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

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

Mineralocorticoids are out of the causes of secondary hypertension. Excess production of mineralocorticoids induces sodium and fluid retention, loss of potassium and metabolic alcalosis. The diagnosis of mineralocorticoid syndromes depends on the interpretation of the functional status of the renin-mineralocorticoid-system, which is in part responsible for the maintenance of normal blood pressure. The classical representative of this group is the syndrome of primary aldosteronism. Causes of mineralocorticoid syndromes associated with hypertension are: 1. autonomous production of mineralo-corticoids by an adrenal adenoma or by idiopathic bilateral adrenal hyperplasia; 2. deficiency of adrenal 17-alpha-hydroxylase or of 11-beta-hydroxylase; 3. secondary aldosteronism associated with primary reninism, or renal arterial stenosis; and 4. pseudo aldosteronism due to excessive ingestion of licorice. Malign or essential hypertension may also often be followed by secondary aldosteronism.
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PMID:[Mineralocorticoid syndromes and hypertension]. 96 85

The Ca2+ antagonistic coronary vasodilator, Nifedipine, was sublingually administered by a dose of 30 mg to 19 patients with hypertension. Blood pressure of patients with with essential hypertension (n=14) decreased from 177 +/- 24 to 123 +/- 13 mmHg systolic and from 108 +/- 12 to 80 +/- 11 mmHg diastolic (mean +/- SD) (p less than 0.01). Plasma renin activity (PRA) increased significantly from 0.73 +/- 0.62 to 1.50 +/- 1.02 ng/ml/h (p less than 0.05). The same tendency was observed in malignant and renovascular hypertension. In primary aldosteronism (n = 2), blood pressure decreased but PRA did not increase. Hypotensive action and increased plasma renin activity by Ca2+ antagonist, Nifedipine, were clearly demonstrated in patients with hypertension.
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PMID:Hypotensive action and increased plasma renin activity by Ca2+ antagonist (Nifedipine) in hypertensive patients. 96 84

To investigate the role of the renin angiotensin system in the pathogenesis of hypertension in Cushing's syndrome two patients with hypercorticism were infused with 20 mg saralasin (1-sar-8-ala-angiotensin II) over a period of 30 minutes under constant blood pressue control. In addition, one patient with primary aldosteronism, an established form of mineralocorticoid hypertension, served as control. Neither in the two patients with Cushing's syndrome nor in the patient with primary aldosteronism could a blood pressure lowering effect of saralasin be observed. In the two patients with hypercoritcism both renin activity and plasma aldosterone increased during saralasin infusion. The patient with primary aldosteronism only showed a weak increase in plasma aldosterone concentration.
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PMID:The effect of saralasin (1sar-8-ala-angiotensin II) on blood pressure in patients with Cushing's syndrome. 97 66

The plasma volume (PV) was determined in 109 patients with chronic arterial hypertension (AH) by 131I-labeled serumalbumin, expressing the results in ml/cm body height. An attempt was made to establish a statistical correlation between PV and diastolic pressure (DP). In essential AH three types of PV were found: normal, hypovolemic and hypervolemic; in hypertensive patients with stenosis of the renal aorta and in those with pheochromocytoma PV was slightly diminished; in hyperaldosteronism it was increased. In AH due to renal parenchymatous lesions the mean PV values were normal, a positive correlation being found between PV and DP (r + 0.929 and p = 0.05) in contrast to the other types of AH, where r was non significant or negative (stenosis of the renal artery, pheochromocytoma, malignant AH).
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PMID:Plasma volume in chronic arterial hypertension. 99 23

A close relationship exists between the endocrine system and hypertension. A brief survey is conducted of the endocrine diseases most frequently associated with high blood pressure. The available means for preoperative differentiation of an aldosterone-producing adenoma from idiopathic aldosteronism with bilateral hyperplasia are considered. For cases where high blood pressure is the principal presenting sign in a patient without overt endocrinopathy, the diagnostic resources for the detection of a hormonal cause--particularly renin--are critically examined.
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PMID:[Endocrinology and arterial hypertension]. 100 37

