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 effects of ketanserin, 40 mg/day (KE40) and 80 mg/day (KE80) on mean arterial pressure, lipids, lipoproteins, and circulating atrial natriuretic factor (ANF) were investigated in a 24-week controlled study in 29 patients suffering from mild to moderate hypertension. A significant decrease in mean arterial pressure (MAP) was observed after 18 weeks of therapy, accompanied by a 64% (P less than .05) and 80% (P less than .02) increase in circulating ANF levels with KE40 and KE80, respectively. There were no significant changes in mean total cholesterol, triglycerides, or cholesterol of the high density lipoproteins (HDL), low density lipoproteins (LDL), and very low density lipoproteins (VLDL) fractions. There was a significant increase in the mean apo B levels and consequently a slight but statistically significant decrease in the ratio of LDL C/B. It is concluded that both doses of KE are effective for monotherapy of mild to moderate essential hypertension. The drug sharply increases circulating ANF levels without significantly altering the plasma lipids. In contrast, by increasing the apolipoprotein B content of the LDL fraction, the beneficial cardiovascular effect of a lowered blood pressure may be partly blunted.
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PMID:Effects of ketanserin on lipids, lipoproteins, and plasma atrial natriuretic factor in patients with essential hypertension. 214 Aug 38

Atrial natriuretic factor (ANF) is a cardiac hormone exerting potent cardiovascular and renal effects but its poor intestinal absorption and rapid inactivation have prevented so far its therapeutic utilisation. However inhibition of endogenous ANF metabolism progressively emerges as a novel therapeutic approach in cardiovascular and renal disorders. The critical role played by enkephalinase (membrane metalloendopeptidase, EC 3.4.24.11) in ANF inactivation was deduced from the effects of inhibitors. These compounds not only protect partially exogenous ANF from hydrolysis by some tissue preparations in vitro but also, in vivo, they increase the half-life of the exogenous hormone in plasma and, even more markedly, its recovery in intact form in kidney, a major target organ. In addition, enkephalinase inhibitors increase by two- to three-fold the circulating level of endogenous ANF, even when the latter is already markedly elevated, such as in patients with chronic heart failure. Finally, enkephalinase inhibitors induce a series of ANF-like responses such as natriuresis, diuresis or increase in cGMP excretion which are attributable to the hormone. These pharmacological observations, as well as preliminary clinical trials, suggest that enkephalinase inhibitors may represent a novel class of therapeutic agents with potential applications in congestive heart failure, essential hypertension and various sodium-retaining states.
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PMID:Enkephalinase (EC 3.4.24.11) inhibitors: protection of endogenous ANF against inactivation and potential therapeutic applications. 214 57

The effect of acute volume expansion (2 liters of saline solution in 2 h) on plasma concentrations of atrial natriuretic factor (ANF), plasma aldosterone concentration (PAC), plasma renin activity (PRA) and their relationship to the renal excretion of urine, sodium and potassium were studied in 6 control subjects and 7 patients with essential hypertension (EH) WHO stage I. Saline infusion provoked comparable rise in plasma ANF in both groups (from 2.98 +/- 0.45 to 12.36 +/- 1.74 pmol/l in the control subjects and from 3.80 +/- 0.72 to 15.78 +/- 2.06 pmol/l in EH patients), significant drop in PRA (from 0.915 +/- 0.419 to 0.256 +/- 0.127 nmol/l/h in controls and from 1.711 +/- 0.324 to 0.714 +/- 0.128 nmol/l/h in EH) and in PAC (from 0.30 +/- 0.07 to 0.14 +/- 0.03 nmol/l in control subjects and from 0.53 +/- 0.13 to 0.24 +/- 0.07 nmol/l in EH). The increase of plasma ANF concentrations after volume expansion might be involved in the suppression of PRA and PAC found after this stimulus. Similar increase in plasma ANF after saline infusion in both groups was associated with significantly greater urine and sodium excretion in EH than in controls. From these results it may be suggested that the acute volume expansion during saline infusion evokes a comparable release of ANF into circulation in both EH patients and controls. In EH patients, however, the similar rise in ANF is accompanied by a more pronounced diuretic and natriuretic response. This exaggerated natriuresis after acute volume and sodium loading cannot be explained solely by a rise in ANF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Humoral and renal response to acute volume loading in patients with essential hypertension. 214 41

