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)

All major enzymes involved in catecholamine synthesis and metabolism have been cloned. In addition to some genetic defects of these enzymes responsible for well-defined clinical syndromes, several enzymatic abnormalities may be due to environmental (e.g. pharmacological and nutritional) or biological (e.g. aging) factors, which may modify genome expression. The enzymes involved in catecholamine metabolism either lead to metabolites which cannot be reconverted to the parent catecholamine (such as products of monoamine oxidation and catechol-O-methylation), or metabolites, which can be reconverted to the free catecholamine from which they are generated (such as products of sulfoconjugation). Reversible sulfoconjugation is partly regulated by the recently cloned enzyme, sulfatase. The importance of this reversible step is that it reconverts inactive into biologically active catecholamines. The balance of the sulfoconjugation-deconjugation interplay may have physiological implications; in addition to catecholamine release, it may determine the availability of free catecholamines during diurnal rhythms and stress or modify their renal excretion. Circumstantial evidence, including a close homology within the aryl sulfatases and steroid sulfatase gene, the first implicated in catecholamine metabolism, the second in steroid metabolism, suggests a genetic defect of sulfatases in essential hypertension. A similar, but secondary, sulfatase defect may affect catecholamine metabolism and action in chronic renal failure.
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PMID:Clinical implications of genetic and acquired defects in catecholamine synthesis and metabolism. 798 99

Besides defining the appropriate doses of frusemide in uraemic patients, A. Heidland's contribution to the treatment of hypertension in chronic renal failure consisted in the following demonstrations: (1) In patients on chronic haemodialysis, calcium antagonists have a beneficial effect on their glucose intolerance and decreased plasma levels of 25OH vitamin D while their effect on blood lipids is neutral. (2) In 5/6 nephrectomized rats, captopril, verapamil, and metoprolol have the same protective effect on their GFR and tubular secretion of protons, at equal blood-pressure-lowering effect. (3) In rats with streptozotocin-induced diabetes, atrial natriuretic peptide does not play a role in their hyperfiltration. (4) Severe retinopathy is observed in patients with uraemic nephropathies at a much smaller elevation of their blood pressure than in patients with essential hypertension. This article reviews the following points: (1) The role of hypertension in the loss of renal function is convincingly demonstrated only in a few experimental models, and in man only in malignant hypertension and diabetic nephropathy but not in essential hypertension nor in non-diabetic nephropathy. However, preliminary results suggests that antihypertensive treatment may retard the progression of renal disease in normotensive patients (DBP <90 mmHg) with either microalbuminuric diabetes and normal renal function or non-diabetic uraemic nephropathy. (2) Only the ACE inhibitors have been proved to have a specific renal protective effect, independent of their diurnal blood-pressure-lowering effect, both in diabetic nephropathy and in non-diabetic uraemic nephropathy.
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PMID:Hypertension and progression of renal insufficiency. 807 21

The primary goal in the treatment of essential hypertension is to reduce all end organ damage, not simply to reduce blood pressure. Hypertension is associated with an increased risk of cerebrovascular, cardiovascular and renal morbidity and mortality. Pharmacological therapy has reduced some, but not all, of these complications. In order to achieve maximal decrease in morbidity and mortality in hypertensive related diseases the overall impact of antihypertensive drug therapy on the pathogenesis of damage to each end organ must be considered. The pharmacological therapy of mild hypertension has reduced complications of most pressure related (arteriolar) damage such as cerebrovascular accidents, congestive heart failure, and some cases of chronic renal failure, but atherosclerotic complications, coronary heart disease, angina, myocardial infarction and sudden death have not been convincingly reduced. A more pathophysiologic and individualized approach to the treatment of hypertension is recommended in place of the traditional stepped care approach which has primarily emphasized diuretics and beta blockers as initial therapy. This new approach in the subsets of hypertension, which is based on eight parameters: (1) Pathophysiology; (2) Haemodynamics; (3) End organ damage; (4) Concomitant medical diseases and problems; (5) Demographics; (6) Adverse effects of drugs and quality of life; (7) Compliance with medication regimen; (8) Total health care costs: direct and indirect costs. Hypertension is not just a disorder of increased intraarterial pressure, but in fact, a syndrome of commonly associated genetic and/or acquired abnormalities including dyslipidaemia, insulin resistance, impaired glucose tolerance, central obesity, renal abnormalities, structural abnormalities of smooth muscle, and abnormal cellular cation transport or membranopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertension and coronary heart disease risk factor management. 819 21

