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)

A sensitive and specific radioimmunoassay for alpha-human atrial natriuretic polypeptide (alpha-hANP) was developed to determine its plasma level. Anti-alpha-hANP rabbit serum was specific for the N-terminus and ring structure of alpha-hANP, and showed no appreciable cross-reactions with other neuropeptides. The lowest level of alpha-hANP detectable by this radioimmunoassay was 4 pg per tube. The intra- and inter-assay coefficients of variation were 4.6-11.4% and 7.9-11.8%, respectively, and the recovery rates at 4 concentrations were 62.6-74.0%. The fasting plasma alpha-hANP concentration in normal subjects were 19.3 +/- 1.0 ng/l (mean +/- SE; n = 54), and there was no sex difference. The plasma alpha-hANP level in normal subjects fell significantly during water deprivation and increased significantly on infusion of hypertonic saline. The mean plasma levels of alpha-hANP were higher than normal in patients with essential hypertension, liver cirrhosis, congestive heart failure and chronic renal failure. Our results indicate that this radioimmunoassay is suitable for determining the alpha-hANP concentration in human plasma and can assess changes in pathological and physiological states.
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PMID:Radioimmunoassay for atrial natriuretic peptide: method and results in normal subjects and patients with various diseases. 294 73

Research on the physiological role of atrial peptides in man is limited, and the potential for these peptides, or more stable analogues, in therapeutics is uncertain. It is clear, however, that plasma levels of immunoreactive atrial natriuretic peptide (IR-ANP) are increased in volunteers taking a high sodium diet, and are elevated in patients with heart failure, chronic renal failure, and primary aldosteronism. There is suggestive evidence that IR-ANP levels are increased also in essential hypertension, although overlap with normotensives is considerable. Injection or infusion of atrial peptides into man results in a diuresis, an increased output of urine electrolytes, a fall in blood pressure and a rise in heart rate, suppression of aldosterone and sometimes of renin also, and stimulation of norepinephrine. In essential hypertensives, urinary effects may be greater than in normotensives. Heart failure patients show a rise in cardiac output and falls in both systemic and pulmonary arterial pressure. Over the next few years and especially if specific antagonists can be developed, the physiologic and pathophysiologic roles of atrial peptides in normal man and in clinical disorders should be clarified. It is possible that stable analogues of atrial peptides will find a place in the treatment of cardiac failure, renal failure, and perhaps hypertension.
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PMID:Atrial natriuretic peptides in man. 296 23

Three types of antihuman atrial natriuretic peptide antiserum were obtained. From the study of cross-reactivity to human atrial natriuretic peptide fragments, it was suggested that antisera-1, -2, and -3 are mostly specific to 1-28, 5-25, and the ring structure, respectively. The estimated values of this hormone were significantly lower in the order of antisera-1, -2, and -3. Moreover, high performance liquid chromatographic study showed that various types of fragments of atrial natriuretic peptide exist in human plasma. These findings suggested that the highly specific antiserum to 1-28 human atrial natriuretic peptide such as antiserum-1 should be used to estimate the 1-28 human atrial natriuretic peptide levels in human plasma. From the study by using antiserum-1, it was concluded that the plasma human atrial natriuretic peptide increased in essential hypertensives, and in patients with primary aldosteronism, chronic renal failure, and malignant hypertension. Regarding the pathophysiological significance of increased plasma atrial natriuretic peptide, it is unlikely that this plays an important role in the etiology of essential hypertension or other hypertensive diseases, because the plasma level of this hormone is elevated in these patients. The increase of plasma atrial natriuretic peptide level in these patients should be considered to be a secondary or compensatory reaction to high blood pressure.
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PMID:Plasma levels of human atrial natriuretic peptide in patients with hypertensive diseases. 296 24

Out of 32 patients (f = 10, m = 22; mean age: 46 +/- 3 years) with untreated essential (primary) hypertension (WHO-classification I-III) and without clinical signs of congestive heart failure or chronic renal failure, 19 showed plasma-ANP base levels above the normal range (greater than 100 pg/ml; normal range: 50 +/- 10 pg/ml). While high sodium loading caused an increase of plasma ANP levels and a concomitant decrease of plasma renin and aldosterone concentrations, low sodium loading caused the opposite pattern of ANP and renin/aldosterone secretion. Some patients with essential hypertension with highly elevated plasma ANP levels (10-20-fold above the normal range) showed an only moderate decrease of ANP and a slight increase of renin under a low sodium diet. Plasma ANP levels were significantly correlated with the heart volume (r = 0.54; p less than 0.05; radiologically determined), the electrocardiographic signs of left ventricular hypertrophy (Sokolow-Lyon index; r = 0.62; p less than 0.05) and with the left atrial diameter (r = 0.34; p less than 0.05; determined by 2-D-echocardiography). We speculate that high levels of plasma ANP in patients with essential hypertension might be interpreted as a compensatory mechanism either for an insufficient excretion of sodium or for myocardial dysfunction.
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PMID:[Atrial natriuretic peptide (ANP) in essential hypertension: a humoral marker for salt sensitivity and hypertensive heart disease at a clinically asymptomatic stage?]. 297 Jan 80

