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

In Europe, about 1% of the women using oral contraceptives develop hypertension. Predisposing factors seem to be age, hypertension problems in past pregnancies, family history of hypertension, personal histories of kidney disorders, diabetes mellitus or adipositas, or diastolic pressure over 80 mm Hg. An overactive renin-angiotensin-aldosterone system may be an important factor in the etiology of this type of hypertension. Oterh possible factors are: reduced excretion of angiotensin 2, increased sensitivity of the arterioles to substances such as angiotensin 2 and noradrenaline, direct effect of ethinyl estradiol and mestranol on the sodium and water system, cardiovascular changes, disorders in the adrenergic system (e.g., catecholamine metabolism). Blood pressure should be checked before beginning any treatment with oral contraceptives and every 3 months after that. For the purpose of differential diagnosis angiotensin 2 in the plasma and catecholanin and its by-products should be checked (24-hour urine samples). In cases of serious hypertension hormone therapy should be discontinued at once. Primary aldosteronism and renal artery stenosis must be excluded in the differential diagnosis, for although these hypertensive disorders exhibit similar biochemical changes, they should be treated by surgical intervention. Usually hypertension is reversible after cessation of therapy with contraceptive steroids. However, some cases of irreversible hypertention, kidney failure, and malignant nephrosclerosis have been described. Hypertensive somen who wish to use oral contraceptives may, under medical supervision try a modified hormonal contraceptive (minipill without estrogen) or sequential or lower dosages.
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PMID:[Clinical aspects of hypertension under contraceptive steroids]. 79 66

Primary hyperaldosteronism is a potentially curable cause of hypertension, and much interest has been shown in methods of diagnosing the associated hypokalaemic hypertension and localising the adrenal adenoma. In two patients the diagnosis of primary aldosteronism was confirmed by colonic potential measurement and the adenoma localised by a new subtraction technique for early adrenal imaging applied to the use of 131I-19-iodocholesterol. Both patients underwent adrenalectomy and in each case an adenoma was removed. Blood pressure and electrolyte levels returned to normal after operation. In one patient bilateral adrenal phlebography had failed to show the tumour, and sampling of aldosterone concentrations in the adrenal veins had been unsatisfactory.
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PMID:Adrenal aldosterone-producing adenoma: use of colonic potential in diagnosis and subtraction scanning technique for localisation. 93 76

The frequency of underlying renal or renal artery disease, and the incidence of vascular complications were reviewed in a series of 136 cases of primary hyperaldosteronism. This was in order to investigate the possible existence of 'tertiary' hyperaldosteronism, and to examine the commonly held view that primary hyperaldosteronism is a relatively benign form of hypertension. Ten cases (7-4 per cent) had evidence of renal artery stenosis and eleven (8-1 per cent) parenchymatous renal disease. In comparison with the reported frequency in large general series of hypertensives, these data show no evidence of an excess of underlying renal disease. It is unlikely, therefore, that autonomous aldosterone secreting adenomata occur commonly as a consequence of prolonged secondary hyperaldosteronism. Four cases (2-9 per cent) had evidence of the malignant-phase of hypertension, and over a mean observation time of 5-9 years, 31 cases (22-8 per cent) developed 39 vascular complications. It appears, therefore, that vascular complications are not rare in primary hyperaldosteronism, and early and effective treatment is thus necessary.
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PMID:Renal abnormalities and vascular complications in primary hyperaldosteronism. Evidence on tertiary hyperaldosteronism. 94 42

Not all the varied clinical disorders in which aldosterone and the mineralocorticoid hormones are involved have been reviewed. Only those disorders in which the mineralocorticoid hormones and their regulatory factors are the principal cause of the biochemical and clinical abnormalities have been examined. These are many and varied. Appreciation of the extent and magnitude of their involvement in the regulation of blood pressure, body fluids, and electrolyte composition continues to grow. The major direct clinical impact of the mineralocorticoid hormones appears to be in two areas: hypertension and potassium homeostasis. Their part in the mosaic of hypertension is established in primary hyperaldosteronism, but they also appear to affect and modify the hypertensive process in primary or essential hypertension. The probe continues. Hypoaldosteronism is more than the rare occurrence associated with Addison's disease. It may be the clue to the presence of nonaldosterone mineralocorticoid excess syndromes, and is obviously of critical importance in an increasing number of patients with chronic renal failure of varied aetiologies.
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PMID:A perspective on aldosterone abnormalities. 97 45

