Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The serum converting enzyme activity (SCEA) was measured in 86 healthy individuals (1.44 +/- 0.82 u, mean +/- SD), 39 patients with essential hypertension (1.53 +/- 0.71 u), 7 patients with hypertension due to renal artery stenosis (1.76 +/- 0.77 u), 14 patients with chronic renal failure (2.10 +/- 0.57 u), 7 patients with renal failure and hypertension (2.62 +/- 0.35 u), 22 normotensive pregnant women (1.02 +/- 0.26 u) and 6 hypertensive pregnant women (1.1 +/- 0.3). No difference was detected between men and women or between normotensives and hypertensives. However, a significant rise in SCEA was found in patients with chromic renal failure (P less than 0.005), in whom an enlarged pulmonary vascular bed and accelerated cellular breakdown are thought to be the causes of the elevated SCEA. During pregnancy, subnormal SCEA was found (P less than 0.005), and this is thought to be due to the enzyme consumption in the kinin system, which is activated during pregnancy. We assume that converting enzyme is not a limiting factor in angiotensin conversion, and most probably it does not contribute significantly to the pathogenesis of hypertension.
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PMID:Serum angiotensin converting enzyme activity in normal adults and patients with different types of hypertension. 609 66

A retrospective cohort study to investigate the association between smoking and renal artery stenosis compared 71 patients with documented renovascular hypertension and 308 age-matched control patients with essential hypertension. 94% (30/32) of men and 74% (29/39) of women with renal artery stenosis had smoked cigarettes compared with only 43% (64/150) of men and 41% (65/158) of women in the control group. This striking relation was true for both patients with fibromuscular disease (71% smokers; 15/21) and patients with atherosclerotic lesions (88% smokers; 44/50). All renal artery stenosis groups had significantly higher systolic and diastolic blood pressures than the relevant control group. When the groups were stratified according to blood pressure, there were significantly more smokers in the renal artery stenosis group at every level of blood pressure.
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PMID:Cigarette smoking and renovascular hypertension. 613 3

Converting enzyme inhibitors (CEI) are efficient antihypertensive medications. The acute and chronic effects of captopril (SQ) on renal function and electrolyte balance are analyzed in the present paper. Acute administration of SQ was associated with renal vasodilatation in the patients with essential hypertension (EH) but had no effect in normal subjects with similar renin levels thus suggesting an enhanced renal vascular response to CEI in EH. A variable effect of CEI on renal function was observed in renovascular hypertension; GFR fell when blood pressure decreased by more than 25 mmHg. Three cases of striking recovery of GFR during chronic SQ in young patients with malignant nephrosclerosis maintained on hemodialysis are reported. Such an improvement in GFR never occurred in patients with primary renal disease. When systemic and renal responses to acute isotonic saline loading were assessed, captopril blunted the exaggerated natriuretic response to saline loading observed in EH and unmasked the volume-dependence of arterial pressure. A case of hyperkalemia during treatment with SQ is reported in a patient with bilateral renal artery stenosis who developed moderate renal failure during treatment. This was associated with high plasma aldosterone whilst fractional excretion of K+ was inappropriately low for the level of serum creatinine thus suggesting that tubular unresponsiveness to aldosterone may have developed during SQ.
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PMID:Renal aspects of treatment by converting enzyme inhibitors in hypertension. 631 75

Among vascular beds, that of the kidney is especially responsive to angiotensin II, perhaps a reflection of the fact that the renin-angiotensin axis is normally a volume-control rather than a pressure-control system. The dose of angiotensin required to induce renal vasoconstriction in a normal subject receiving a typical, liberal sodium intake, for example, is about an order of magnitude lower than that required to induce a pressor response. Indeed, compelling arguments can be made for a local, intrarenal role as angiotensin's first action in phylogeny, with additional cardiovascular and endocrine responses arising later. In patients with essential hypertension, in whom renal vascular tone is commonly increased, converting enzyme inhibitors such as teprotide and captopril induce a potentiated acute renal vascular response: renal blood flow increases more than it does in normal subjects. The result is a consistent, early increase in sodium excretion and an occasional increase in glomerular filtration rate. Reduced aldosterone release consequent to the block of angiotensin II formation also contributes to the natriuresis and results in positive potassium balance. With long-term therapy, renal function tends to be very well maintained. In renal artery stenosis the situation is more complex: as perfusion pressure distal to the stenosis falls, typically afferent arteriolar dilatation exists and glomerular capillary pressure tends to be maintained by an increase in postglomerular resistance. To the extent that this increase is angiotensin-mediated, suppression of angiotensin formation with captopril can reduce glomerular capillary pressure and thus filtration rate. This is well tolerated in the patient with unilateral stenosis and a healthy contralateral kidney, but can provoke renal failure when the stenosis is bilateral or involves a solitary kidney. The available evidence suggests that the converting enzyme inhibitor's influence on the kidney primarily reflects reduced angiotensin II formation, although reduced kinin degradation or increased prostaglandin synthesis may also have an influence. Whatever the mechanism responsible for the renal response, there are compelling reasons for suspecting that the salutary action of captopril on the kidney makes a substantial contribution to its over-all efficacy in the treatment of hypertension.
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PMID:Renal hemodynamics in essential and renovascular hypertension. Influence of captopril. 632 83

