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

The study was undertaken to examine 30 healthy males and 67 patients with arterial hypertension. The author studied urinary excretion of 17-KS and blood levels of cortisol and adrenocorticotropic hormone before and after emotional stress induced by the "hour/compass" test. It was found that due to the stress, the release of the metabolites corticosteroids was higher in intensity than changes in blood concentrations of cortisol and adrenocorticotropic hormone in borderline hypertension and Stage I hypertensive disease, whereas these parameters were in an inverse ratio in Stage II hypertensive disease. Such changes occurred in patients with secondary hypertension. The ratio should be used as a diagnostic test.
 ...
PMID:[The participation of the hypothalamo-hypophyseal-adrenal system in the raising of the arterial pressure under the influence of emotional stress in arterial hypertension]. 839 12

A case of adrenal tumor producing 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone and aldosterone is reported. A 55-year-old woman had hypertension, hypokalemia, low plasma renin activity and an adrenal tumor. The plasma level of aldosterone was normal, and the levels of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone were extremely high. After the tumor removal, the plasma level of aldosterone decreased and plasma levels of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone were normalized. The tumor was benign adenoma and the production of steroid hormones was under control of adrenocorticotropic hormone. The enzyme activity of 21-hydroxylation in the tumor was elevated and that of 11 beta-hydroxylation was decreased compared with the adjacent tissue.
 ...
PMID:Adrenal tumor producing 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone and aldosterone. 868 Jan

A 57-year-old white man presented with metabolic alkalosis, hypokalemia (pH 7.58, HCO3 >50 mEq/L, serum K 1.8 mEq/L) and hypertension. The initial evaluation was significant for markedly elevated serum cortisol and adrenocorticotropic hormone (ACTH) level; neither hormone showed circadian rhythm or suppression with high-dose dexamethasone. Perihilar and supraclavicular masses were found to consist of undifferentiated small cell carcinoma. Ectopic ACTH syndrome was diagnosed. In spite of progressively rising hormone levels (ACTH, 723 pg/dL; and cortisol, 212 microgram/dL), his severe metabolic alkalosis was largely corrected by aggressive treatment with potassium chloride alone. Possible mechanisms of these clinical findings are discussed.
 ...
PMID:Correction of metabolic alkalosis by potassium chloride in ectopic adrenocorticotropic hormone syndrome. 884 Sep 54

The effects of acute foot shock on cardiovascular and sympathoadrenal responses were investigated in chronically stressed borderline hypertensive rats (BHR) and Wistar-Kyoto (WKY) rats. Male BHRs were divided into two groups; the maturation group (Mat) was not stressed, whereas the chronic stress group (AJS) received 8 wk (5 days/wk, 30 min/day) of air-jet stress coupled with immobilization. After chronic stress, the rats were cannulated in the femoral artery and jugular vein. Resting mean arterial pressure (MAP), heart rate (HR), and plasma norepinephrine (NE) levels were higher in the AJS group. In contrast, chronic stress failed to increase basal arterial pressure or HR in WKY rats. In response to acute foot shock, the Mat group had higher MAP increases, at which they plateaued, whereas the AJS rats displayed a progressive decline in MAP. This was associated with higher plasma NE and epinephrine levels but a smaller increase in adrenocorticotropic hormone in AJS versus Mat rats. This hyperactivity in the sympathoadrenal system of chronically stressed BHRs may, in part, account for their mild hypertension.
 ...
PMID:Chronic stress induces sensitization in sympathoadrenal responses to stress in borderline hypertensive rats. 908 43

A 72-year-old man was admitted to our hospital because of a tumor-like shadow on a chest X-ray film. At the initial examination, he had clinical signs of Cushing's syndrome: moon face, central obesity, and hypertension. A computed tomographic scan of chest showed an abnormal shadow in the lung (5 x 6 cm) with involvement of the right paratracheal and anterior tracheal lymph nodes, and a right-sided pleural effusion. Small cell lung cancer (extended disease; T2N2M6 stage IV) was diagnosed after a transbronchial biopsy. The concentrations of adrenocorticotropic hormone, cortisol, and parathyroid hormone in plasma were markedly elevated, and there was no circadian rhythm (336 pg/ml. more than 60.1 micrograms ml. and 805 pg/ml, respectively). Fluid obtained by thoracentasis had malignant cells, and the levels of adrenocorticotropic hormone and parathyroid hormone in the effusion (1120 pg/ml and 1810 pg/ml, respectively) were higher than those in serum, which indicates that these hormones were produced by the tumor cells. The patient received chemotherapy and responded well, but he died of respiratory failure 26 months later. The response rate to chemotherapy in elderly patients with lung cancer is said to be comparable to that in younger patients, but treatment may be difficult because of poor performance status and diminished physical capacity. Although patients with lung cancer complicated by Cushing's syndrome have a poor prognosis, this patient survived for more than 2 years after the disease was diagnosed.
 ...
PMID:[Cushing's syndrome due to small cell lung cancer with ectopic production of adrenocorticotropic and parathyroid hormone]. 915 97

