Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prescription of cardiac glycosides is usually controlled by immunological measurement of their plasma concentration. The observation of false positive digoxin measurements in patients free of this drug and the hypothesis that endogenous digitalis-like compounds might participate in body sodium and water homeostasis have led us to investigate the presence in plasma of compounds interacting with digoxin-antibodies under various physiological and pathological conditions in man and rats. The apparent levels of digoxin-equivalents in plasma of healthy control subjects (n = 21) and patients with essential hypertension (n = 48) or end-stage renal failure (n = 13) were 24.7 +/- 3.2, 34.4 +/- 4.4 and 98.7 +/- 17.4 pg/ml, p less than 0.05 and p less than 0.01 respectively. Positive correlations were observed between systolic and diastolic blood pressure and the apparent immunoreactivity of either whole or deproteinized plasma, in particular when only male subjects were considered. No relationship was found with the renal Na+ excretion or the plasma renin activity and the apparent immunoreactivity of the plasma. Its levels were however correlated with its ability to inhibit ouabain binding to the erythrocyte Na+ pump and to its capacity to reduce the renal Na+, K+-ATPase activity. In rats with experimental hypertension, induced by chronic excess salt intake either alone or associated with reduced renal mass, the cross reactivity with antidigoxin antibodies was also enhanced when compared to control rats (71.6 +/- 10.2 pg/ml, n = 12 and 57.3 +/- 5.0 pg/ml, n = 33 respectively compared to 43.4 +/- 3.7 pg/ml, n = 36, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Compounds of the digoxin type in essential and experimental hypertension]. 243 46

Renal effects of 1,4-dihydropyridine (DHP)-type calcium antagonists (nitrendipine and nisoldipine) were analyzed in diverse conditions, such as long-term antihypertensive treatment, acute saline-loading, and acute renal failure in rats. In spontaneously hypertensive rats (SHR), 60-week treatment with nitrendipine resulted in normotensive blood pressure values without increasing body weight, an indicator of salt-water retention, or increasing plasma renin activity and plasma aldosterone concentration compared with the untreated rats. After acute saline-loading of normotensive or hypertensive rats, administration of calcium antagonists nitrendipine and nisoldipine increased urinary volume and sodium excretion. This was in contrast to the effects observed with the vasodilator minoxidil, with which salt-water retention was shown. In acute renal failure induced by 60-min renal ischemia in uninephrectomized rats, administration of nisoldipine decreased mortality rate and improved kidney function. The increase in renal tissue calcium content and the decrease in ATP content associated with the renal failure was abolished by nisoldipine treatment. In conclusion, renal protective effects are present with DHP-type calcium antagonists; however, mechanisms in situations such as hypertension or acute renal failure might be different and deserve further analysis.
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PMID:Renal effects of 1,4-dihydropyridines in animal models of hypertension and renal failure. 244 Nov 91

ANF is an exciting, newly discovered hormone that has significant potential for furthering our understanding of the complex interactions involved in fluid and electrolyte balance. In addition to effects on water and salt balance, it is a potent vasodilator, as well as inhibitor of renin, angiotensin II, aldosterone, and vasopressin. ANF is primarily produced in the atria, but production in the brain is suggestive of action as a neuropeptide and as a potential regulator of CSF production. Receptors are found throughout the heart, vascular tree, kidney, adrenal gland, and brain. The stimulus for release appears to be atrial stretch, which may be secondary to intravascular fluid changes. It causes hemoconcentration and may be an important regulator of interstitial fluid distribution as well as capillary permeability. Patients with CHF and renal failure have been found to have elevated levels that decrease in response to treatment. Potentially, it may be useful as a therapeutic agent in acute renal failure, CHF and other fluid disturbances. ANF is a testament to the incredible advances in peptide biology. Within 2 years of the discovery, ANF was sequenced and cloned. Since that time, literally thousands of papers describing its actions have been published. Our knowledge about this hormone grows at an exponential rate. It is clear that this hormone is intimately involved in the regulation of fluid and electrolyte balance, vascular tone, and the pathophysiology of CHF but many questions remain unanswered. Continued research will provide many of the missing pieces to this very complex, new hormone system.
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PMID:Atrial natriuretic factor. 252 98

