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

One hundred and ten cases of hypertensive disorders in pregnancy were analyzed retrospectively. There were 16 cases of gestational hypertension, 36 cases of mild preeclampsia, 43 cases of severe preeclampsia, 6 cases of eclampsia, and 9 cases of chronic hypertension with superimposed severe preeclampsia. The principle of management was conservative in order to prolong pregnancy for patients remote from term. Corticosteroids were used to accelerate fetal lung maturity for patients with gestations of less than 36 weeks and magnesium sulfate was administered to prevent seizures. Fetal heart rate monitoring was done routinely and doppler blood flow velocity time wave form study of uterine and umbilical arteries was also performed in the latter part of the study. The cesarean section rate in gestational hypertension and mild preeclampsia was comparable to the general obstetric population in our institute (26.9% vs. 21.2%), but the rate of severe forms of the disease including severe preeclampsia, eclampsia, and chronic hypertension with superimposed severe preeclampsia was as high as 77.6%. Fetal distress was the main indication of section. There were 2 cases (6.9%) of mild respiratory distress syndrome, and all recovered uneventfully. The patients with severe forms of the disease had a higher incidence of small infants for gestational age (72%) and delivery at less than 36 weeks' gestation (48.2%). The corrected perinatal mortality rate was 5.4%. No maternal death was encountered. It was concluded that pregnancy could be prolonged in the interest of fetal lung maturity under meticulous maternal-fetal monitoring without endangering the mother.
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PMID:Hypertensive disorders in pregnancy: analysis of 110 cases. 279 58

An apparent increase of calmodulin (CaM) activity was previously observed in the heart and kidney but not in the liver of spontaneously-hypertensive rats (SHR) and mice compared with their corresponding normotensive controls. As this change was due to an elevated recovery of CaM in the organs of the hypertensive animals, the present study was designed to evaluate its activity in hypertension. A CaM activator, detected in heart and kidney supernatants from hypertensive animals, was found to be responsible for this enhanced recovery. Similar results were obtained with passaged, cultured aortic smooth muscle cells from SHR, indicating that the anomaly was not a mere consequence of elevated blood pressure but rather a genetic expression of cells of hypertensive origin. The activator was heat stable, nondialyzable, and recovered in the fraction precipitated with 30-50% ammonium sulfate. Preliminary extraction studies suggest that the activator is contained in a glycolipid fraction. The stimulation of phosphodiesterase by this activator was calcium and CaM dependent. The activator appears to affect the affinity of the phosphodiesterase for CaM rather than the maximal stimulation. The activator was also present at a low concentration in the heart and kidney of normotensive animals. These findings indicate that at least some of the calcium abnormalities implicated in the pathogenesis of hypertension could be the result of interactions between CaM, calcium, and this activator.
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PMID:Abnormality of calmodulin activity in hypertension. Evidence of the presence of an activator. 283 48

In order to identify a specific endogenous Na+,K+-ATPase inhibitor which could possibly be related to salt-dependent hypertension, we looked for substances in the methanol extract of bovine whole adrenal which show all of the following properties: (i) inhibitory activity for Na+,K+-ATPase; (ii) competitive displacing activity against [3H]ouabain binding to the enzyme; (iii) inhibitory activity for 86Rb uptake into intact human erythrocytes; and (iv) cross-reactivity with sheep anti-digoxin-specific antibody. After stepwise fractionation of the methanol extract of bovine adrenal glands by chromatography on a C18 open column, a 0-15% acetonitrile fraction was fractionated by high-performance liquid chromatography on a Zorbax octadecylsilane column. One of the most active fractions in 0-15% acetonitrile was found to exhibit all of the four types of the activities. It was soluble in water and was distinct from various substances which have been known to inhibit Na+,K+-ATPase such as unsaturated free fatty acids, lysophosphatidylcholines, vanadate, dihydroxyeicosatrienoic acid, dehydroepiandrosterone sulfate, dopamine, lignan, ascorbic acid, etc. This substance was further purified by using an additional five steps of high-performance liquid chromatography with five different types of columns. Molecular mass was estimated as below 350 by fast atom bombardment mass spectroscopy and ultrafiltration. Heat treatment at 250 degrees C for 2 h and acid treatment with 6 N HCl at 115 degrees C for 21 h almost completely destroyed the inhibitory activity of the purified substance for Na+ pump activity. Additionally, alkaline treatment with 0.2 N NaOH at 23 degrees C for 2 h destroyed approximately 70% of the inhibitory activity, whereas boiling for 10 min and various enzyme digestion did not destroy the activity. The dose dependency for the four types of the activities for this substance paralleled those of ouabain, spanning 2 orders of magnitude in concentration range. The inhibitory potencies of the purified substance for Na+,K+-ATPase, Na+ pump, and ouabain binding activities were diminished with increasing K+ concentration, exhibiting a characteristic typical of cardiac glycosides. This substance had no effect on the Ca2+-ATPase activity or the Ca2+ loading rate into the vesicle prepared from skeletal muscle sarcoplasmic reticulum. These results strongly suggest that this water-soluble nonpeptidic Na+,K+-ATPase inhibitor may be a specific endogenous regulator for the ATPase.
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PMID:Isolation and characterization of a specific endogenous Na+,K+-ATPase inhibitor from bovine adrenal. 284 24