1. The effects of L-arginine treatment on dexamethasone-induced hypertension were examined in the Sprague-Dawley rat. Seventy rats were randomly divided into the following eight groups: sham, dexamethasone (5 and 10 micrograms/day, L-arginine (100 and 500 mg/kg per day), L-arginine (100 or 500 mg/kg per day) + dexamethasone (10 micrograms/day), L-arginine (520-797 mg/kg per day in food) + dexamethasone (5 micrograms/day). Systolic blood pressure (SBP), bodyweight and plasma nitrate/nitrite concentration were measured. 2. Dexamethasone (5 and 10 micrograms/day) increased SBP in both sham and L-arginine-treated rats. Dexamethasone at 10 micrograms/day decreased bodyweight, but did not alter plasma nitrate/nitrite concentrations. 3. L-Arginine (500 mg/kg per day, i.p.) increased plasma nitrate/nitrite concentrations in 10 micrograms/day dexamethasone-treated rats. L-Arginine did not alter blood pressure in either sham or dexamethasone-treated rats. 4. Dexamethasone-induced hypertension differs from adrenocorticotropic hormone (ACTH)-induced hypertension in the rat in that it is not modified by L-arginine. Thus, ACTH-induced hypertension cannot be explained simply in terms of glucocorticoid activity.
 ...
PMID:Dexamethasone-induced hypertension in the rat: effects of L-arginine. 931 78

To study the effects of elevated maternal levels of adrenocorticotropic hormone (ACTH) on the fetus, nine chronically catheterized pregnant ewes (132 +/- 0.9 days of gestation) were infused intravenously for 3 days with Synacthen (5 micrograms.kg-1.day-1). Four ewes were given 0.15 M saline intravenously over the same period. ACTH induced hypertension in the ewe. Mean arterial pressure (MAP) increased from 101 +/- 4.4 to 114 +/- 3.9 mmHg at 48 h (P < 0.05); cardiac output increased from 8.6 +/- 0.5 to 10.4 +/- 1.0 l/min after 24 h (P < 0.05). Within 2-4 h, maternal cortisol levels increased from 24.6 +/- 6.3 to 287 +/- 30 nM (P < 0.05) and remained high. Fetal plasma cortisol levels increased from 20 +/- 4.5 to 60 +/- 4.5 nM (P < 0.05) within 2-4 h and then increased further. Fetal MAP was increased at 24 h. There was no effect on fetal blood gases or pH. Ewes became hyperglycemic and lactacidemic by 24 h (P < 0.05), and the fetuses were also hyperglycemic and lactacidemic (P < 0.05) at this time. There were no changes in fetuses carried by saline-infused ewes. Both ewes and fetuses had raised plasma osmolalities and, since hematocrit fell, retained fluid. Ewes became hypokalemic; the fetuses did not, but there was an increase in fetal K excretion. Thus ACTH-induced hypertension in the ewe had minimal effects on fetal MAP, fetal blood gas status, and pH. The fetus, however, did show many of the other effects of maternal glucocorticoid and mineralocorticoid excess, partly because its cortisol levels were increased but also as a consequence of metabolic and endocrine changes in the ewe.
 ...
PMID:Effects of infusions of ACTH in the chronically catheterized pregnant ewe and her fetus. 948 3

