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

The adrenal glands produce glucocorticoids (approximately 25 mg cortisol/day), mineralocorticoids (approximately 100 micrograms aldosterone/day) and androgens (e.g. dehydroepiandrosterone = DHEA approximately 10 mg/day) in their cortex and catecholamines in their medulla. Excessive cortisol production leads to Cushing's syndrome. In approximately 2/3 of the cases this is due to ACTH oversecretion most often from a pituitary adenoma and can be cured by removal of this adenoma. Cushing's syndrome caused by an adrenal adenoma, carcinoma or bilateral nodular adrenal hyperplasia is treated by adrenal surgery. Nelson's syndrome consists of hyperpigmentation of the skin and an often aggressively growing pituitary adenoma which secretes excessive amounts of ACTH. Treatment is surgical. Conn's syndrome (primary hyperaldosteronism) is due to aldosterone hypersecretion most often from an adrenal adenoma (therapy: unilateral adrenalectomy), more seldom from bilaterally hyperplastic adrenals (therapy: spironolactone). Excessive adrenal androgen secretion is found in the adrenogenital syndrome in which defective cortisol biosynthesis leads to ACTH oversecretion and ACTH-stimulated overproduction of cortisol precursors, some of which are androgens. Treatment consists of glucocorticoids which suppress the ACTH oversecretion. Pheochromocytomas produce excessive amounts of catecholamines and cause hypertension which can be persistent as well as episodic. Therapy consists of adrenalectomy. Malignant tumors of the adrenals have a poor prognosis. Incidentally found adrenal masses ("incidentalomas") are observed at regular intervals if they are small and should be surgically removed if they have a tendency to grow or are large (greater than or equal to 5 cm phi).
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PMID:[Normal and pathologic endocrinology of the adrenal glands]. 268 Oct 84

Ketoconazole, an oral antimycotic agent, is known to have a potent inhibitory effect on adrenal steroid production. It was given at a dose of 1200 mg/day to a 52-year-old female patient with a virilizing adrenocortical carcinoma in order to achieve better metabolic control pre-operatively. Together with a rapid normalisation of hypertension and hyperglycemia, a dramatic fall was noticed in serum and urinary adrenal steroids after a few days. Levels of total testosterone (20 nmol/l), androstenedione (greater than 35 nmol/l) and DHEA-sulphate (greater than 28 nmol/l) fell to normal levels in 6 days. By contrast, levels of 17-OH-progesterone (30 nmol/l) and progesterone (2.45 nmol/l) increased slightly, indicating inhibition of adrenal 17,20-lyase. Cortisol (620 nmol/l at 08.00 h) fell to very low levels (50 nmol/l) on day 6 of the trial. We conclude that ketoconazole is very effective in suppression of adrenal tumoural steroidogenesis and merits consideration in pre-operative use. We warn against dangerous hypoadrenalism which seems to occur earlier in tumoural than in normal adrenal metabolism.
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PMID:Use of ketoconazole in the treatment of a virilizing adrenocortical carcinoma. 277 22

Properties of cardiac beta-adrenergic receptors from two kidney-one clip hypertension and control rats were studied to determine whether or not alterations in the receptor contribute to the decreased responsiveness of two kidney-one clip rat hearts to adrenergic stimulation. The number and affinity of the beta-receptors were assessed by the binding of [3H]DHA in an enriched ventricular membrane fraction obtained from the rat hearts 3 and 4 weeks after the application of the clip. In the rats with 3 weeks of development of hypertension no significant difference was found neither in the number nor in the affinity of receptors (30.9 +/- 5.3 fmol/mg protein, KD: 1.62 +/- 0.43 nM) compared to the control rats (33.3 +/- 6.3 fmol/mg protein, KD: 2.21 +/- 0.59 nM). In rats with 4 weeks of development of hypertension, there was an increased number of receptors (54.7 +/- 3.7 fmol/mg protein, KD: 1.41 +/- 0.17 nM) compared with control rats studied in paralleled conditions (40.0 +/- 2.3 fmol/mg protein, KD: 1.13 +/- 0.12 nM). These results suggest that the reported beta-adrenergic subsensitivity in this model of hypertensive rats could be mediated by a biochemical mechanism other than a direct alteration of the beta adrenergic receptors, and that there is a compensatory increase in the density of receptors during the development of the hypertension.
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PMID:[Myocardial beta adrenergic receptors in experimental renal hypertension, type Goldblatt II]. 286 67

