thyroid, and the adrenal increase in frequency with aging. Finally, the reproductive system is primarily altered by endocrine cell death, by unknown mechanisms, resulting in decreased estrogen and testosterone levels in women and men. This most obvious age-related endocrine change turns out to be incompletely understood and is not representative of most age-related endocrine changes. Despite characterization of these many age-related alterations in endocrine systems, therapeutic issues often remain unexplored, and more data are needed in many areas.
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PMID:Age and the endocrine system. 391 1

To better define the effect of age on blood pressure in patients with hyperthyroidism, the blood pressures of 321 patients with hyperthyroidism were compared with those of 324 euthyroid controls. Subjects were divided into four age groups by decade from 20 to 59 years. The systolic, but not diastolic, blood pressure in the patients with hyperthyroidism was significantly higher in all age groups. Among the euthyroid controls, the systolic blood pressure increased with age. However, no age-related increase was apparent among the hyperthyroid patients because of the relatively high systolic blood pressure in young patients. Effective antithyroid treatment reduced the systolic blood pressure significantly in hyperthyroid patients. The reduction of systolic blood pressure was greater in the younger hyperthyroid patients than that in the older ones, so that an age-related increase in systolic blood pressure was present after a euthyroid state had been achieved. These results provide evidence against the report that in hyperthyroidism, hypertension tends to occur in older patients, and suggest that the effect of excessive thyroid hormone on the systolic blood pressure may differ according to age.
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PMID:The effect of age on blood pressure in hyperthyroidism. 396 51

A large prospective study investigated prenatal and perinatal antecedents of chronic motor dysfunction (cerebral palsy [CP]), evaluating approximately 400 characteristics of the mothers, pregnancies, or deliveries. In addition to confirming some, but not all, of the classic risk factors for CP, this study observed relatively large increases in the CP rate in association with maternal mental retardation, seizure disorders, hyperthyroidism, or with the administration of thyroid hormone and estrogen in pregnancy. Some risk factors were predictive of CP only insofar as they were associated with low birth weight or low Apgar scores. Among factors not significantly related to CP rate were maternal age, parity, socioeconomic status, smoking history, maternal diabetes, first trimester vaginal bleeding, kidney or bladder infection, moderate hypertension, long cord, use of anesthetic agents, or use of oxytoxics for initiation or augmentation of labor. Duration of labor, whether precipitate or prolonged, was not a risk factor for CP.
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PMID:Antecedents of cerebral palsy. I. Univariate analysis of risks. 403 90

Plasma cAMP was determined using the method of Tovey et al. in normal pregnant women with a mean concentration of 18.9 +/- 0.8 pmol/ml (x- +/- SEM). Between weeks 9-12 and 33-36 of gestation, there were two peaks, with a mean cAMP of 22.5 +/- 2.4 which were significantly increased in comparison to the other weeks of pregnancy. Significantly decreased values were found in patients with threatened abortion (weeks 12-28) which terminated in abortion (11.6 +/- 2.4; p < 0.01). In premature labor no differences were found. During therapy with fenoterol there were highly significantly increased plasma cAMP levels (48.2 +/- 2.8; p < 0.0005). During thyroid hormone therapy in euthyroid goiter, cAMP was significantly decreased (14.0 +/- 1.4; p < 0.05). 1 week after cessation of therapy a highly significant increase of cAMP was observed (38.2 +/- 6.9; p < 0.0005). There was a negative linear regression between T3 and cAMP (2p < 0.01). In pregnancy with hypertension cAMP was significantly elevated (30.5 +/- 3.8 p < 0.0005), but nearly normal under antihypertensive therapy. In pregnancy with edema only, no difference was found. Induction of labor with PGE2 alpha was followed by a decrease of plasma cAMP.
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PMID:Plasma cAMP in normal and abnormal human pregnancy. 625 65

Endocrine function was studied in a 24 year old female with lipoatrophic diabetes (LD). Baseline endocrine studies (serum triglycerides: 2600 mg/dl) demonstrated hyperprolactinemia (serum prolactin 51 ng/ml), increased ACTH levels, absence of suppression of ACTH to a high dose of dexamethasone which suppressed serum cortisol normally and, hyperresponsiveness of TSH to stimulation with TRH. Thyroid hormone levels (total and free fraction) were essentially normal. Major metabolites of thyroid hormone (T3, rT3, 3, 3'-T2, and 3', 5'-T2) were also normal and exhibited a normal response to the administration of L-thyroxine and propylthiouracil. Exchange of 84% of the patient's plasma resulted in a decrease in serum triglycerides (700 mg/dl) which was followed by a rebound to the original level in seven days. After the sixth plasmapheresis serum triglycerides stabilized at less than 1000 mg/dl. Plasmapheresis was associated with the appearance of amenorrhea and galactorrhea; also hypertension and proliferative retinopathy developed during this therapy. Repeat endocrine function studies (serum triglycerides: 700 mg/dl) showed a further rise in serum prolactin (greater than 160 ng/ml), persistence of abnormal ACTH secretion and normalization of TSH responsiveness. Lipoatrophic diabetes is associated with abnormal central endocrine function but appropriate peripheral target gland secretion. A course of plasmapheresis improves the hypertriglyceridemia but not the endocrine dysfunction. In this patient with LD the most important side effect of plasmapheresis was the development of cardiovascular complications.
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PMID:Lipoatrophic diabetes: endocrine dysfunction and the response to control hypertriglyceridemia. 628 8