The effects of xylazine on heart rate (HR) and mean arterial blood pressure (ABP) were studied in 5 conscious male dogs. An IV injection of xylazine (1 mg/kg) caused a decrease in HR, which was accompanied by sinus arrhythmia. Xylazine administration also caused an initial increase in ABP, which was followed by a decrease. Atropine sulfate (0.045 mg/kg, IM) increased both the ABP and HR, but prevented xylazine-induced bradycardia only in 3 of 5 dogs. The other 2 dogs had to be given a supplemental dose of atropine sulfate (0.01 mg/kg, IV) before xylazine-induced bradycardia was antagonized. In addition, atropine sulfate potentiated xylazine-induced hypertension for 60 minutes. Yohimbine, an alpha 2-adrenoreceptor blocking agent, given IV at a dosage of 0.1 mg/kg, antagonized hypertension, hypotension, and bradycardia induced by xylazine. In addition, doxapram HCl, given IV at a dosage of 5.5 mg/kg, antagonized bradycardia but potentiated xylazine-induced hypertension, and an IV injection of 4-aminopyridine at a dosage of 0.5 mg/kg did not affect the cardiovascular actions of xylazine. It was concluded that atropine sulfate at the IM dosage of 0.045 mg/kg may be insufficient to antagonize xylazine-induced bradycardia but may potentiate xylazine-induced hypertension, and yohimbine may be useful in antagonizing these untoward reactions associated with xylazine administration. Doxapram and 4-aminopyridine were not found to be beneficial.
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PMID:Effect of xylazine on heart rate and arterial blood pressure in conscious dogs, as influenced by atropine, 4-aminopyridine, doxapram, and yohimbine. 285 5

Several significant interrelations among variation in blood pressure, body fat, and adrenal androgen levels, as assessed by serum dehydroepiandrosterone sulfate concentrations, were found in black male and female adolescents, aged 12 to 16 years. In girls, high levels of dehydroepiandrosterone sulfate were associated with significantly higher levels of blood pressure (alpha = 0.05), even after adjusting for the significant association between increased levels of dehydroepiandrosterone sulfate and body fat. The increased body fat (i.e., body mass index) found with higher levels of dehydroepiandrosterone sulfate in girls was related to significantly greater (alpha = 0.05) accumulations of fat in the upper trunk, as opposed to the limb. In boys, high levels of serum dehydroepiandrosterone sulfate, low body mass index, and significantly higher blood pressure were interrelated (alpha = 0.05). In addition to the interaction of increased body mass index or body fat and increased levels of dehydroepiandrosterone sulfate in association with higher blood pressure, high levels of the adrenal androgen, even in boys with low body mass index, were associated independently with relatively higher blood pressure. Body proportion analyses for these boys indicated that they were tall and thin, in contrast to the other boys with low body mass index, who were generally short and thin.
Hypertension 1986 Apr
PMID:Blood pressure, body fat, and dehydroepiandrosterone sulfate variation in adolescence. 293 23

The practicability and tolerability of trilostane, a competitive inhibitor of 3 beta-hydroxysteroid-delta 5-dehydrogenase, for the therapy of primary aldosteronism was assessed in 1 patient with aldosterone-producing adenoma (APA) and 3 subjects with idiopathic adrenal hyperplasia (IHA). Trilostane afforded reduction of plasma levels of aldosterone, progesterone, deoxycorticosterone, 17-OH progesterone, cortisol, delta 4-androstenedione, and urinary excretion of 17-hydroxycorticosteroid. Conversely, circulating levels of dehydroepiandrosterone, dehydroepiandrosterone sulfate, and urinary excretion of 17-ketosteroids were increased following this drug therapy. Suppression of mineralo- or glucocorticoid biosynthesis was accompanied by an increase in plasma renin activity. One patient with APA or 3 subjects with IHA showed slight or remarkable improvement of hypertension and hypokalemia. Based on these findings, efficacy and tolerability of trilostane appear to aid in the treatment of IHA.
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PMID:Primary aldosteronism treated by trilostane (3 beta-hydroxysteroid dehydrogenase inhibitor). 298 27