The acute antihypertensive effect of a new long-acting oral angiotensin I-converting enzyme (ACE) inhibitor, enalapril maleate, was assessed in 20 hypertensive patients, of whom 14 had essential hypertension, 4 had renovascular hypertension, one had hypertension associated with chronic renal failure, and one had primary aldosteronism. Enalapril maleate significantly lowered the blood pressure in either low-renin or normal- and high-renin hypertensives. There was a significant correlation for all patients as a group between the pretreatment levels of serum ACE activity and the reduction in mean blood pressure (r = -0.454, p less than 0.05, n = 20) 2 h after drug administration. The serum ACE activity decreased maximally 3 to 4 hours after drug administration and did not return to baseline levels within 24 h. There was a significant correlation between the reduction in mean blood pressure and changes in ACE activity 90 min and 2 h after drug administration, respectively, for all patients as a group (r = 0.495, p less than 0.05, n = 20, at 90 min; r = 0.508, p less than 0.05, n = 20, at 2 h). The plasma renin activity (PRA) significantly increased in normal- and high-renin hypertensives but not in low-renin hypertensives. There was a close correlation between the reduction in mean blood pressure and the PRA 8 h after drug administration in normal- and high-renin patients (r = -0.623, p less than 0.05, n = 13), while no such relationship was observed in low-renin patients. The plasma aldosterone concentration (PAC) significantly decreased within 3 h, the lowest values occurring at 8 h after drug administration, and it returned to baseline levels within 24 h in all patients. No relationship was found between the reduction in mean blood pressure and changes in PAC after drug administration in either low-renin or normal- and high-renin hypertensives. The plasma bradykinin concentration (PBC) increased within 1 h, the highest values occurring at 3 h after drug administration, and returned to baseline levels within 24 h in low-renin hypertensives, while the PBC was significantly increased at 4 h and had not returned to baseline levels within 24 h in normal- and high-renin hypertensives. There was a significant correlation between percentage changes in mean blood pressure and those in PBC 90 min after drug administration in normal- and high-renin hypertensives (r = -0.556, p less than 0.05, n = 13), while no relationship was observed between them in low-renin hypertensives.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The acute effects of the new angiotensin I-converting enzyme inhibitor, enalapril maleate, on blood pressure, plasma renin, aldosterone and kinins in hypertensive patients]. 299 Oct 35

The acute effect on the renin-angiotensin system and the pharmacokinetic properties of delapril, a new angiotensin converting enzyme inhibitor and its active diacid metabolites (delapril diacid and 5-hydroxy delapril diacid) arising from delapril in vivo were investigated in 4 hypertensive patients with chronic renal failure (CRF: 4 males, average age 49.5 (37-64) years, mean Ccr 22.2 ml/min/1.73 m2) and 9 patients with essential hypertension (EH: 6 males, 3 females, average age 42.8 (28-61) years, mean Ccr 79.3 ml/min/1.73 m2). In CRF, following a single dose of delapril hydrochloride (30 mg), the biological half lives (t1/2) of delapril diacid and 5-OH-delapril diacid were 4.69, 12.88 hours, the maximum serum concentration (Cmax) and the area under the plasma concentration-time curve ([AUC]24(0)) of delapril and its diacid metabolites were 414, 797 and 435 ng/ml, and 658, 6400 and 5068 ng X h/ml, respectively. In EH, the t1/2 of delapril diacid and 5-OH-delapril diacid were 1.21, 1.40 hours and the Cmax and [AUC]24(0) of delapril and its diacid metabolites were 489, 635 and 229 ng/ml, and 572, 1859 and 948 ng X h/ml, respectively. The [AUC]24(0) in CRF were significantly increased as compared with those in EH. The cumulative urinary excretions were significantly lower in CRF than in EH. The serum angiotensin converting enzyme (ACE) was markedly inhibited in both groups up to 24 hours. The plasma concentration of angiotensin II decreased in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacokinetics and acute effect on the renin-angiotensin system of delapril in patients with chronic renal failure. 303 May 95