The author found that the onset of hypertension or hypotension is relatively often associated with infections or development of so-called "sneezing due to allergy to pollen or dust," with or without headache, or due to trauma to the occipital area of the head. Using the "Bi-Digital O-ring Test," it was possible to demonstrate that, among bacterial and viral infections, the most common cause of infection associated with the appearance of hypertension is chlamydia, herpes simplex virus, cytomegalovirus, or Epstein-Barr virus. Particularly chlamydia and/or herpes simplex virus, with or without coexistence of other microbes, is usually present at the heart representation area of the medulla oblongata, especially at the left ventricular representation area, often accompanied by upper respiratory infection, cephalic, cervical or facial pain, with or without coexisting genito-urinary infection. The left ventricular representation area of the medulla oblongata is usually located at the right side. In most hypertensive patients, the left ventricular representation area of the medulla oblongata is enlarged up to 3 or 4 times normal size. Sufficient antibiotic treatment of chlamydia with erythromycin sometimes eliminated severe hypertension which appeared after chlamydia infection. In the presence of viral infections, such as herpes simplex, which is also causing severe pain in the head or neck, oral administration of acyclovir, erythromycin, or EPA (Eicosa Pentaenoic acid)-DHA (docosa hexaenoic acid) Omega 3 fish oil often reduced associated intractable pain and hypertension toward the normal level. Thus, the author is proposing new possible mechanisms as among the causes of so-called essential hypertension as a result of microbial infection or trauma of the cardiovascular representation area, particularly that of the left ventricular representation area at the right side of the medulla oblongata.
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PMID:Microbial infection or trauma at cardiovascular representation area of medulla oblongata as some of the possible causes of hypertension or hypotension. 290 10

The effect of cardiac hypertrophy on beta-adrenergic receptor density and affinity was studied under 4 experimental conditions: in the spontaneously hypertensive rat (SHR), in the 2K-1C renal hypertensive rat (RHR), and following subcutaneous infusions of 2 pressor agents; epinephrine (E) and angiotensin II(AII). Using the antagonist 3H-dihydroalprenolol [( 3H]-DHA), the number of binding sites was shown to significantly decrease at both 13 and 24 weeks of age in the SHR when compared to age-matched WKY, with no change in affinity. In the RHR a significant increase in binding sites was observed at both 6 and 10 weeks after clipping, returning towards normal levels following removal of the clipped kidney. Cardiac hypertrophy and hypertension were induced by subcutaneous infusions for up to 2 weeks of both E and AII. E caused an alteration in receptor density, causing a significant decrease with no change in affinity. In contradistinction, although the degree of hypertrophy was the same following AII, no changes in receptor density or affinity were seen. These present experiments confirm our hypothesis that different models of hypertensive hypertrophy are associated with varying changes in beta-adrenergic receptors. This suggests that any consequential changes in myocardial function may be a result of other post receptor mechanisms.
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PMID:Beta-adrenergic receptors in rat myocardium during the development and reversal of hypertrophy and following chronic infusions of angiotensin II and epinephrine. 299 Mar 66

To study potential central adrenoceptor alterations in the hypertension, we have determined alpha 1, alpha 2 and beta-adrenoceptors using [3H]WB4101, [3H]yohimbine and [3H]DHA in the brain regions of spontaneously hypertensive rats (SHR), stroke-prone SHR (SHRSP) and renal hypertensive rats. There was a significant increase in specific [3H]WB4101 binding only in the hypothalamus of SHR and SHRSP at 16-24 weeks of age compared to that of age-matched Wistar-Kyoto rats (WKY). Scatchard analysis revealed a 28-33% increase in the Bmax value for hypothalamic [3H]WB4101 binding without a change in the Kd value, suggesting a change in the receptor density. An increased density of alpha 1-adrenoceptors was consistently observed in the prehypertensive (5 weeks) and developmental (10 weeks) stages of spontaneous hypertension. In contrast, there was no alpha 1-adrenoceptor alteration in the hypothalamus of rats with renal hypertension. The receptor alteration in the SHRSP hypothalamus was not abolished by a chronic hypotensive treatment which prevented the development of hypertension, thereby suggesting that an increased density of the alpha 1-adrenoceptors in spontaneous hypertension does not occur secondarily to the elevation of blood pressure. The SHRSP hypothalamus showed significantly lowered levels of noradrenaline. There was no change in specific binding of [3H]yohimbine and [3H]DHA in the brain regions of SHRSP, except the brainstem which showed a significant decrease in the [3H]yohimbine binding. Thus, the present study suggests an important role for hypothalamic alpha 1-adrenoceptors in the pathogenesis of spontaneous hypertension.
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PMID:Specific increase of hypothalamic alpha 1-adrenoceptors in spontaneously hypertensive rats: effect of hypotensive drug treatment. 299 33