Investigations were performed in 26 patients with essential hypertension and 24 with unilateral renal artery stenosis. In each patient blood was drawn simultaneously and in triplicate, from both renal veins and aorta, for measurement of plasma concentrations of active and inactive renin and of angiotensin II. In 19 patients estimates of individual renal plasma flow were obtained in order to calculate secretion rates for active and inactive renin, and to assess the contribution of renin secretion rate and of renal plasma flow to the renal vein renin ratio. In patients with essential hypertension there was evidence that the kidney secreted active renin (18% mean increase in renal vein concentration above that of arterial plasma; P less than 0.001), but no evidence of secretion of inactive renin (4% mean increase; NS). There was a tendency for the kidney to extract angiotensin II (8% mean decrease in renal vein concentration below that of arterial plasma; P = 0.07). The affected kidney in patients with renal artery stenosis showed marked secretion of active renin (364% mean increase; P less than 0.001) and also secreted inactive renin (80% mean increase; P less than 0.05) with net generation of angiotensin II across the renal circulation (100% mean increase; P less than 0.05). The contralateral kidney exhibited suppressed secretion of active renin (3% mean increase; NS) with no evidence of secretion of inactive renin (2% mean increase; NS), and marked extraction of angiotensin II (50% mean decrease; P less than 0.001). The correlation between combined secretion rate of active renin by both kidneys and the arterial concentration of active renin in patients with essential and renovascular hypertension taken together was strongly positive (r = 0.82; P less than 0.01). The same correlation for inactive renin was weak (r = 0.32; NS). The correlation between the combined secretion rates of active renin by both kidneys and the circulating plasma concentration of angiotensin II (r = +0.60; P less than 0.05) was both significant and positive. By contrast, the total 'secretion' rate of angiotensin II by both kidneys was inversely related to arterial plasma angiotensin II (r = -0.92; P less than 0.001). This latter relationship suggests an important role for the kidney in clearing angiotensin II from the circulation, this being more marked the higher the arterial angiotensin II concentration.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in active and inactive renin and in angiotensin II across the kidney in essential hypertension and renal artery stenosis. 639 32

Measurements of exchangeable sodium, arterial pressure and plasma concentrations of active renin, angiotensin II, aldosterone, sodium and potassium were made in 35 hypertensive patients with renal artery stenosis, 30 having unilateral renal arterial lesions. Plasma urea was below 7 mmol/l in 24 of the patients with unilateral lesions. In these and in the whole group of 35 patients there were significant inverse correlations between exchangeable sodium and diastolic blood pressure and between plasma sodium concentration and diastolic pressure. Six patients had hyponatraemia with a plasma sodium concentration less than 135 mmol/l. All were sodium-deplete with secondary hyperaldosteronism, three also having malignant-phase hypertension. Twelve of the patients with unilateral renal artery stenosis underwent bilateral ureteric catheterization. Sodium excretion was greater from the contralateral kidney than from the affected kidney and the rate of sodium excretion from the former, but not from the latter, was significantly related to arterial pressure. The relation of diastolic blood pressure and exchangeable sodium is the opposite of the positive correlation found in essential hypertension and Conn's syndrome. In renal artery stenosis the inverse correlation could result from a natriuretic effect of increased arterial pressure occurring mainly in the contralateral kidney.
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PMID:Inverse relation of exchangeable sodium and blood pressure in hypertensive patients with renal artery stenosis. 639 20

The renal extraction ratios of 131I-sodium iodohippurate (131I-Hippuran) and 125I-thalamate were greatly reduced on the affected side by 50 mg captopril in seven out of 14 patients with unilateral renal artery stenosis. With long term captopril 150 mg daily the uptake of 99mTc-diethylenetriaminepenta-acetic acid by the affected kidney, which was determined by scintillation camera renography, became almost zero in these seven patients, indicating severe reduction of the glomerular filtration rate. Function of the affected kidney returned on discontinuing treatment. The reduced extraction of sodium iodohippurate probably reflected a shortened plasma transit time through the kidney due to intrarenal vasodilatation. The reduced extraction of thalamate reflected a low filtration fraction, suggesting that the vasodilatation was, at least in part, at the level of the postglomerular arterioles. Captopril had little effect on the contralateral kidney and on the kidneys of 17 patients with essential hypertension, and serum creatinine concentrations showed minor changes. Radioisotope renography should be performed after beginning captopril treatment in patients with renal artery stenosis. This is also recommended for patients given captopril as a third line drug when renal artery stenosis has not been excluded. Hypertension is these patients is often severe and difficult to control. Renal artery disease is not rare in this difficult group and finding seriously impaired renal function on one side during captopril treatment may be diagnostic.
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PMID:Splint renal function after captopril in unilateral renal artery stenosis. 642 29