Autonomous hypersecretion of aldosterone (primary hyperaldosteronism) is caused by either hyperplasia (usually bilateral) or an adenoma (frequently unilateral) of the adrenal cortex. Systemic hypertension due to an aldosteronoma is a potentially curable condition through surgical extirpation of the offending organ. In our experience with 37 patients clinically suspected to have primary hyperaldosteronism, radiological methods contributed significantly in preoperative diagnosis. These included (1) selective bilateral adrenal vein catheterization and blood sample collection, (2) adrenal venography, and (3) radioisotope adrenal scan. Unilateral hyperfunction could be accurately detected by the aldosterone assays from the collected samples. When adrenal venography was technically satisfactory, a nodule or aggregate of nodules measuring at least 7 mm and located on the margin of the gland or 1.5 cm or more in diameter when located in the center of the gland were readily identified. Enlarged adrenal gland on venography, in itself, was not a dependable index of a hyperfunctioning gland. Presence of a higher uptake on one side on the radioisotope adrenal scan did not always indicate the hyperfunctioning gland, but lack of lateralization of adrenal hyperfunction was more accurately predicted on the radioisotope scan than by venography. Four histopathological patterns were recognized in the surgically removed adrenal glands, but no correlation between these patterns and clinical behavior or postoperative course was found.
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PMID:Radiology in primary hyperaldosteronism. 97 62

The urinary excretion of free noradrenaline (NA), adrenaline (A), dopamine (DA), the DA/NA ratio in the urine, plasma renin activity (PRA) and their mutual relationship were investigated in 71 patients suffering from different types of arterial hypertension. In spite of the fact that the mean values of excreted catecholamines, with the exception of pheochromocytoma, lie within the range of values found in healthy controls, certain differences were found in spectrum of excreted catecholamines. In patients with labile, malignant and renovascular hypertension and in pheochromcytoma the higher mean excretion of NA and the low DA/NA ratio was accompanied by the higher PRA in comparison with fixed benign essential hypertension. On the other hand, in hypertension with low PRA (essential hypertension with suppressed renin and Conn's syndrome) a low excretion of NA and high DA/NA ratio was found. There was a significant, if not even very close negative correlation between the PRA and DA/NA ratios both in recumbent and upright position. The rise of PRA on standing up was followed by an increased excretion of NA while the excretion of DA did not change or decreased. Hence the DA/NA ratio when standing up showed a decreasing tendency as compared with values when lying down. Application of the beta-blocker Inderal decreased the PRA and the blood pressure not only in juvenile hypertensive patients with hyperkinetic circulation but also in the early phases of renovascular hypertension. It thus appears that endogenous catecholamines, first of all the ratio between the renin-inhibiting DA and the renin-stimulating NA, participate as one of several factors in the regulation of secretion and of the plasma levels of renin not only in juvenile hypertensive patients with hyperkinetic circulation but also in other types of hypertension.
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PMID:Relationship between plasma renin activity and urinary catecholamines in various types of hypertension. 97 8

The content of total metabolizing sodium was studied in 74 patients with hypertension of different genesis, using the Na24-isotope dilution technique. Among these patients 31 had essential hypertension, 43--symptomatic hypertension (40--renal, and 3--adrenal). In Stage IB and IIA hypertension, a reduction of the level of total metabolizing sodium and its increased urine excretion were found. At late stages of essential hypertension, like in symptomatic renal hypertension, normal levels of total metabolizing sodium were found, or a slight tendency towards its elevation. In cases of adrenal hypertension (Conn's syndrome, pheochromocytoma) the level of total metabolizing sodium is significantly elevated. No correlation was seen between the levels of total metabolizing sodium, and plasma and erythrocytes sodium. The decrease of total metabolizing sodium at early stages of essential hypertension must be an adaptative reaction of the body, which is proved by the increased urine excretion of sodium.
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PMID:[Content of total metabolic sodium in arterial hypertension of varying origin]. 97 79

