Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of abrupt withdrawal of propranolol on serum concentrations of triiodothyronine (T3) and thyroxine (T4) was investigated in 5 patients with uncomplicated essential hypertension. The patients had been treated from 2 to 18 mo before the study was begun. Doses varied from 160 to 480 mg propranolol daily. Four of the patients studied developed tachycardia, sweating, or tremor within 2 to 6 days after withdrawal of propranolol. In 1 patient reversible ischemic ECG changes were recorded. The serum concentrations of free T3 increased in the 4 patients suffering from withdrawal symptoms. The mean increase on the day the symptoms started was 51% (range, 22 to 74, 2 p = 0.01). This increase in serum-free T3 correlated positively with the serum propranolol concentration on the last day propranolol was given (r = 0.91, 2 p = 0.03). In the one patient, who did not develop withdrawal symptoms, the serum concentration of propranolol was very low, and the free T3 level remained unchanged. No significant changes in serum concentrations of free T4 or total thyroid hormones were found in any of the patients. We suggest that the propranolol withdrawal symptoms are, at least partially, caused by an increase in the thyroid hormone, T3.
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PMID:Propranolol withdrawal and thyroid hormones in patients with essential hypertension. 64 76

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 circadian variation of blood pressure (BP) and heart rate (HR) was examined in 18 normal subjects, 15 patients with essential hypertension treated with beta-blockers and 21 patients with hyperthyroidism. Most of the patients with hyperthyroidism were also treated with beta-blockers. The 24 hr BP was measured with an ambulatory blood pressure monitoring device (UBP-100) every 5 min. A nocturnal fall in BP and HR was observed in the patients with essential hypertension treated with beta-blockers and the patients with mild to moderate hyperthyroidism as well as normal subjects. On the other hand, in patients with severe hyperthyroidism the nocturnal fall was observed in HR alone, and the fall was small in its amplitude. There was a significant negative correlation between triiodothyronine (T3) level and percentage amplitude of the nocturnal fall in systolic BP (n = 21, r = -0.5, p less than 0.01). However, this relation was not significant in diastolic BP and HR. These results indicate that excess thyroid hormone may modulate the circadian variation of BP and HR.
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PMID:The circadian variation of blood pressure and heart rate in patients with hyperthyroidism. 257 56

Recent reports suggest a role for serotonin in the pathogenesis of primary hypertension and left ventricular (LV) hypertrophy. In this study, we have induced LV hypertrophy by oral feeding of thyroxine at increasing dosages (150-450 micrograms/kg b.wt.) over a 5-week period. The effects of hyperthyroidism on cardiovascular parameters, blood and myocardial serotonin concentrations were assessed. Water-fed rats and formerly hyperthyroid recovered animals served as controls. Thyroxine caused a significant LV hypertrophy: hyperthyroid rats 2.19 +/- 0.16*; controls 1.65 +/- 0.13 g/kg b.wt. (mean +/- SD; *P less than 0.05). An almost complete regression of LV hypertrophy occurred in the recovery group (1.66 +/- 0.20 g/kg b.wt.) 3 weeks after cessation of thyroid hormone application. Thyroxine-treated animals showed a significant increase of serotonin blood levels (thyroxine rats: 2108 +/- 781*, recovery: 1132 +/- 726, controls: 705 +/- 480 ng/ml; *P less than 0.05). The concentrations of serotonin in left ventricular myocardium were increased after thyroid hormone application, whereas the highest levels were found in the recovery group (thyroxine rats: 139.1 +/- 30.4, recovery: 167.2 +/- 43.1, controls: 68.9 +/- 27.9 mg/ml homogenate). Serotonin-containing cells in the left ventricular myocardium were stained immunohistochemically. They were localized perivascularly and were assumed to represent tissue mast cells. In experimental hyperthyroidism the serotonin levels in blood and heart are increased possibly indicating an interaction of both hormones in thyroxine-induced cardiomyopathy.
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PMID:Influence of experimental hyperthyroidism on blood and myocardial serotonin in rats. 323 76

Subnormal activity of the Na+-K+-ATPase appears to be a common feature of essential hypertension, and may in fact play a pathogenic role in this disorder. If so, methods which relieve inhibition or enhance the activity of the sodium pump should have therapeutic or preventive value. Diuretics enhance the activity of the sodium pump in hypertensives, apparently by suppressing secretion of an inhibitory natriuretic factor, and it is likely that low-sodium diets have a similar effect. Activity of the Na+-K+-ATPase is also stimulated by thyroid hormone and insulin, and there are indications that thyroid therapy, as well as various measures which increase tissue insulin sensitivity, may have therapeutic value in essential hypertension. Nutritional measures which may enhance sodium pump activity include potassium supplementation, insurance of adequate magnesium intake, and consumption of rich sources of gamma-linolenic acid.
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PMID:Hormonal and nutritional enhancement of Na+-K+-ATPase activity may aid the prevention and treatment of essential hypertension. 632 33