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)

An enzyme immunoassay of 19-nor-deoxycorticosterone in rat serum was established. The normal value of 19-nor-DOC in rat serum obtained from 9:00 am to 10:00 am was 148 +/- 30 ng/dl (mean +/- SE,n = 10). Serum levels of this steroid decreased in rats with adrenal regeneration hypertension during the course of the experiment up to 8 weeks, while systolic blood pressure rose progressively. We concluded that this mineralocorticoid is not involved at least as a circulating hormone in the pathogenesis of adrenal regeneration hypertension in rats.
Steroids 1983 Jan
PMID:Decreased serum 19-nor-deoxycorticosterone (21-hydroxy-19-nor-4-pregnene-3, 20-dione) level in adrenal regeneration hypertensive rats. 665 66

Intracranial hypertension is caused by various pathologic processes. From oncologic point of view, they are 1) intracranial space-occupying lesions, especially malignant tumors, 2) leptomeningeal tumors, 3) hemorrhage in the brain tumors, 4) intracranial hemorrhage due to hemorrhagic diathesis related to the malignant tumors, and 5) cerebral thrombosis or embolism due to increased blood coagulability secondary to malignancy. In the increase of intracranial pressure, brain edema or disturbance of cerebrospinal fluid (CSF) circulation due to the presence of brain tumors play more important role than the tumor bulk itself. CT scan is useful for demonstrating the process causing the intracranial hypertension. Therapeutic measures in all patients with increased intracranial pressure are initiated promptly to restore the cardiopulmonary dysfunction if any. Hyperventilation and intravenous infusion of hyperosmolar agents such as mannitol and glycerol have an immediate effect in reducing intracranial pressure when brain edema plays role in increasing it. Steroids are also very effective in reducing brain edema; the effect is less immediate but long lasting. CSF drainage or shunt operation is necessary when dilated ventricular system plays role in the intracranial hypertension. The radical treatment of the intracranial hypertension is a removal of the tumor causing it; however, if not indicated, the second choice is the internal or external decompressions. Postoperative radiotherapy and chemotherapy are also indicated for the malignant brain tumors.
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PMID:[Intracranial hypertension]. 688 68

The bioactivity of 5 alpha-reduced sex steroids such as 5 alpha-dihydrotestosterone has increased interest in an analogous role for 5 alpha-reduced mineralocorticoids in hypertensive syndromes. In view of its relatively high mineralocorticoid receptor affinity despite relatively low electrolyte-altering effects, 5-alpha-dihydro-11-deoxycorticosterone, or 5 alpha DHDOC (2) was compared to 11-deoxycorticosterone acetate (DOCA) for blood pressure-altering ability by continuous subcutaneous infusion into uninephrectomized saline-drinking Sprague-Dawley male rats, at doses selected on the basis of relative mineralocorticoid receptor affinity. After three weeks of treatment, DOCA significantly raised blood pressure, body weight, heart and kidney weight, and produced a discernible increase in fluid intake; 5 alpha DHDOC failed to affect any of these parameters commonly influenced by mineralocorticoids. We conclude that 1) the ability of 5 alpha DHDOC to affect blood pressure was not predicted by its relatively high affinity for the mineralocorticoid receptor, and 2) these data do not support a role for 5 alpha DHDOC in mineralocorticoid hypertension, although differences in protein binding and clearance could affect its blood pressure-altering activity.
Steroids 1981 Jan
PMID:5 alpha-Dihydro-11-deoxycorticosterone: effect on blood pressure in the rat. 722 41

A 32-year-old woman was bedridden for a year because of chronic pain and headaches. She had insomnia, depression, suicidal thoughts and a severe chemical allergy. She had been on steroid therapy for two years and became Cushingoid with striae in the arm pits, groins and abdomen. However, she had no hypertension, nor the buffalo fat and hirsutism. She was very edematous, with a weight gain from 112 to 180 lbs. The fluid retention did not conform to the syndrome of inappropriate antidiuretic hormone. Studies revealed abnormal scalp EEG discharges and high-voltage seizure discharges in the posterior thalamus. Electrothalamic stimulation suppressed the thalamic discharges and relieved the patient's pelvic pain and headaches. After one month of several thalamic stimulations per day, she was able to get out of bed and ambulate. In addition, the patient no longer was edematous and was tolerating perfumes and floor detergents. Steroids were progressively reduced without complications of withdrawal. She went from a completely steroid dependent state to independent during the first 1-1/2 yrs of thalamic stimulation. With continued thalamic stimulation she has done well for 8-1/2 yrs, weighs 112 lbs, keeps house and drives a car. It's speculated the illness is a chronic pain multiple syndrome predominantly due to mesothalamic discharges and body infirmities. The mesothalamic discharge implicated neural networks, which represent biologic systems, i.e. pain, sleep, fluid retention, etc. Therapeutic stimulation attenuates the discharges and the neural networks return to their normal set points of homeostasis.
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PMID:Mesothalamic discharge in a chronic pain, allergy and fluid retention syndrome (case report). 766 2

