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

The urinary excretion of 3beta,16beta-dihydroxy-5-androsten-17-one (16beta-OH-DHEA) is increased in patients with low renin essential hypertension. This steroid and its isomer 3beta,17beta-dihydroxy-5-androsten-16-one (16-oxo-A) have also been reported to have mineralocorticoid activity in adrenalectomized rats. These findings have led to the postulate that excessive secretion of 16beta-OH-DHEA may be responsible for the production of low renin essential hypertension. In this study unilaterally nephrectomized salt loaded rats injected once a week with 30 mg of 11-desoxycorticosterone acetate per/kg of body weight for 2 month periods developed hypertension. Rats given similar amounts of 16beta-OH-DHEA or 16-oxo-A and rats given no steroids did not develop hypertension. We conclude that it is unlikely that 16beta-OH-DHEA and 16-oxo-A are direct causative factors in the production of low renin essential hypertension.
Steroids 1977 Jan
PMID:Blood pressure changes following chronic administration to rats of 3beta,16beta-dihydroxy-5-androsten-17-one, 3beta,17beta-dihydroxy-5-androsten-16-one and 21-hydroxy-4-pregnene-3,20-dione-21-acetate. 13 80

Anaesthesia for nine patients with the carcinoid syndrome is described. With the exception of one case in which severe bronchospasm and hypertension occurred, complications were minor. Steroids, aprotonin and methotrimeprazine appear to be useful agents in the management of such patients. An anaesthetic technique employing thiopentone, pancuronium and nitrous oxide proved satisfactory.
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PMID:Anaesthesia for the carcinoid syndrome: a report of nine cases. 30 68

A time course study to measure adrenal cortical function was undertaken for the period prior to the development of hypertension until the onset of hypertension in the adrenal-regeneration hypertension (ARH) model. Quiescent rat kills were used so that all adrenal cortical parameters investigated would reflect basal or resting levels for controls. Thus a more accurate determination of the differences between control and experimental animals could be made. A radioimmunoassay procedure for deoxycorticosterone was developed to measure this steroid in individual rat serum samples. Elevated serum deoxycorticosterone levels were observed in rats with regenerating adrenals when they were killed under quiescent conditions. This agreed with our recently reported in vitro finding of restoration of cholesterol side chain cleavage activity while 11beta-hydroxylase activity remained imparied 25 days after adrenal enucleation. When rats were killed after ether stress, deoxycorticosterone levels were elevated in both control rats and in rats with regenerating adrenals but the difference was not significant. In contrast, after ether stress serum corticosterone levels were lower in rats with regenerating adrenals than in controls. These studies, in conjunction with our previous in vitro findings, point to the importance of deoxycorticosterone in the pathogenesis of adrenal regeneration hypertension and help to explain the anomalous corticosteroid secretion rate data found in this experimental hypertension model.
Steroids 1975 Mar
PMID:Serum 11-deoxycorticosterone levels in adrenal-regeneration hypertension under conditions of quiescence and stress. 114 70

16Alpha, 18-Dihydroxydeoxycorticosterone (16alpha, 18-dihydroxy-DOC) (1) and 1, 2-3H-16alpha, 18-dihydroxy-DOC (1,2-3H-16alpha, 18-dihydroxy-DOC) of high specific activity were obtained in good yield by microbiological hydroxylation of 18-OH-DOC and 1,2-3H-18-OH-DOC by Streptomyces roseochromogenus (ATCC 13400). The identity of the fermentation product to human adrenal produced 16alpha, 18-dihydroxy-DOC was established by chromatographic studies, derivative formation and gas-liquid chromatography. Yield of the product was about 30% of sutstrate and, allowing for losses in recovery, about 60% of the substrate 18-OH-DOC was converted to this product. A second product of fermentation isolated in lower yield appeared to be a dimer of 16alpha, 18-dihydroxy-DOC found in the acidic conditions of the fermentation. This method of synthesis of 16alpha, 18-dihydroxy-DOC is a practical way to make large quantities of the compound for further study of its possible role in human and experimental hypertension.
Steroids 1975 Dec
PMID:Microbiological synthesis of 16alpha, 18-dihydroxydeoxycorticosterone. 121 57