It is here proposed that disordered redox balance leads to congestive heart failure in a variety of diverse clinical situations. These conditions include those associated with an excess of reducing agents, such as catecholamines and thyroid hormone, or impaired oxidant defenses, such as in selenium deficiency. The clinical situations include hypertension, hyperthyroidism, progressive congestive heart failure, amphetamine overdose and hemochromatosis. The molecular damage to the cardiac muscle is postulated to be mediated via reaction oxygen radicals.
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PMID:An etiologic basis for congestive heart failure on the molecular level. 632 33

A 48-year-old woman with a known history of hypothyroidism was admitted to the intensive care unit with a diagnosis of thyroid storm secondary to acute thyroid hormone poisoning and the possible hyperfunction of a singular thyroid nodule. Her clinical manifestations included pyrexia, tachycardia, tachypnea, hypertension, RUQ abdominal pain, psychotic behavior, and pharyngitis. She was successfully treated with sodium iodide, PTU, propranolol, antibiotics, and a hypothermia mattress, with her serum T4 level returning to normal range prior to discharge. The patient was discharged 9 days after admission in good medical health with no medication. This article clearly shows that the functions of the endocrine system remain a frontier in today's medicine. With research, perhaps one day we might fully understand the intricate pathophysiology that results in thyroid storm. The potential problem format has been utilized in the development of the nursing care plan to assist the nurse with identifying and defining her patient's problems, as well as directing her assessment and nursing intervention. As more is learned about thyroid storm, nurses should update their knowledge so that they will be prepared to care for the patient with these difficult nursing problems.
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PMID:Thyroid storm--a nursing crisis. 655 51

A patient on a regimen of 400 mg/day of propranolol hydrochloride was observed to have elevated thyroxine (T4) and free T4 levels with a normal thyrotropin response to protirelin. This led us to study the prevalence of hyperthyroxinemia in 14 consecutively treated patients with hypertension on daily doses of propranolol of 320 mg or more. Four of 14 patients had elevated serum T4 levels. As a group, the patients on propranolol therapy had higher serum T4 levels, free T4 indices, and triiodothyronine levels than did healthy controls. The use of high-dosage propranolol may be associated with euthyroid hyperthyroxinemia and be a source of diagnostic confusion. All patients receiving therapy with high-dosage propranolol should undergo protirelin testing before one can conclude that their elevated thyroid hormone levels are due to hyperthyroidism.
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PMID:Propranolol-induced hyperthyroxinemia. 663 43

To study whether there is an association between hypertension and hypothyroidism, measurements of blood pressure and thyroid function were determined in 477 female patients with chronic thyroiditis. Based on the blood levels of thyroxine (T4) and thyroid stimulating hormone (TSH), 308 patients were considered euthyroid and 169 were hypothyroid [T4 = 2.9 +/- 0.1 micrograms/dl and TSH = 105.8 +/- 6.8 microU/ml (mean +/- SEM)]. Diastolic, but not systolic, blood pressure in hypothyroid patients over 50 years was higher than in euthyroid patients of corresponding age groups. The prevalence of hypertension was higher in hypothyroid patients when hypertension was defined as the systolic and/or diastolic blood pressure above 160/95 mm Hg (14.8% vs 5.5%; p less than 0.01). Correlations between diastolic, but not systolic, blood pressure and either the blood level of triiodothyronine (T3) or T4 was significant (r = - 0.174, p less than 0.01, and r = 0.208, p less than 0.01, respectively) when data from both euthyroid and hypothyroid patients were combined. Adequate thyroid hormone replacement therapy for an average 14.8 months in 14 patients resulted in a normalization of thyroid function and a reduction of blood pressure (p less than 0.01). In four who showed no change in thyroid function due to inadequate replacement therapy, blood pressure remained elevated. These results suggest a close association between hypertension and hypothyroidism.
Hypertension
PMID:Hypothyroidism as a cause of hypertension. 684 58


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