Atrial natriuretic peptide is a recently discovered cardiac hormone with natriuretic, vasodilatory and hypotensive activities. The role of this hormone in the pathophysiology of hypertension is of particular interest. In contrast to an earlier concept, a deficiency of the atrial peptide could not be found in animal models of hypertension or in patients. ANP plasma levels were elevated in SHR with accelerated hypertension, in salt-sensitive Dahl rats, in rats with DOCA-salt-hypertension and in animals with renovascular hypertension. Elevated ANP levels under these conditions can be explained by an expansion of the intravascular volume or by an elevated atrial wall stretch induced by the hypertension itself. In patients with primary hypertension, plasma levels of the peptide are raised in some patients and are normal in others. Plasma ANP levels correlate with age, blood pressure and signs of left ventricular hypertrophy. A negative correlation is described between ANP and renin. Measurement of plasma ANP levels does not allow a differentiation between primary and secondary forms of hypertension. Elevated ANP levels are also found in primary hyperaldosteronism and in renal failure. Stimulation of ANP secretion by physical exercise and dietary salt loading is maintained in hypertension. Infusion of 1-28-hANP leads to a reduction in systemic arterial pressure in normotensives and hypertensives. The natriuresis induced by exogenous ANP is more pronounced in hypertensives. Stimulation of endogenous ANP secretion does not prevent the rise in blood pressure possibly due to a reduction in ANP receptors in target tissues.
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PMID:[Atrial natriuretic peptide and its significance for arterial hypertension]. 253 Dec 53

In patients with chronic renal disease, hypertension represents an important risk factor for the development of cardiovascular complications. Moreover, it appears possible that the progression of chronic renal failure may be slowed by carefully adjusted antihypertensive therapy. Therefore, blood pressure needs to be monitored very closely in patients with kidney disease and, when indicated, antihypertensive treatment should be started as soon as blood pressure begins to rise. Antihypertensive treatment of patients with non-oliguric renal failure has usually been started with dietary salt restriction and diuretic monotherapy. Other drugs, such as beta-blockers, sympathicolytic and/or vasodilating agents have been added successively. The possibility of beginning antihypertensive therapy with alternative compounds (beta-blocker, calcium antagonists and converting enzyme inhibitors) in patients with non-oliguric renal failure is discussed.
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PMID:[Treatment of arterial hypertension in non-oliguric renal failure]. 267 36

The performance of the renin-angiotensin-aldosterone system and water-salt balance was studied in 69 patients with various patterns (both clinical and morphological) of glomerulonephritis. The author revealed that the levels of total and nonactive renin in the plasma of patients prone to membranous proliferative nephritis were higher than both in controls and in the patients with mesangial proliferative disease. Though there was no difference in the levels of active renin. Besides, it was stated that the renin-angiotensin system more strongly governed the pathogenesis of arterial hypertension in patients with membranous proliferative nephritis than in those who suffered from mesangial proliferative patterns of the disease. As the blood pressure levels turned to be dependent both on the levels of plasma and total renin the author established the existence of a mixed mechanism of hypertension occurrence in the patients with glomerulonephritis. Conversion of the nonactive part of renin into the active one promoted the rise of blood pressure. Therefore, in this case the increased levels of the renin nonactive fraction could be regarded as a risk factor for the occurrence of the hypertensive syndrome. The patients with glomerulonephritis enrolled in the study and 15 controls demonstrated a significant feedback correlation between the levels of total and nonactive renin as well as between the exchangeable sodium and its extracellular levels; the degree of correlation in hypertensive patients varied. It was demonstrated that hyperkalemia could be a reason for an increase in aldosterone levels observed in patients with renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in the renin-angiotensin-aldosterone system in glomerulonephritis]. 268 49