Peripheral plasma renin activity (PRA), vena cava and renal veins PRA were measured in 85 patients; arterial PRA was also measured in several cases. 25 patients had essential hypertension or primary aldosteronism; whereas in 60 patients renal or renovascular abnormalities were present. Peripheral PRA was elevated in 17/30 patients with parenchimal or excretory tract diseases. The following ratios came from the results of vena cava, and renal veins PRA were calculated: Ra/Rc and Rc/P according to Stockigt et al. and V-A/A according to Vaughan et al. The ratios were calculated only when v. cava PRA was greater than 4 ng/ml/3 hrs. A good correlation was found between v. cava can arterial PRA. Among the 60 cases with renal hypertension, 26 underwent either revascularization or nephrectomy surgery. Eleven of the 15 patients operated on for renovascular diseases showed a significant reduction of blood pressure (greater than 30 mmHg); all had high peripheral PRA and 6 had significant Ra/Rc and Rc/P (respectively greater than or equal to 1,5 and less than or equal to 1,3). The same patients also had V-A/A of the affected kidney greater than or equal to 0,48 and 5 also V-A/A of the controlateral kidney less than or equal to 0,23, both values being significant for a unilateral renin secretion and controlateral suppression. Among the 4 patients who were unsuccessfully operated on, only 2 had elevated peripheral PRA and 1 had Ra/Rc and Va-A/A greater than normal, but not significant values of Rc/P and Vc-A/A. 11 patients with small kidney or other forms underwent surgery; among the 6 cases with satisfactory results, 5 had high peripheral PRA, 2 showed significant ratios Ra/Rc and 3 a significant V-A/A for both kidneys. Only 1 of the patients not cured by surgery had supernormal peripheral PRA and none had any significant ratio. Therefore both methods for elaborating data obtained from the measurement of PRA in renal veins seem to offer similar prognostic indications. The finding of significant ratios is an almost sure criterium for predicting a surgical cure of renal hypertension, whereas the cases where we may expect a failure present ratios which are not significant. However, patients of the latter group may sometimes have successful results at surgery too, which demonstrates that other mechanisms may also be involved in the pathogenesis of this form of hypertension.
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PMID:[Plasma renin activity in renal veins in different types of arterial hypertension (author's transl)]. 101 Feb 16

Intravenous diazoxide (300 mg) was administered to 29 hypertensive patients previously classified in subgroups according to their plasma renin and urinary aldosterone levels. The blood pressure was measured before and periodically after injection and plasma renin activity (PRA) and plasma aldosterone before and after 2 hours. The mean systolic and diastolic blood pressure fell notably from 193/118 to 155 93 mmHg; whereas PRA increased from 7.51 to 13.21 ng/ml/3 hrs and plasma aldosterone did not change significantly (71.3 and 102.8 ng%). Examining the individual sub-groups, a significant decrease in blood pressure was observed in 15 patients with low, posture unresponsive PRA, both in subjects with normal urinary aldosterone and those with surgically proven primary aldosteronism. In the former only the mean PRA showed a slight but sigificant increase, while in the latter the changes for both PRA and aldosterone were not significant. In the subgroups of patients with normal renin and urinary aldosterone the arterial pressure also significantly and promptly decreased. However, in this group the mean PRA substantially increased whereas the plasma aldosterone levels remained constant. The same blood pressure decline was observed in those patients with high PRA and aldosterone, including 1 case of pheocromocytoma. The mean PRA showed a further modest increase while the plasma aldosterone did not change significantly. These results indicate that the antihypertensive action of diazoxide is similar in the different types of hypertension (volume, vasoconstrictor or mixed form according to Laragh's classification), being independent of the basal plasma renin and aldosterone levels. Furthermore, the response of the blood pressure to diazoxide is not related in any way to the induced changes in PRA and plasma aldosterone values.
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PMID:[Effect of diazoxide on blood pressure, PRA and plasma aldosterone in hypertensive patients (author's transl)]. 101 Feb 35

The angiotensin antagonist saralasin (1-sar-8-ala-angiotensin II) was given to 27 patients with different forms of secondary hypertension. The blood pressure fell in 6 of 7 patients with renal artery stenosis and in 4 of 10 patients with terminal renal failure on regular hemodialysis. No change or a rise in blood pressure was observed in 3 patients with Cushing's syndrome, 4 patients with primary aldosteronism, 3 patients with hypertension and a unilateral small kidney of other than renovascular origin, and 6 patients with terminal renal failure. It can be concluded from the results that angiotensin II is involved in the pathogenesis of renovascular hypertension and in some cases of hypertension accompanying chronic renal failure.
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PMID:[Effect of the angiotensin antagonist saralasin (1-sar-8-ala-angiotensin II) on the blood pressure in secondary hypertension]. 101 96

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


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