Racial and ethnic variations in serum testosterone levels were investigated among a large sample of male Vietnam era veterans. Based on geometric means, significant average differences were found between 3,654 non-Hispanic white and 525 black individuals. The geometric mean for testosterone levels among 200 Hispanic individuals was similar to that of non-Hispanic white individuals. Regarding two other racial/ethnic groups (Asian/Pacific Islanders and Native Americans), no significant differences were found, due perhaps to small sample sizes. Results were interpreted as having considerable potential for explaining some of the race differences in the incidences of cardiovascular diseases, hypertension, and prostate cancer.
Steroids 1992 Feb
PMID:Racial/ethnic variations in male testosterone levels: a probable contributor to group differences in health. 162 Dec 59

19-Nordeoxycorticosterone (19-norDOC) is a powerful mineralocorticoid that has been postulated to play a role in the pathogenesis of some forms of hypertension in the rat. We measured the daily excretion of 19-norDOC, aldosterone, and corticosterone in intact male and female SR/jr rats for 20 consecutive days. The excretion of corticosterone and aldosterone was higher during the first 4 days of collection and remained relatively stable for the rest of the collection period. The excretion of corticosterone and aldosterone was not different between male and female rats. The excretion of 19-norDOC, which, as has been reported previously, was significantly higher in female than male rats, varied over 600% from day to day in some individual rats. The variability in the excretion of 19-norDOC did not correlate with the excretion of aldosterone or corticosterone and did not appear to coincide with an estrous cycle. These studies also indicate that when the urinary excretion of steroids is intended to be used as an indication of steroid production in the basal state, a period of at least 4 days of acclimatization in metabolic cages, even for animals accustomed to handling, is necessary to obtain stable excretions.
Steroids 1991 Aug
PMID:19-Nordeoxycorticosterone, aldosterone, and corticosterone excretion in sequential urine samples from male and female rats. 178 63

Anabolic/androgenic steroid abuse is an increasing medical and public health problem. The uncontrolled use of these agents has been associated with numerous toxic side-effects including deleterious cardiovascular changes. The most widely reported to these latter changes include the development of adverse lipid profiles and hypertension. Acute thrombosis has only recently been linked to androgen abuse. Such a causative link has been proposed in reports of acute myocardial infarction and stroke in several athletes using androgens. Unfortunately, there exists no direct evidence that androgens are thrombogenic in humans. However, indirect experimental data suggests that androgens affect platelet aggregation, coagulation proteins and the vascular system in ways that facilitate thrombosis. Androgens also increase several anticoagulant and fibrinolytic proteins. However, they have not been shown to protect from thrombosis in high risk patients. Existing data supports a possible thrombogenic effect of exogenous androgens. Further studies are needed to clarify the hemostatic influence associated with androgen abuse in weightlifters. The abuse of these agents may diminish if acute thrombosis becomes clearly and scientifically associated with their uncontrolled use.
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PMID:Anabolic/androgenic steroid abuse and thrombosis: is there a connection? 192 73