The indication of low salt diet for the management of hypertension associated with pregnancy is controversial. We studied the effect of a low-salt diet (less than 5g/day) on pregnancy-induced hypertension compared to patients with hypertension due to chronic renal failure and essential hypertension. In chronic renal failure, mean blood pressure decreased from 115.3 +/- 3.0mmHg to 92.1 +/- 2.6mmHg (p < 0.001) and in essential hypertension, from 117.7 +/- 3.1mmHg to 108.5 +/- 3.5mmHg (p < 0.01). However, in pregnancy-induced hypertension, the blood pressure did not change significantly. CUA/Ccr ratio, the indicator of plasma volume, decreased significantly from 8.7 +/- 1.5% to 3.8 +/- 0.7% (p < 0.001) after salt restriction. CUA and mean blood pressure in patients with preeclampsia were negatively correlated significantly (r = -0.51, p < 0.05). There was a significant correlation between CUA and urinary sodium excretion (r = 0.67, p < 0.001). These results indicate that a low-salt diet is not only ineffective, but also accelerates volume depletion in preeclampsia.
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PMID:[Effect of salt restriction on preeclampsia]. 819 19

In recent years, substantial investigative attention has focused on therapeutic regimens that could retard the progression of chronic renal insufficiency. Emphasis has been placed on the effects of antihypertensive treatment on renal hemodynamics and preservation of renal function. It has been suggested that some classes of antihypertensive agents may confer a greater renoprotective effect, especially agents that lower glomerular capillary pressure. Conversely, by virtue of their ability to preferentially dilate the afferent arteriole calcium antagonists theoretically could favor an increase in glomerular capillary pressure thereby accelerating the decline of renal function. In this review we survey the literature critically and conclude that in patients with essential hypertension and in patients with chronic renal insufficiency, calcium antagonists effectively reduce systemic blood pressure while maintaining glomerular filtration rate and effective renal plasma flow. Preliminary results from a few long-term studies suggest that calcium antagonists may even attenuate the decline in renal function of patients with chronic renal failure. The majority of studies in humans, however, have been nonrandomized, of too short duration, or confounded by investigative difficulties precluding definite conclusions whether calcium antagonists have renoprotective effects. Although the possibility that calcium antagonists may retard progression of renal disease remains to be ascertained, the available evidence indicates that calcium antagonists may be used in patients with renal functional impairment without further exacerbating renal function.
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PMID:Effects of calcium antagonists on renal hemodynamics and progression of nondiabetic chronic renal disease. 820 87

It was reported recently that the endogenous digitalis-like factor ouabain may mainly originate from the adrenal gland. To ascertain the pathophysiological significance of endogenous ouabain and to examine if it originates in the adrenal gland, we determined plasma immunoreactive ouabain levels in patients with various cardiovascular and endocrine diseases. Plasma immunoreactive ouabain levels were also determined in the adrenal venous blood by adrenal venous sampling. Plasma immunoreactive ouabain levels were significantly increased in patients with essential hypertension, primary aldosteronism, Cushing's syndrome, pheochromocytoma, acromegaly, and chronic renal failure. Plasma immunoreactive ouabain levels were decreased in patients with primary aldosteronism after unilateral adrenalectomy, acromegaly after pituitary adenomectomy, and chronic renal failure after hemodialysis. Plasma immunoreactive ouabain levels in patients after bilateral adrenalectomy were similar to those in healthy subjects. There was no significant step-up of immunoreactive ouabain levels in the adrenal vein from the peripheral vein in three patients, whereas one patient with hypertension and right adrenal tumor but without any known adrenal hormone excess showed higher plasma immunoreactive ouabain levels in the right adrenal vein than those in the peripheral vein. These results suggest an important pathophysiological significance of endogenous ouabain in various cardiovascular and endocrine diseases. It is unlikely that the adrenal gland is a major source of plasma ouabain, although a possible excess production of ouabain by the adrenal tumor remains to be elucidated.
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PMID:Does plasma immunoreactive ouabain originate from the adrenal gland? 828 39

