Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have assessed the presence of VIP/PHI/secretin receptors in heart by: (1) testing the ability of the corresponding peptides to activate adenylate cyclase in cardiac membranes from rat, dog, Cynomolgus monkey and man, and (2) examining the ability of the same peptides to exert inotropic and chronotropic effects on heart preparations from rat and Cynomolgus monkey in vitro. Based on their affinity for natural peptides and synthetic analogs, two types of VIP/PHI/secretin receptors were characterized: the relatively nonspecific "secretin/VIP receptor" of rat heart (that is "secretin-preferring" only in that secretin was more efficient than VIP in stimulating adenylate cyclase), and the "VIP/PHI-preferring" receptor of man, monkey and dog heart. Four physiopathological situations affecting secretin/VIP receptors in rat heart were explored: In male rats from the Okamoto strain and the Lyon strain, two strains presenting spontaneous hypertension, heart membranes exhibited a markedly decreased response of adenylate cyclase to secretin/VIP, with lesser alterations in the responses to isoproterenol and glucagon. This impairment developed in parallel with the occurrence of hypertension and was reproduced in normotensive rats submitted to chronic isoproterenol treatment (but not in Goldblatt hypertensive rats). These findings are consistent with a hyperactivity of norepinephrine pathways in spontaneously hypertensive rats, leading to a reduced number of cardiac post-junctional secretin/VIP receptors bound to adenylate cyclase. Heart membranes from genetically obese (fa/fa) Zucker rats also exhibited severely decreased responses to secretin/VIP with lesser alterations in the responses to glucagon and isoproterenol. These anomalies were specific for the heart, and developed in concomitance with obesity. The first anomaly could not be corrected by severe food restriction. Secretin stimulation of heart adenylate cyclase was also selectively altered in streptozotocin-diabetic rats. Thus, two types of diabetic cardiomyopathy were characterized by a severe local alteration of secretin/VIP receptors coupled to adenylate cyclase. Hypothyroidism, provoked in rat by thyroidectomy or propylthiouracil treatment, again induced a marked decrease in secretin-stimulated cardiac adenylate cyclase activity. In rat papillary muscle electrically stimulated in vitro, secretin exerted a positive inotropic effect. This effect was reduced in obese (fa/fa) Zucker rats. In rat right atrium, secretin also exerted a positive chronotropic effects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Heart receptors for VIP, PHI and secretin are able to activate adenylate cyclase and to mediate inotropic and chronotropic effects. Species variations and physiopathology. 608 34

Pharmacological treatment of hypertension can cause clinically significant alterations in endocrine function through effects on glucose homeostasis, thyroid and parathyroid hormones, adrenal steroid metabolism and reproductive/pituitary physiology. Long term use of thiazide diuretics causes deterioration in glucose tolerance, probably secondary to potassium depletion. Hypoglycaemic complications of beta-blockers (mainly the non-selective compounds) can be dramatic, especially in type I diabetics. Clonidine, diazoxide and calcium antagonists have all been associated with deterioration in glucose tolerance and their long term use should be avoided in type II diabetics if possible. Propranolol lowers T3 levels by decreasing the conversion of T4 to T3. Prazosin causes elevations in T4 and thyroid-stimulating hormone, while sodium nitroprusside use may result in hypothyroidism. Numerous agents are associated with sexual dysfunction, including methyldopa, reserpine, clonidine and spironolactone. Thiazide diuretics may cause hypercalcaemia, particularly in patients with hyperparathyroidism, by decreasing urinary calcium as well as directly influencing bone and gut calcium handling. Conversely, propranolol may decrease circulating parathyroid hormone levels and correct the hypercalcaemia seen in hyperparathyroidism. Awareness of drug-induced changes in endocrine function will facilitate the rational management of the hypertensive patient.
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PMID:Effects of antihypertensive drugs on endocrine function. 614 2

High plasma noradrenaline (PNA) levels have been reported in hypothyroid patients and hypothyroidism has been associated with hypertension. To explore the relationship between PNA and blood pressure (BP) in hypothyroid patients, and the effects of gradual thyroxine replacement, a prospective study was performed comparing BP, heart rate (HR) and PNA in a normotensive and a hypertensive group of hypothyroid patients before and during gradual thyroxine substitution. Thyroxine treatment reduced the BP; the reduction in supine BP was greater in the hypertensive than in the normotensive group. HR increased similarly in both groups during treatment. PNA was elevated in the normotensive group before treatment and decreased gradually during thyroxine treatment. The hypertensive group had normal PNA levels. The present study indicates that normotensive, in contrast to hypertensive, hypothyroid patients have increased sympathetic nervous activity. Although the mechanism is unclear, thyroid replacement therapy can reverse hypertension in hypothyroid patients.
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PMID:Plasma noradrenaline and blood pressure in hypothyroid patients: effect of gradual thyroxine treatment. 646 35