Diagnosis of pheochromocytoma has been made by the determination of urinary noradrenaline and adrenaline excretion for 24 hours. The assay procedure and the collection of urine for 24 hrs. are intricate. In the present study, we have ascertained the clinical significance of urinary normetanephrine (NM) and metanephrine (M), chemically stable metabolites of catecholamines, in single voided urine for a diagnosis of pheochromocytoma. Urine and plasma samples were collected from 361 normal subjects, 59 patients with essential hypertension, 22 patients with chronic renal failure and 22 patients with pheochromocytoma. Urinary NM and M concentrations were determined by radioimmunoassay with prior hydrolysis by acidification with 1N HCl. Plasma NM and M concentrations in normal subjects were 71.8 +/- 30.7 pg/ml and 41.5 +/- 8.61 pg/ml, respectively. Plasma NM was increased in 8 and plasma M was increased in 20 of 21 patients with pheochromocytoma, although many of these overlapped with those patients with chronic renal failure (NM, 285.9 +/- 175.1 pg/ml; M, 206.3 +/- 186.7 pg/ml) and essential hypertension (NM, 107.7 +/- 90.7 pg/ml; M, 46.7 +/- 20.2 pg/ml). Urinary NM and M concentrations did not show specific diurnal variation and there was significant correlations between the values in single voided urine and those in the 24 hour urine. Urinary NM and M concentrations in normal controls were 197.5 +/- 46.7 ng/mg Cr. and 125.3 +/- 37.1 ng/mg Cr., respectively. Urinary NM concentration was increased in 14 and urinary M concentration was increased in all of 17 patients with pheochromocytoma. In addition, urinary M concentration was higher in most of the 17 patients with pheochromocytoma than that in the patients with chronic renal failure and essential hypertension. However, the values in three patients with Sipple's syndrome with a small adrenal tumor or recurrent cases overlapped with those in other diseases. Relationships between urinary concentrations of NM and/or M and tumor size showed positive correlations. Urinary NM and M concentrations showed significant decreases after surgical removal of the tumors. These results suggest that NM and/or M concentrations in single voided urine could be a sensitive and specific diagnostic tool for pheochromocytoma.
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PMID:[Biochemical diagnosis of pheochromocytoma by determining normetanephrine and metanephrine concentrations in single voided urine]. 322 27

Novel approaches to managing refractory arterial hypertension (AH) have been tested in 130 patients aged 28 to 59 years with severe or malignant hypertension. Hemosorption was performed in 70 patients in whom AH was caused by chronic diffuse glomerulonephritis (49 cases) or chronic pyelonephritis (21 cases) accompanied by the appearance of chronic renal failure. In all patients, blood pressure after hemosorption decreased by 15% to 16% on the average, resulting in progressively improved renal function and a nearly 2.0-fold reduction in plasma aldosterone concentration (PAC), and allowing the doses of antihypertensive drugs to be reduced. Plasmapheresis was performed in 31 patients with refractory severe or malignant AH due to essential hypertension or parenchymatous diseases of the kidneys. After two to four plasmapheresis sessions with up to 2 L of plasma exchanged, blood pressure dropped by 24% compared to baseline while the doses of antihypertensive drugs were diminished and some were discontinued completely in several cases. Analysis of the sensitivity to antihypertensive drugs after plasmapheresis using the rosette technique revealed a significant decrease in the number of rosette-forming cells. The level of angiotensin II and urinary excretion of aldosterone-18-glucuronide declined progressively by nearly 50% after plasmapheresis, correlating with the antihypertensive effect of plasmapheresis. In 32 patients with severe AH complicated by refractory cardiac failure, isolated ultrafiltration was used. After one to eight sessions and the removal of 1.0 L to 35.8 L of fluid, the signs of cardiac failure diminished, the blood pressure level responded to drug therapy, and the PAC level decreased significantly. Although the mechanisms of the antihypertensive actions of hemosorption, plasmapheresis, and isolated ultracentrifugation are still not completely elucidated, these data suggest that hemosorption may act by removing nitrogenous residues from the body and reducing PAC, plasmapheresis by deblocking receptors for antihypertensive drugs and reducing the concentration of angiotensin II and the synthesis of aldosterone in the body, and isolated ultrafiltration by eliminating hyperhydration and edema of the parenchymatous organs.
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PMID:Extracorporeal methods in the management of severe and malignant arterial hypertension. 324 17

The endogenous digoxin-like substance seems to play an important role in the aetiology and pathogenesis of essential and secondary hypertension. Immunoreactive digoxin-like substance was determined in 52 subjects: 17 healthy ones, 15 patients with essential hypertension, 10 cases of chronic renal failure and 10 patients with acromegaly. The substance was not found in healthy subjects, in acromegaly and essential hypertension. In chronic renal failure detectable concentrations of the substance were observed but they showed no correlation with the creatinine level and other clinical data.
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PMID:[Endogenous digoxin-like substance level in essential arterial hypertension, renal failure and acromegaly]. 327 65

Effects of captopril on arterial pressure (AP) and renal function were investigated in patients with non-malignant "benign" or malignant phase essential hypertension (EH group), or with chronic renal failure (CRF group). After captopril administration, AP and renal vascular resistance (RVR) decreased significantly, and renal blood flow (RBF) and plasma renin activity (PRA) increased in both groups. Glomerular filtration rate (GFR) increased in the EH group, but was unchanged in CRF. Filtration fraction decreased in the malignant hypertension and CRF groups. Significant correlations were found between baseline PRA and baseline RVR, and the captopril-induced decrease in mean AP, decrease in RVR, increase in RBF, and increase in GFR in the EH group, while these associations were not observed in CRF. These results indicate that the high AP, RVR, suppressed RBF and GFR in the EH group were closely related to activity of the renin-angiotensin system, but not so the low RBF and GFR in CRF. Small doses of captopril may improve impaired renal function in EH, and may not cause deterioration in the CRF group.
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PMID:Renal haemodynamics and comparative effects of captopril in patients with benign- or malignant-essential hypertension, or with chronic renal failure. 330 Oct 82


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