The activities of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) and 5 beta-reductase were analyzed in 39 normotensive controls and 128 patients with essential hypertension. The activity of 11 beta-HSD was obtained by dividing the 24-hour urinary tetrahydrocortisone by the sum of tetrahydrocortisol (THF) and allotetrahydrocortisol (aTHF), whereas the activity of 5 beta-reductase was obtained by dividing the 24-hour urinary THF by aTHF. The activity of 5 beta-reductase was significantly lower in essential hypertensives compared with normotensive controls (P < 0.05). However, the activity of 11 beta-HSD did not differ between normotensive controls and essential hypertensives. A positive correlation between the activities of 11 beta-HSD and 5 beta-reductase was observed in essential hypertensives (r = 0.60, P < 0.01). Neither 11 beta-HSD nor 5 beta-reductase activity correlated with indices of renal mineralocorticoid receptor activation, which were assessed by determination of plasma potassium and urinary excretion of sodium as well as potassium. Taken together, these results suggest that disturbances of one of the inactivation pathways of cortisol may contribute to the pathogenesis of hypertension.
Steroids 1994 Nov
PMID:The activities of 5 beta-reductase and 11 beta-hydroxysteroid dehydrogenase in essential hypertension. 770 42

Potassium canrenoate (K-Can) prevents hypertension in Milan hypertensive strain (MHS) but not in spontaneously hypertensive rats (SHR). Essential hypertensive patients (HT) may have differential sensitivity to diuretics, since a subgroup of HT insensitive to hydrochlorothiazide (HCTZ) but sensitive to K-Can has previously been found. The aims of this study were: 1) to seek markers of response in essential hypertensive patients selectively sensitive to K-Can: and 2) to test whether selective sensitivity to furosemide may also be demonstrated. After 2 weeks of placebo (P) 50 uncomplicated, mild to moderate HT (46 +/- 9 yrs, mean +/- SD) received K-Can (50 mg/day) for 4 weeks. After 2 more weeks of P, patients received HCTZ (25 mg) and furosemide (25 mg) for 4 weeks each in a single blind crossover design, with 2 weeks P between each treatment. Dosages were doubled after 2 weeks if diastolic blood pressure (DBP) was > 90 mmHg. Responders (R) were those HT whose DBP was < or = 90 mmHg and/or at least 10 mmHg lower than before treatment. Systolic blood pressure (SBP)/DBP was measured every 2 weeks with plasma renin activity (PRA), red blood cell Na(+)-K(+)-Cl- cotransport (COT) and Na(+)-K+ ATPase pump activity measured at the end of the first P period, and serum electrolytes at the end of each period. Four HT dropped out because of low compliance, 6 because of reversible side effects, and 1 because blood pressure was not back to pre-treatment value after the second placebo period.(ABSTRACT TRUNCATED AT 250 WORDS)
Steroids 1995 Jan
PMID:Recognition of markers of response to potassium-canrenoate in essential hypertension. 779 93