Twelve male patients with mild essential hypertension were put on a diet supplemented with 2 cans of mackerel/day (= 2.2 g daily of eicosapentaenoic acid, EPA, C20:5 n-3 and 2.8 g daily of docosahexaenoic acid, DHA, C22:6 n-3) for 2 weeks within an isocaloric regimen and then with 3 cans/week (= 3.3 g/week, equivalent to 0.47 g daily of EPA and 4.2 g/week, equivalent to 0.69 g daily of DHA) for 8 months with a subsequent period of 2 months on normal diet. Eleven male hypertensives matched for age, body weight index, blood pressure and serum lipids with no change in their nutritional habits served as controls. After the first dietary period (2 weeks) a significant decrease of serum triglycerides (TG), total and LDL-cholesterol, blood pressure and thromboxane B2 (TxB2) was found, whereas HDL cholesterol and potassium in erythrocytes were significantly increased. During the second dietary period (8 months) providing the lower dose of EPA, serum lipids and the other biochemical parameters returned to the initial values. Blood pressure, however, remained significantly lower and rose to the basal levels only after the third period (2 months) on normal diet. In the control group no alterations could be seen. The data suggest a dose-related differential effect of dietary EPA on serum lipids, lipoproteins, TxB2 and blood pressure in subjects with mild hypertension.
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PMID:Long-term effect of mackerel diet on blood pressure, serum lipids and thromboxane formation in patients with mild essential hypertension. 302 12

The binding of 3H-dihydroalprenolol, a beta-antagonist, with the fat cell plasma membrane was studied in spontaneously hypertensive rats and in patients with essential hypertension. It was found that, as compared to control rats, hypertensive animals had an increased maximum number of 3H-DHA binding sites in the membranes and diminished affinity of beta-adrenoreceptors. It is suggested that these differences may play an essential role in the latered sensitivity to adrenalin in hypertensive rats. Removal of the adrenal, i. e. deprivation of the stabilizing corticosteroid effect, leads to marked changes in the state of the beta-adrenoreceptors in hypertensive animals. Thus, the maximum number of binding sites reduces in hypertensive rats but remains unaltered in the controls; following adrenalectomy the affinity of beta-adrenoreceptors increases in rats with hypertension, but in normal rats, on the contrary, does not change or rather has a tendency to decrease.
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PMID:[Characteristics of 3H-dihydroalprenolol binding to beta-receptors in the fat cells of rats and spontaneous genetic hypertension and in hypertensive disease]. 624 54

The possible contribution of changes in cardiac beta-adrenoceptors to alterations in cardiac responses to isoprenaline were investigated in hearts isolated from rats with renovascular hypertension (two-kidney, one-clip Goldblatt), 6, 12 and 18 weeks after renal artery clipping. Cardiac responses were determined in vitro (Langendorff preparation), and ventricular beta-adrenoceptors [( 3H]dihydroalprenolol, [3H]DHA) were then assayed in the same 44 hearts. There was no difference between renovascular hypertensive rats (RHR) and matched normotensive controls as regards chronotropic responses to isoprenaline or in atrial beta-adrenoceptor numbers or apparent affinity. Inotropic responses were significantly lower in all stages of RHR than in matched normotensive controls. There was also a significant (P less than 0.001) decrease in ventricular beta-adrenoceptor density with no significant change in apparent affinity (Kd). Inotropic responsiveness to isoprenaline (max. increment in peak dP/dt) was significantly correlated with ventricular beta-adrenoceptor density (r = 0.54, P = 0.0005). These results suggest that the reduction of ventricular beta-adrenoceptor density in that model of hypertension was responsible, at least partially, for the lowered inotropic responsiveness of the same hearts to isoprenaline.
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PMID:Beta-adrenoceptors and responsiveness in cardiac hypertrophy associated with renal hypertension in renovascular hypertensive rats. 632 88

A thermostable urinary homologue of the plasma aldosterone-binding globulin (ABG), designated ABG-TsU, was isolated and purified by differential ultrafiltration, ion exchange chromatography, and gel filtration to electrophoretic homogeneity. Scatchard plot analysis using highly purified ABG-TsU demonstrated reversible high-affinity low-capacity binding at separate sites for aldosterone and dehydroepiandrosterone sulfate (DHEA-SO4). ABG-TsU injected intraperitoneally (i.p.) in male rats resulted in sustained hypertension after 5 to 8 days, characterized after 12 days by no changes in plasma Na+ K+, aldosterone, or plasma renin activity (PRA). No histological changes could be detected in the kidneys, brains, or hearts, nor evidence of adrenocortical hyperplasia. This hypertension appears to be aldosterone-dependent since it is prevented by bilateral adrenalectomy or administration of a spironolactone, but not by adrenalectomy when aldosterone is given concomitantly with ABG-TsU. Hemodynamic characterization of this hypertension was carried out in rats after treatment with ABG-TsU or saline i.p. for 14 days. Cardiac output (CO) was measured using the reference sample microsphere method. ABG-TsU-treated rats had significantly higher mean arterial pressure (MAP), systolic blood pressure (SBP), diastolic blood pressure (DBP), and CO, while no difference in total peripheral resistance (TPR) was detected. This new animal model of borderline essential hypertension (EH) induced by ABG-TsU, which has a reversible high-affinity binding for aldosterone, results in adrenal-dependent hypertension due at this early phase to an increase in CO without any change in TPR, which remains inappropriately normal.
Hypertension
PMID:Aldosterone-binding globulin-induced hypertension in the rat. A new experimental model. 636 Aug 79


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