Rectal electrical potential difference (P.D.), plasma aldosterone and plasma renin activity were measured in 25 normal subjects, 80 patients with untreated essential hypertension, 4 patients with primary and 9 patients with secondary hyperaldosteronism. In normal subjects the rectal P.D. was 26 +/- 10 mV (+/- S.D.); in patients with hyperaldosteronism it was 51 +/- 7 mV. Plasma aldosterone and rectal P.D. were correlated significantly (r = 0.84, p less than 0.001) in these two groups combined. In 29% of patients with low-renin hypertension, in 9% of patients with normal-renin hypertension and in 3 out of 8 patients with high-renin hypertension, rectal P.D. was found to be elevated in the presence of normal plasma and urinary aldosterone and no correlation was observed between plasma aldosterone and rectal P.D. (r = --0.09, n.s.). In 3 out of 7 patients with low-renin hypertension and high rectal P.D., plasma and urinary aldosterone were consistently suppressed. Since patients with low renin and high rectal P.D. responded favourably to spironolactone therapy it is suggested that mineralocorticoids other than aldosterone may contribute to the pathogenesis of the hypertension in these cases. The aetiology of raised rectal P.D. in normal and high-renin hypertension is not clear, but both catecholamines and angiotensin II may be involved. The measurement of rectal P.D. alone is of limited value as a screening test for primary hyperaldosteronism in hypertensive patients, but combined with renin measurements it is a valuable tool for further investigation of patients with suspected mineralocorticoid excess syndromes, as well as for adjusting therapy with competitive aldosterone antagonists in patients with proven primary or secondary hyperaldosteronism.
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PMID:[Rectal electrical potential difference and plasma aldosterone in hyperaldosteronism and low-, normal- and high-renin hypertension]. 101 11

In a series comprising 482 patients with hypertension requiring treatment 79 percent had to be classified as essential hypertension. Bilateral renal disease was found in 9 percent, unilateral renal disease in 3.3 percent, but only one patient underwent surgery. Renal artery stenosis was found in 24 patients (5 percent), but only 5 (1 percent) were operated on. Two cases of primary hyperaldosteronism and one of phaeochromocytoma were found; in all three surgical intervention was successful. Oral contraceptives had caused the elevated BP in 7 patients (1.5 percent). It is emphasized that the frequency of curable hypertension is still very low and this should be taken into account when routine examination of patients with hypertension requiring treatment is discussed.
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PMID:The frequency of secondary hypertension. 112 62

The responses of blood pressure, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) to infusion of either angiotensin II (10 ng/Kg/min) or norepinephrine (100 ng/Kg/min) were observed in 25 patients with essential hypertension. The difference in modes of response between low renin essential hypertension and normal or high renin essential hypertension was analyzed. For comparison, 5 patients with Conn's syndrome, 4 with renovascular hypertension, and 5 normotensive subjects were also studied. Following infusion of antiotensin II the changes in diastolic blood pressure (DBP) were +24+/-3.0 mmHg in low renin essential hypertension and +25+/-3.1 mmHg in normal or high renin essential hypertension in PRA -0.28+/-0.06 ng/ml/h in low renin essential hypertension and -0.69+/-0.02 mg/ml/h in order and in PAC +3.7+/-1.4 and +7.6+/-1.8 ng/100 ml respectively. There was a significant difference in magnitude of response in PRA between the 2 groups of essential hypertension (p less than 0.05). Norepinephrine induced rise in DBP with decreases both in PRA and PAC. The mean changes in DPB were +6+/-1.4 mmHg in low renin essential hypertension and +16+/-2.2 mmHg in another and the pressor response in the later was significantly greater (p less than 0.01). The changes in PRA were -0.14+/-0.07 ng/ml/h in low renin essential hypertension and -0.67+/-0.26 ng/ml/h in normal or high renin essential hypertension, and in PAC -4.9+/-1.3 and -3.3+/-1.9 ng/100 ml respectively. The greater fall in PRA in normal or high renin essential hypertension was observed but the difference between the 2 groups of essential hypertension was not significant. The changes in PAC did not parallel the changes in PRA. Angiotensin II indcued essentially similar effects on blood pressure in both groups but the greater feedback inhibition of PRA was produced by this peptide in normal or high renin essential hypertension than in low renin essential hypertension. Norepinephrine induced significantly greater pressor effect in normal or high renin essential hypertension. The adopted dose of norepinephrine suppressed both PRA and PAC and a tendency to the greater fall in PRA was observed in normal or high renin essential hypertension. There was no difference in responses of PAC to both agents between the 2 groups of essential hypertension.
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PMID:Effect of pressor agents on blood pressure, plasma renin activity and plasma aldosterone concentration in essential hypertension. 115 95


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