Hypertension is very common in the elderly patient with renal insufficiency and may be primary or secondary to the kidney disease. In these patients, hypertension is usually associated with an increase in peripheral vascular resistance and salt sensitivity (the latter related to the degree of renal failure.) Therapy should be tailored to the individual patient, particularly when the elevated blood pressure and renal insufficiency are associated with other significant medical problems. Most of the drugs used in younger hypertensives may be used in the elderly patient with renal insufficiency, but in general, starting and maintenance doses should be lower because of the greater sensitivity due to age and/or the renal failure. The goal in the elderly hypertensive patient with renal failure is similar to that in other hypertensive patients: blood pressure should be brought to 140/90 mm Hg or lower. In the elderly patient with resistant hypertension or who manifests a decrease in kidney function as blood pressure is lowered, an effort must be made to look for associated renovascular disease.
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PMID:Managing hypertension in chronic renal disease. 287 73

The discovery of the atrial natriuretic factor (ANF) has opened a new field in modern biology. After rapid isolation and identification of this new peptide from atrial granules, it is now evident that this new hormone has a wide variety of actions with general implication in the control of vascular tone, sodium and water balance, hormonal secretion as well as neuronal functions. The major mode of action of this hormone is transmitted via its interaction with a membrane enzyme, particulate guanylate cyclase, leading to increases of cGMP levels. This nucleotide is a faithful marker of ANF action correlating with all functions ascribed to ANF up to date. Significant increases of ANF as well as of cGMP have been discovered in heart and renal failure, secondary hypertension and other states with altered salt-water balance, impairment of heart function and particularly increase of atrial pressure. The increases of levels and relative inefficiency of increased ANF have to be carefully interpreted in face of increased levels of cGMP. It can be expected that new pharmacological developments will occur in this area issuing from both our increasing knowledge concerning the peripheral mode of action of this hormone, its physiological implications as well as its pharmacological effectiveness in diseases with altered salt-water balance, cardiac function and blood pressure disregulation.
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PMID:[Physiological and physiopathological aspects of the atrial natriuretic factor]. 288 82

In this simple, sensitive radioimmunoassay (RIA) of atrial natriuretic polypeptide (hANP) in human plasma, nonspecific interference is minimized by deproteinizing the plasma by heat treatment at 85 degrees C for 10 min. We directly measure alpha-hANP in the supernates by RIA, with use of antiserum that recognizes the N-terminal region of alpha-hANP. The minimal detectable value was 0.4 pg per tube. The intra-assay CV was 6.6% (n = 8). The mean concentration of hANP in plasma of 54 healthy volunteers was 41 (SD 29) ng/L. Concentrations of hANP in plasma increased after saline infusion and high salt intake for one week in patients with essential hypertension. High concentrations were also measured in patients with renal failure and congestive heart failure. This method, which requires no extraction or purification with column chromatography, is especially useful for simultaneous measurement of several samples.
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PMID:Radioimmunoassay of atrial natriuretic polypeptide in heat-treated human plasma. 295 77

The control of sodium balance plays a vital role in the regulation of both intravascular and extravascular fluid volume. The discovery and synthesis of the atrial natriuretic peptides has led to the suggestion that they may be an important hormone in the control of sodium and water balance. Studies in man have confirmed that, when injected, they are natriuretic and that the plasma level, as measured by radioimmunoassay, changes with physiological changes in extracellular volume particularly those that occur with alteration of salt intake, the levels of atrial peptide rising as salt intake is increased. A recent study with a low dose infusion of atrial peptides has shown an increase in sodium excretion at the same plasma levels as those found with saline infusion, confirming that the atrial peptides are a natriuretic hormone in man. These findings allow a better interpretation of the raised levels that are already being described in patients with heart failure, renal failure and high blood pressure.
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PMID:Are the atrial peptides a natriuretic hormone? 295 5


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