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

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

A 38-year-old obese woman with concurrent hypothyroidism and pseudotumor cerebri was monitored with serial thyroid function tests and CSF pressure determinations during levothyroxine sodium replacement therapy. Following normalization of the patient's thyroid status, assessed by both clinical and chemical indexes (serum thyroxine level, 1.5 to 11.0 micrograms/dL; serum thyrotropin level, 128 to 1.5 micro units/mL), intracranial hypertension persisted for more than four months. After weight loss, acetazolamide therapy, and intermittent CSF drainage failed to produce remission, glucocorticoid therapy was associated with prompt, sustained resolution of the pseudotumor cerebri. Contrary to previous reports, this patient's clinical course suggests that thyroid hormone deficiency and pseudotumor cerebri are not causally related.
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PMID:Pseudotumor cerebri and hypothyroidism. 684 97

In order to study the prognosis of Graves' disease, 236 patients, who had been diagnosed as having had Graves' disease more than 10 years before, were examined. Although one patient had died of leukemia and 2 patients had been operated on for breast cancer after 131I therapy, and another 6 patients had died between the ages of 20 and 50, the patients were doing quite well. Generally, the prognosis of Graves' disease is not considered to be serious if the thyroid function is controlled. Among the 72 patients who had been treated with 131I therapy, 15 patients (21%) showed low serum levels of both T3 and T4 and were considered to be suffering from late-onset hypothyroidism. About 67% of the 131I-treated patients were considered to be almost euthyroid, but serum TSH levels were high in half of them, suggesting latent hypothyroidism. The incidence of hypertension seemed to be significantly higher in the TSH-elevated euthyroid group compared with the TSH-nonelevated patients. An excessive reaction of the hypothalamus and/or pituitary gland might have an unfavorable effect not only on the apparent hypothyroidism, but also on the latent hypothyroidism after the therapy for Graves' disease.
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PMID:[Primary hypothyroidism as a possible cause of hypertension from long-term follow-up studies of patients with Graves' disease (author's transl)]. 689 8

Described here is a 27-year-old female, who had centripetal obesity, broad reddish-purple striae on the lower abdomen and hypertension. Serum cortisol levels, the results of a dexamethasone suppression test and an adrenal scintigram with 131I-19-iodocholesterol were all compatible with Cushing's syndrome due to an adrenal adenoma that secretes cortisol autonomously. This was confirmed by gross and microscopic examination of the removed adrenal tumor. In addition, the patient had markedly diminished T4 and T3 concentrations in serum. Basal TSH levels were not elevated and did not rise significantly after TRH injection. Serum T4 and T3 concentrations were elevated to the normal range when the hyperadrenocorticism was corrected. The results indicate that the patient had "'corticogenic hypothyroidism."
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PMID:Cushing's syndrome associated with corticogenic hypothyroidism: a case study. 730 57

Six patients with hypothyroidism and hypertension whose blood pressure fell to normal when treated with thyroxine (172 +/- 7.2/112 +/- 2.1 to 140 +/- 3.2/84+/- 1.6 mmHg, P < 0.001) are described. Plasma renin activity (1.76 +/- 0.63 ng angiotensin I.ml-1.h-1) was low before treatment. Hypertension with low plasma renin is consistent with sodium retention. Hypertension in the hypothyroid patient only requires further evaluation if it persists after adequate treatment with thyroxine.
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PMID:Reversible hypertension and hypothyroidism. 743 75

The two isomers of the positive inotropic compound EMD 53998, (+)EMD 57033 and (-)EMD 57439, possess selective calcium sensitizing and phosphodiesterase (PDE) inhibitory properties, respectively. We measured the pharmacological responses to both enantiomers in isolated rat cardiac and vascular tissues and in muscles from severely failing human hearts. We also measured positive inotropic and chronotropic responses to EMD 57033 in cardiac tissues from rats with thyroid dysfunction, diabetes, or hypertension. Both compounds increased force of contraction in isolated rat cardiac tissues, although the ventricular response to EMD 57439 was only approximately 10% that of calcium chloride. Forskolin pretreatment potentiated responses to both compounds in atria but only to EMD 57439 in ventricles. Hyperthyroidism increased ventricular responses to EMD 57033 relative to calcium chloride; hypothyroidism and diabetes decreased these responses. Ventricular responses were unchanged in hypertensive rats. Both enantiomers produced positive inotropy in human isolated right atrial trabeculae, although the maximal increases were only 14% (EMD 57033) and 26% (EMD 57439) that of calcium chloride. In rat thoracic aortic rings, both enantiomers produced relaxation; the responses due to EMD 57033 were endothelium dependent. Thus, calcium sensitization produces positive inotropy and vascular relaxation in rats. Positive chronotropic responses to EMD 57033 are most likely due to PDE inhibition. The limited inotropic response in severely failing human myocardium, together with possible vasorelaxation, may provide cardiac support in heart failure without an excessive increase in cardiac O2 demand.
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PMID:Calcium sensitization as a positive inotropic mechanism in diseased rat and human heart. 752 44


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