Calcium antagonists are increasingly used in the treatment of primary and secondary hypertension. A new substance of this group, isobutyl methyl 1,4-dihydro-2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridinecarboxylate (nisoldipine, Bay k 5552) inhibits the calcium-induced contraction of arteries and veins in concentrations 5-20 times lower compared to those of nifedipine in vitro. The effect of nisoldipine (10 mg orally) on blood pressure and heart rate in supine and upright position, on serum electrolytes (Na+, K+, Ca2+) and on serum aldosterone and serum hydrocortisone (cortisol) was comparatively studied in patients with essential hypertension (n = 6, 57 +/- 7 years), in patients with hypertension and chronic renal failure (n = 6, 46 +/- 4 years, serum creatinine 2.1 +/- 0.5 mg/100 ml) and in 6 patients with unilateral renal artery stenosis. In patients with essential hypertension, systolic blood pressure (BP) dropped by 26 mmHg; diastolic BP was lowered by 17 mmHg after 150 min compared to placebo. In patients with chronic renal failure, decrement in BP was 25/16 mmHg (systolic and diastolic BP, respectively). In patients with renal artery stenosis, blood pressure declined by 31/18 mmHg after nisoldipine. Serum electrolytes (Na+, K+ and Ca2+) and serum aldosterone as well as serum hydrocortisone remained unchanged. The hypotensive action of nisoldipine seems to be independent of the type of hypertension. However, the hypotensive activity correlates with the level of the baseline blood pressure.
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PMID:[Hypotensive properties of nisoldipine. Comparative study in essential, renal and renovascular hypertension]. 654 May 81

1. The renin-angiotensin system because of its unique relationship to both aldosterone secretion and vascular reactivity is important in the control of blood pressure and may be useful in determining the cause of hypertension. 2. Patients with volume expanded hypertension almost invariably have low renin levels. Some of these patients have primary aldosteronism, others have excess production of nonaldosterone mineralocorticoids. The majority have essential hypertension. 3. Many patients with low renin essential hypertension have an enhanced adrenal response to angiotensin II as the underlying mechanism. 4. Fifteen to twenty per cent of patients with an elevated blood pressure have renin-dependent angiotensinogenic hypertension. Some of these patients have renal lesions to account for the elevated renin levels, for example, renal artery stenosis. However, some patients with high renin essential hypertension have a decreased adrenal response to angiotensin II as the primary mechanism for their high renin levels and potentially for their elevated blood pressure. 5. Patients who fall into this latter group may not only have alterations in angiotensin's interaction with the adrenal but also with other target tissues, for example, renal vasculature. 6. Thus, as many as 60% of patients with essential hypertension may have an alteration in the interaction of angiotensin II with its target tissues which could be the major factor underlying the pathogenesis of their elevated blood pressure.
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PMID:The renin-angiotensin system and hypertension. 675 84

The diagnostic accuracy of renal vein renin (RVR) analyses was evaluated in 63 hypertensive patients treated with sodium depletion and/or hydralazine prior to selective renal vein sampling. A positive RVR study (i.e., lateralization of RVR) was defined as a ratio greater than or equal to 1.5 when RVR from the kidney with renal artery stenosis was compared to RVR from the contralateral kidney. Approximately 40% of patients with essential hypertension had positive RVR studies. Among patients with renal artery stenosis, surgical outcome was correctly predicted in 5 of 8 patients (63%) treated with sodium depletion, whereas outcome was accurately predicted in 11 of 12 patients (92%) treated with hydralazine. These observations demonstrate that a high percentage of patients with essential hypertension have positive RVR studies despite arteriographically normal renal vasculature. Results obtained in patients with renal artery stenosis suggest that stimulation of renin secretion by hydralazine may be of particular advantage prior to renal vein sampling. However, additional data are required to confirm whether activation of specific mechanisms for renin release improves the reliability of the RVR test.
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PMID:Influence of salt depletion and hydralazine-induced vasodilatation on accuracy of selective renal vein sampling in patients with essential hypertension and renal artery stenosis. 676 63


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