It has been suggested that endogenous substances (known as ouabain-like factors, OLF), secreted from the central nervous system in response to salt and water retention, inhibit the cell membrane Na+/K+ pump in the renal tubules and reduce sodium reabsorption. However, by also acting upon vascular smooth muscle cells, they may induce cell Na+ and Ca++ accumulation, vasoconstriction and systemic hypertension. Recently, an endogenous Na+/K+ pump inhibitor was isolated from human plasma; this inhibitor is indistinguishable from the cardiac glycoside ouabain based on biochemical and immunological criteria. Its plasma concentration is close to the therapeutic range for ouabain (around 0.4 nmol/L). Since plant ouabain promotes natriuresis, vasoconstriction, and hypertension; endogenous ouabain may therefore control extracellular fluid volume and blood pressure. The highest plasma concentrations of endogenous ouabain and OLF were found in congestive heart failure, aldosterone producing adenoma, human and animal models of volume expanded hypertension (reduced renal mass and DOCA-salt hypertension), and in Milan hypertensive rats (MHS). Aldosterone antagonists (canrenone and canrenoate) exert both agonist and antagonist effects on the digitalis receptor site of the Na+/K+ pump. They are effective antihypertensive agents in animal models of hypertension sustained by OLF (reduced renal mass-Na+ and DOCA-salt hypertension in rats). Moreover, in a subgroup of essential hypertensives, 4 weeks of canrenoate administration reduced blood pressure, heightened red blood cell Na+/K+ pump activity, and antagonized ouabain-induced vasoconstriction. None of these effects was seen in the other hypertensives. These data suggest that aldosterone antagonists stimulate the Na+/K+ pump inhibited by endogenous ouabain and exert their antihypertensive action at least in part through this mechanism.
Steroids 1995 Jan
PMID:Ouabain-inhibiting activity of aldosterone antagonists. 779 94

We have previously reported our studies on glucocorticoid (GC) effects on Na+ influx in vascular smooth muscle (VSM) cells. We now report a parallel study on the effect of mineralocorticoid (MC) on Na+ influx in VSM cells. Unidirectional influx of Na+ was measured in cultured cells of rabbit aortic media with 22Na as tracer. Cells were treated with near physiologic (5 nM) or supraphysiologic (50 nM) aldosterone (ALDO) for 24 or 48 hours, or for 7 to 10 days, in the presence of competitive inhibitors of MC-receptor binding, K-prorenoate (PRN), or GC-receptor binding, RU 486. ALDO at 5 nM increased Na+ influx by 98% +/- 12%, but only after 7-10 days of treatment. This effect was inhibited by PRN, but not by RU 486, and blocked by amiloride but not by ethylisopropyl-amiloride or by dichlorobenzamil (DCB). In VSM cell membranes from aortae of rabbits treated in vivo with ALDO (2 mg/day) for 4 weeks. Na+ channels were quantified by determination of specific [3H]amiloride binding in the presence of excess of DCB and EIPA to exclude tracer binding from the Na+/Ca2+ exchanger and the Na+/H+ antiporter. ALDO doubled the number of of Na+ channels in such isolated cell membranes, as determined by Bmax per mg membrane protein. We propose that this vascular effect of ALDO may constitute an important pathogenetic mechanism of hypertension induced by chronic excess of MC, in addition to the well known renal mechanism.
Steroids 1995 Jan
PMID:Aldosterone (ALDO) increases transmembrane influx of Na+ in vascular smooth muscle (VSM) cells through increased synthesis of Na+ channels. 779 95

Chronic mineralocorticoid (MC) excess, whether due to elevated plasma aldosterone (ALDO) or deoxycorticosterone (DOC), is associated with a perivascular fibrosis of systemic and coronary arterioles. This remodeling of resistance vessels contributes to the appearance of hypertension. Chronic MC excess is also accompanied by cardiac myocyte necrosis, secondary to myocardial potassium depletion, and a subsequent reparative fibrosis that appears in the normotensive, nonhypertrophied right and hypertensive, hypertrophied left ventricles. Fibrosis contributes to the appearance of ventricular arrhythmias and dysfunction. Herein, clinical and experimental evidence linking chronic, inappropriate (relative to dietary sodium) elevations in circulating ALDO and DOC with these reactive and reparative forms of fibrous tissue formation in the heart and other tissues is presented.
Steroids 1995 Jan
PMID:Chronic mineralocorticoid excess and cardiovascular remodeling. 779 97

Uninephrectomized rats maintained on 0.9% NaCl as drinking fluid and infused for 8 weeks with aldosterone 0.75 micrograms/h via subcutaneous osmotic minipumps respond with hypertension, cardiac hypertrophy, and both interstitial and perivascular cardiac fibrosis. Similar animals injected with desoxycorticosterone (20 mg/week), or the glucocorticoid antagonist RU 486 (2 mg/day) show interstitial cardiac fibrosis to a lesser degree than animals injected with aldosterone, and show perivascular fibrosis to a greater degree. These findings suggest that glucocorticoid antagonist activity may play a role in exacerbating perivascular collagen deposition in response to chronic mineralocorticoid and salt imbalance.
Steroids 1995 Jan
PMID:Adrenal steroids and cardiac fibrosis. 779 98


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