The authors investigated dynamic changes and the interaction of the plasma renin activity (PRA), plasma aldosterone (PAC), i.e. the main representatives of sodium retaining systems, and of the atrial natriuretic factor (ANF) the decisive natriuretic substance in acute expansion of the extracellular volume (ECV) by infusion of two litres of saline in six controls, seven patients with essential hypertension and liver cirrhosis without ascites (6 patients) and with ascites (6 patients). The expansion evoked controversial changes of these systems. It led to a rise of ANF and suppression of PAC and PRA. Although ANF rose after infusion to the roughly similar range (12.4 to 15.7 pmol/l), the natriuretic response to expansion differed significantly in different groups of patients. It was most marked in hypertonic subjects (517.2 to 93.2 mumols/min) and practically zero in ascitic liver cirrhosis (54.2 +/- 44.2 mumols/min). The explanation of this finding may be the persistence of high activity of the renin-angiotensin-aldosterone system despite its partial inhibition by infusion of saline in cirrhosis of the liver (PRA 1.69 +/- 0.66 nmols/l/hr., PAC 1.12 nmol/l). For the renal response to acute expansion of the ECV thus not only the absolute plasma concentration of ANF is decisive but also its ratio to the activity of the sodium retaining renin-angiotensin-aldosterone system.
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PMID:[Mutual interaction of the renin-angiotensin system and the atrial natriuretic factor in the renal response to acute volume loading]. 214 4

Calcitonin gene-related peptide (CGRP) is a 37-amine acid bioactive polypeptide and known to be a powerful vascular relaxant. CGRP was measured in 45 cases with essential hypertension (EH). The results suggested that plasma CGRP level in patients with EH was lower than that in normal subjects (P less than 0.001). It was found that decrease of plasma CGRP was closely related with the severity of hypertension. However, the level of plasma atrial natriuretic factor (ANF) in EH patients was significantly increased as compared with normal subjects (P less than 0.01). A negative correlation between plasma CGRP and ANF (r = -0.3615, P less than 0.02) was found. These data suggested that decrease of plasma CGRP may play an important role in the pathogenesis of hypertension.
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PMID:[Plasma calcitonin gene-related peptide (CGRP) level in patients with essential hypertension]. 215 Jul 97

The C-terminal fragment of atrial natriuretic factor (ANF) was infused intravenously at 0.5 pmol/kg/min during 12 hours in 6 patients with mild to moderate essential hypertension, and in 6 normotensive volunteers, all recumbent and well hydrated, under a daily intake of 200 and 120 mmoles of sodium and potassium, respectively. Plasma C-terminal ANF tended to increase during ANF and to decrease during vehicle infusions. Plasma concentrations of the N-terminal fragment of ANF decreased by 20 to 40% (p less than 0.05) during ANF and remained unchanged following vehicle infusion, suggesting that exogenous ANF reduces endogenous ANF secretion. ANF increased significantly plasma cyclic guanosine monophosphate (p less than 0.01) from 3.1 +/- 0.4 to 4.3 +/- 0.8 and from 2.8 +/- 0.4 to 5.1 +/- 0.5 nmol/L in controls and patients respectively. ANF reduced systolic diastolic blood pressure during the last 8 hours of the infusion, by about 5% (p = 0.055) in patients, but did not alter blood pressure in controls. Sodium excretion during ANF increased 42% vs vehicle (p less than 0.05), in the patients group and remained unchanged in controls. Hematocrit levels increased significantly in both groups with ANF infusion. We conclude that a prolonged infusion of ANF at a physiological rate causes a modest increase in plasma cyclic guanosine monophosphate, hemoconcentration, and reduces endogenous ANF secretion. It also stimulates diuresis and natriuresis and slightly reduces systolic blood pressure in patients with essential hypertension.
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PMID:Prolonged low dose infusion of atrial natriuretic factor in essential hypertension. 215 74