1. Recent studies in animals have linked fetal exposure to excess maternal glucocorticoids with the later occurrence of cardiovascular disorders, particularly hypertension. 2. To test the hypothesis that prenatal treatment could impact on adult blood pressure two groups of pregnant ewes were transported from the farm to the Institute at either 22-29 days of pregnancy (pretreatment group 1) or 59-66 days of pregnancy (pretreatment group 2), subjected to 48 h treatment with dexamethasone (0.28 mg day-1 kg-1 for 2 days) and then returned to the farm. The control group remained at the farm for the entire pregnancy. Lambs were then studied at approximately 4, 10 and 19 months after birth. 3. The basal mean arterial pressure in pretreatment group 1 (80 +/- 1 mmHg at 124 days; 83 +/- 1 mmHg at 309 days and 89 +/- 1 mmHg at 558 days; n = 6) was significantly different (P < 0.05 in all groups) from that in the control group of lambs (74 +/- 2 mmHg at 110 days; 76 +/- 1 mmHg at 323 days and 81 +/- 1 mmHg at 568 days; n = 7). However, prenatal glucocorticoid exposure did not alter vascular sensitivity to noradrenaline, angiotensin II and adrenocorticotropic hormone in these sheep at any of the ages studied, nor did it affect basal or adrenocorticotropic hormone-induced concentrations of cortisol or basal plasma renin concentrations in the lambs at any age. 4. These data support the hypothesis that excess glucocorticoid exposure in early pregnancy, during a critical developmental stage or 'window', programmes higher blood pressure that persists in later life.
 ...
PMID:An early prenatal exposure to excess glucocorticoid leads to hypertensive offspring in sheep. 953 23

A 61-year-old Japanese woman was hospitalized because of general malaise. The patient demonstrated hypertension, hypokalemia and chronic renal failure (CRF). Plasma aldosterone concentration and urinary excretion of aldosterone were elevated. Abdominal computed tomographic scan revealed right adrenal tumor and multiple cysts in both kidneys. Adrenal scintigram using 131I-adosterol disclosed uptake of the isotope in the area corresponding to the adrenal tumor. Plasma aldosterone concentration and renin activity (PRA) in an upright posture and daily variations in adrenocorticotropic hormone, cortisol, aldosterone levels and PRA were compatible with aldosterone-producing adrenocortical adenoma. After administration of spironolactone and manidipine hydrochloride, a calcium antagonist, general malaise disappeared, and blood pressure and serum potassium level returned to the normal range without adrenalectomy. Although adrenalectomy is known to be effective for the treatment of aldosterone-producing adrenocortical adenoma, several papers reporting cases of aldosterone-producing adrenocortical adenoma with CRF indicated that surgical therapy was not always optimal in terms of postoperative conditions. Taken together, the conservative therapy may be one of the choices considering the prognoses of hypertension and renal dysfunction in patients with aldosterone-producing adrenocortical adenoma with CRF.
 ...
PMID:Aldosterone-producing adrenocortical adenoma complicated by chronic renal failure. Case report and review of the literature. 984 33

Mibefradil is a new cardiovascular drug with peculiar Ca++ antagonistic properties. The most remarkable feature of mibefradil is its unique relative selectivity for T type calcium channels, a property that has been proposed to explain in part the beneficial pharmacological and clinical profiles of this drug. In adrenal glomerulosa cells, aldosterone biosynthesis and secretion in response to angiotensin II or extracellular potassium is dependent on a sustained influx of Ca++ through T type Ca++ channels. The effect of mibefradil on the steroidogenic function of glomerulosa cells was therefore investigated. Using the patch clamp technique, we found that mibefradil inhibits selectively and in a concentration-dependent manner (IC50 = 3 microM)++ T type currents in bovine glomerulosa cells. In addition to this tonic (voltage independent) inhibition, the drug also induced a shift of the steady-state inactivation curve of these channels toward hyperpolarized voltages, contributing to its efficacy to prevent Ca++ influx into the cell through T type channels. Concomitantly, mibefradil reduced the cytosolic calcium responses to potassium and angiotensin II (as assessed with fluorescent probes), without affecting the capacitative Ca++ influx, and inhibited pregnenolone and aldosterone formation. This inhibition of steroidogenesis was not exclusively due to mibefradil action on voltage-operated Ca++ channels, because this agent also partially reduced steroid synthesis induced by adrenocorticotropic hormone or forskolin, two activators of the cyclic AMP pathway. In conclusion, mibefradil is highly effective in adrenal glomerulosa cells in reducing T type channel activity and aldosterone biosynthesis, two actions that should contribute to the beneficial effect of the drug in the treatment of hypertension.
 ...
PMID:Inhibitory action of mibefradil on calcium signaling and aldosterone synthesis in bovine adrenal glomerulosa cells. 986 60


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>