The human heart secretes both atrial natriuretic peptide and brain natriuretic peptide. This study attempts to clarify the pathophysiological significance of the peptides in cardiovascular diseases. Using immunoradiometric assay, plasma brain natriuretic peptide and atrial natriuretic peptide levels in essential hypertension, various secondary hypertension, chronic renal failure, chronic heart failure during cardiac pacing, and acute myocardial infarction were determined. Mean plasma brain natriuretic peptide and atrial natriuretic peptide levels in healthy subjects were 3.7 +/- 0.3 and 5.7 +/- 0.3 pmol/L, respectively, and increased as a function of age. Plasma brain natriuretic peptide levels showed a larger increase than atrial natriuretic peptide levels in various cardiovascular diseases. In chronic renal failure, whereas plasma atrial natriuretic peptide levels decreased significantly after hemodialysis and were correlated with the changes in body weight, changes in plasma brain natriuretic peptide levels were less prominent and did not show such a correlation. In chronic heart failure, both basal plasma brain natriuretic peptide and atrial natriuretic peptide levels were also significantly elevated. However, in response to acute ventricular or atrial pacing, brain natriuretic peptide levels did not show any increase in contrast to the marked increase of atrial natriuretic peptide levels. In acute myocardial infarction, brain natriuretic peptide levels showed more prominent changes than atrial natriuretic peptide levels and were correlated with serum levels of creatine kinase and cardiac myosin light chain I in most patients. These results suggest that both brain and atrial natriuretic peptides play an important role in the regulation of cardiovascular homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial and brain natriuretic peptides in cardiovascular diseases. 828 65

The existence of a relationship between the kidney and arterial hypertension has long been known. Renal participation in the development of arterial hypertension has been clearly shown in different animal models that mimic human essential hypertension. Some data obtained in hypertensive humans also seem to support the prevalence of the kidney in the initiation of this particular type of arterial hypertension. On the other hand, renal vasculature can also suffer the consequences of essential hypertension and, as a result, chronic renal failure can develop. The role of antihypertensive therapy in preventing renal damage has been sufficiently addressed. However, investigation of the potential for facilitating the antihypertensive capacity of drugs through their renal effects and investigation of the differing abilities of particular groups of antihypertensive agents to prevent or slow the progression of renal damage constitutes a challenge for future research.
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PMID:Kidney and aetiology, pathology and management of essential hypertension. 848 48

The aim of this study was to test basal and after treatment erythrocyte sodium and calcium concentrations, and calcium-ATPase activity and platelet cytosolic free calcium and pH in 20 normotensive controls, 20 hemodialysis-dependent chronic renal failure patients and in 18 essential hypertensives. Prior to treatment, essential hypertensive and uremic patients presented similar higher platelet calcium concentrations and lower pH than the normotensive control group. The erythrocyte sodium, calcium, and magnesium concentrations were only significantly elevated in chronic renal failure, with a significant decrease in the calcium-ATPase activity in the latter population. Hemodialysis partially reversed these intracellular ionic abnormalities with normalization of platelet pH. Significant correlations have been noted between weight loss and decreases in platelet calcium concentration (r = 0.60, p < 0.01) or in erythrocyte sodium (r = 0.50, p < 0.05). The systolic blood pressure decrease was only correlated to the increase in calcium-ATPase activity (r = 0.57, p < 0.05). Antihypertensive treatment (captopril and nifedipine) only tended to normalize the intracellular calcium concentration with correlation between the decrease of the latter and blood pressure decrease (r = 0.64 for the systolic blood pressure and 0.68 for the diastolic blood pressure, p < 0.01). Thus, in essential hypertension and in uremia, some cellular ionic abnormalities exist in platelets in baseline condition. Moreover, in uremia, erythrocyte presents abnormal ionic pattern. Some, but not all of these abnormalities could be corrected by treatment affecting blood pressure (cellular calcium) in essential hypertension or by hemodialysis (cellular sodium, calcium, and pH). In the latter treatment, the changes are linked to extracellular fluid modification. In essential hypertension, the intracellular calcium reduction was linked to blood pressure decrease.
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PMID:Intracellular cation concentrations in essential hypertension and chronic renal failure. 849 May 92

The mechanism by which hypertension produces renal damage remains poorly defined. Experimental evidence suggests that glomerular hypertension/hyperfiltration constitutes a potential mechanism by which hypertension leads to chronic renal failure. Renal functional reserve has been used to investigate the presence or absence of hyperfiltration, both in experimental animals and humans. Micropuncture studies using the two-kidney, one-clip hypertension model have shown that glomerular hypertension/hyperfiltration is associated with loss of renal functional reserve. However, loss of renal functional reserve in this experimental model is not always indicative of hyperfiltration because some antihypertensive agents (Verapamil, Losartan) correct glomerular hypertension/hyperfiltration, but do not restore renal reserve. Renal reserve has also been evaluated in patients with essential hypertension. Some investigators have shown that hypertension is associated with loss of renal functional reserve which can be restored in some studies with antihypertensive therapy. However, normal renal reserve has also been shown in hypertensive patients. Altogether, these data suggest that renal functional reserve cannot be used to assess the role of hemodynamic mechanisms in hypertension-induced renal injury. Long-term follow-up studies are required to establish if loss of renal reserve is indicative of risk factors leading to renal failure in patients with systemic hypertension.
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PMID:Renal reserve in patients with high blood pressure. 852 52


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