Angiotensin-converting enzyme, the polypeptide that converts angiotensin I to angiotensin II, was measured in the serum of 114 pregnant women who had normal blood pressure, pregnancy-induced hypertension-preeclampsia, and chronic hypertension with or without pregnancy-induced hypertension. Angiotensin-converting enzyme levels were unrelated to weeks of gestation. The angiotensin-converting enzyme levels were similar in normotensive women (21.1 +/- 6.9 units/ml), women with chronic hypertension without pregnancy-induced hypertension (23.1 +/- 2.7 units/ml), and patients with pregnancy-induced hypertension where magnesium sulfate (22.6 +/- 8.7 units/ml) had been administered prior to angiotensin-converting enzyme assay, but these values were significantly less than those in patients with pregnancy-induced hypertension with no magnesium sulfate (29.1 +/- 6.5 units/ml) therapy and in women with chronic hypertension with superimposed pregnancy-induced hypertension (30.7 +/- 4.4 units/ml) (p less than 0.005). Maternal venous and umbilical venous and arterial angiotensin-converting enzyme levels were as follows: The maternal venous level was less than the cord venous level and greater than the cord arterial value. Neither neonatal size nor twin gestation influenced the angiotensin-converting enzyme levels. Patients with diabetes mellitus had variable angiotensin-converting enzyme values regardless of the status of the blood pressure. The physiologic theories of blood pressure control in pregnant women are discussed in relation to the renin-angiotensin, bradykinin, and prostaglandin systems.
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PMID:The relation of angiotensin-converting enzyme to the pregnancy-induced hypertension-preeclampsia syndrome. 300 58

Angiotensin-converting enzyme is a peptidase involved in the formation of angiotensin II and the inactivation of bradykinin. In a previous study we found elevated angiotensin-converting enzyme activity in women with pregnancy-induced hypertension prior to magnesium sulfate therapy and lower levels during therapy. This prospective study was undertaken in order to determine if angiotensin-converting enzyme activity indeed decreased after magnesium sulfate therapy. Sixteen patients with pregnancy-induced hypertension were studied before and during magnesium sulfate therapy. Angiotensin-converting enzyme activity was found to decrease 1 to 8 hours into therapy and then plateau between 9 and 24 hours. Possible mechanisms for this observation are discussed.
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PMID:Angiotensin-converting enzyme activity in hypertensive subjects after magnesium sulfate therapy. 303 26

The vascular proteoglycans probably have an important influence on the biomechanical properties of blood vessels and, therefore, may play a role in the development or maintenance of hypertension. In the aorta of the spontaneously hypertensive rat, the authors previously observed an increased content of chondroitin sulfate, an increased incorporation of [35S]sulfate into proteoglycans, and qualitative alterations in the [35S]polysaccharides compared to the normotensive Wistar Kyoto rat. To determine if these differences were related to hypertension or to strain variations, normotensive and hypertensive Dahl S rats were studied. There was a significant elevation (70%) in the aorta content of chondroitin sulfate, whereas the dermatan sulfate and hyaluronic acid contents were similar in the two groups. The in vitro incorporation of [35S]sulfate was increased 2.6-fold in the hypertensive animals. No differences between the two groups were observed with respect to the gel chromatographic profiles of the [35S]proteoglycans or the charge density of the [35S]glycosaminoglycans, as assessed by ion exchange chromatography. It was concluded that the increase in chondroitin sulfate and [35S]sulfate incorporation into proteoglycans occurred as a result of hypertension, regardless of genetic factors.
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PMID:Proteoglycans and hypertension: III: Aorta proteoglycans in Dahl salt-sensitive hypertensive rats. 310 11

17 alpha-hydroxylase deficiency is a rare form of congenital abnormality in steroid synthesis, usually associated with moderate arterial hypertension and suppression of the renin-angiotensin system in a young adult. We report on a 45 years old woman with malignant hypertension (220/135 mmHg, severe retinopathy with papilledema, progressive renal insufficiency with serum creatinine over 300 mumol/l) of recent onset. Biological exploration revealed a metabolic alkalosis, a moderate hypokalemia (3 mmol/l), with elevated urinary excretion of potassium. Plasma aldosterone concentration (33 ng/dl) and plasma renin activity (17 ng/ml/h) were elevated. Acute captopril administration was followed by a marked (-29 p. 100) decrease in mean arterial pressure. In this 46 XX patient, a primary amenorrhea had never been explored; clinical examination disclosed the absence of female secondary sex characteristics. Plasma cortisol was low (203 mmol/l) as were plasma androgens (testosterone 0.55, androstene dione 0.19, delta HEA less than 0.1 nmol/l respectively) and oestrogens (oestradiol 59 nmol/l). Elevated levels of progesterone and pregnenolone sulfate (12.1 and 2027 nmol/l respectively) contrasted with decreased levels of 17 OH progesterone (0.35 nmol/l). Computed tomography revealed a subnormal right adrenal gland and a pseudo-tumoral aspect on the left side. Treatment with dexamethasone and combined antihypertensive drugs (captopril, nifedipine and atenolol) resulted in normalisation of blood pressure and secretion of renin and aldosterone but renal function did not fully recovered. Thus, the hypertension of 17 alpha-hydroxylase deficiency can follow a malignant course in association with a marked activation of the renin-angiotensin system.
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PMID:[Malignant arterial hypertension disclosing late congenital adrenal hyperplasia due to 17 alpha-hydroxylase deficiency]. 314 37


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