The current investigation was designed to study the effect(s) of high calcium diet on the development of high blood pressure (BP) in both young intact spontaneously hypertensive rats (SHRs) and in young adrenalectomized (ADX) male SHRs treated with aldosterone (ALDO). Weaned SHRs were fed either a control calcium diet (0.5% Ca as PO4) (CCaDiet), a high calcium diet (2.5% Ca, 0.5% as PO4 and 2% as CO3) (HCaDiet), or Agway ProLab rat food containing 2.5% Ca (HCaPLDiet). The HCaDiet significantly blunted the development of high BP in young intact SHRs (P less than 0.001; n = 8 to 10). At 6 weeks of age, BP was 117 +/- 2 mm Hg (HCaDiet) compared with 135 +/- 3 mm Hg (CCaDiet); by 12.7 weeks of age, BP was 192 +/- 4 mm Hg (HCaDiet) compared with 233 +/- 3 mm Hg (CCaDiet). Similar results were observed in age-matched SHRs fed the HCaPLDiet. The results show that subcutaneous infusion of ALDO (1.0 microgram/d, osmotic pumps) for 2 weeks to young ADX male SHRs raised on the CCaDiet caused a significant increase in systolic BP when compared with SHRs implanted with Sham pumps (P less than 0.001). High BP associated with ALDO infusion was attenuated by the HCaDiet (BP after 2 weeks was 138 +/- 8 mm Hg for the HCaDiet group compared with 200 +/- 5 mm Hg for the CCaDiet group, P less than 0.001; n = 4 to 6). The results show that the HCaDiet blunts the development of high BP in intact SHRs and may protect against the development of ALDO hypertension in ADX young SHRs.
Steroids 1991 Mar
PMID:Effect of high calcium diet on the development of high blood pressure in intact spontaneously hypertensive rats and in adrenalectomized spontaneously hypertensive rats treated with aldosterone. 204 31

Post-transplant hypertension remains an important risk factor for cardiovascular mortality and graft function. There are multiple mechanisms responsible for post-transplant hypertension. The details of these mechanisms are poorly understood. Steroids, acute and chronic rejection, recurrent renal disease, native kidney disease, and renal artery stenosis have all been implicated in causing post-transplant hypertension. With the addition of cyclosporine, a known hypertensive agent, to the immunosuppressive armamentarium, the evaluation of post-transplantation hypertension has become difficult. Presently, medical therapy is initially directed toward the complications of cyclosporine nephrotoxicity. Empirically, converting enzyme inhibitors are added to the antihypertensive regimen. Further management is aimed at identification of specific causes of post-transplant hypertension. Unfortunately, because of the multifactorial etiology of post-transplant hypertension and a lack of detailed information about the mechanisms, medical and surgical therapy are often unrewarding. Further study is needed to clarify the mechanisms involved in post-transplant hypertension, and thus direct therapy.
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PMID:Post-transplant hypertension. 222 80

A male to female ration of coronary disease of 2:1 has been a consistent finding. This differential persists event when the classic risk factors for coronary disease--hypertension, smoking, obesity, diabetes, and hyperlipidemia--are controlled for gender. The most likely ultimate cause of this phenomenon is male-female differences in sex hormone patterns. Clinical studies in this area have either compared the sex hormone profiles of men and women with and without coronary disease or computed the relative prevalence of disease in populations that differ in their sex hormone patterns. In general, research findings have disputed the hypothesis that persons with coronary disease have low levels of a protective factor such as estrogen or progesterone and high levels of testosterone. Coronary disease patients actually have elevated estrogen levels and low testosterone levels; endogenous progesterone levels are normal before infarction but show a stress-mediated increase in the immediate postinfarction period. Findings of a low prevalence of coronary disease in premenopausal women, a loss of protection after menopause, and a low prevalence of coronary disease in men with cirrhosis-related hyperestrogenemia suggest that natural estrogens are antiatherogenic. The protective effect of pregnancy against myocardial infarction, despite concomitant potentially thrombogenic levels of estrogen at the time, seems to indicate that progesterone, whose levels are also extremely high during pregnancy, plays a major anti-infarction protective effect distinct from that of estrogen. Studies of women oral contraceptive (OC) users and men taking estrogens for brief periods have found that these exogenous hormones produce coronary thrombosis but not atherosclerosis. Finally, the finding of increased coronary disease risk in long-term OC users indicates that synthetic estrogens favor coronary atherosclerosis by suppressing natural estrogen and progesterone production.
Steroids 1990 Aug
PMID:Sex hormones and coronary disease: a review of the clinical studies. 223 42


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