In a comparative study the influence of changes in dietary sodium intake on blood pressure, renal function, extracellular fluid volume, the renin-angiotensin-aldosterone system and plasma concentrations of arginine vasopressin, atrial natriuretic factor and cyclic guanosine monophosphate (GMP) was investigated in 12 patients with essential hypertension and in 10 normotensive controls. The subjects were studied after 4 days on a low (50 mmol/day), medium (180 mmol/day) or high (380 mmol/day) sodium intake. Renal sodium handling was assessed by simultaneous measurements of 51Cr-ethylenediaminetetraacetic acid (EDTA), lithium and sodium clearances. Identical values for the extracellular fluid volume, glomerular filtration rate and proximal and distal tubular resorption rates of sodium and water were found in the hypertensive patients and the controls at all three levels of sodium intake. In both groups, raising the sodium intake from low to high significantly increased 51Cr-EDTA and lithium clearance (an indirect measure of end-proximal fluid delivery), with intermediate values for the medium-sodium diet. The estimated values of fractional proximal and distal sodium resorption decreased when sodium intake was raised; the absolute proximal sodium resorption rate did not change, whereas the absolute distal sodium resorption rate as well as the extracellular fluid volume and sodium clearance increased. Blood pressure and the heart rate were unaffected by sodium intake. In both hypertensives and controls, plasma concentrations of active renin, angiotensin II and aldosterone decreased with increasing sodium intake, arginine vasopressin did not change, and atrial natriuretic factor and cyclic GMP increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Normal renal tubular response to changes of sodium intake in hypertensive man. 215 2

Endothelin-1 is a novel endothelium-derived vasoconstrictive peptide. Using a highly specific and sensitive radioimmunoassay for endothelin-1, plasma levels of immunoreactive endothelin-1 were measured in 32 research subjects with normal renal function (21 normal subjects and 11 patients with essential hypertension), 24 patients with nondialyzed chronic renal failure, and 51 patients undergoing maintenance hemodialysis. Although there was no significant difference in plasma immunoreactive endothelin-1 levels among the three groups, patients with essential hypertension had significantly higher plasma endothelin-1 levels than normal subjects (2.29 +/- 1.09 vs. 1.41 +/- 0.50 pg/ml, p less than 0.025). When nondialyzed and hemodialyzed patients were divided into hypertensive and normotensive groups, the nondialyzed hypertensive group (n = 17) had higher plasma endothelin-1 levels than the comparable normotensive group (n = 7) (3.08 +/- 3.43 vs. 0.73 +/- 0.34 pg/ml, p less than 0.05), and the hemodialyzed hypertensive group (n = 18) had higher plasma endothelin-1 levels than the comparable normotensive group (n = 33) (2.66 +/- 1.92 vs. 1.35 +/- 0.73 pg/ml, p less than 0.005). Plasma atrial natriuretic factor, arginine vasopressin, renin activity, and aldosterone concentration did not show significant differences between hypertensive and normotensive individuals or a correlation with plasma endothelin-1 levels. These data suggest that circulating endothelin-1 may be partly involved in the development or maintenance of hypertension in humans.
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PMID:Plasma endothelin levels in hypertension and chronic renal failure. 218 51

We studied two groups of hypertensive patients in order to ascertain whether the acute natriuretic effect of nifedipine is mediated by humoral factors such as renal kallikrein or atrial natriuretic factor (ANF). First, 17 patients with mild to moderate essential hypertension maintained on a 130-mmol/day diet, received either nifedipine (10 mg orally) or placebo during a 6-h infusion of the kallikrein inhibitor aprotinin (2 x 10(6) KIU) or saline as control. Aprotinin, while significantly reducing urinary kallikrein activity, did not interfere with the acute effects of nifedipine on blood pressure, heart rate, urinary volume, urinary Na+ and creatinine clearance. In another group of eight patients on a constant daily Na+ intake of 130 mmol and in the supine position, placebo or nifedipine (10 mg sublingually) were administered, and blood pressure, heart rate, plasma renin activity, plasma aldosterone and plasma ANF, urinary Na+, urine volume and creatinine clearance, were monitored for 2 h. While placebo did not induce changes in any of the above parameters, nifedipine administration induced a significant decrease in blood pressure and increase in urinary Na+, urine volume and creatinine clearance, and a significant rise in ANF levels, from 19.4 +/- 2.8 pg/ml to a maximum of 23.9 +/- 2.5 and 24.1 +/- 2.2 pg/ml (P less than 0.05) at 60 and 90 min, respectively. In conclusion, our data do not support a role for renal kallikrein as a humoral mediator of the natriuretic effect of calcium antagonists, but do not exclude the possibility that ANF might participate in the nifedipine-induced increase in sodium and water excretion.
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PMID:Studies on the natriuretic effect of nifedipine in hypertensive patients: increase in levels of plasma atrial natriuretic factor without participation of the renal kallikrein-kinin system. 245 Jan 87

Atrial distension and pressure have been reported to be important for the release of atrial natriuretic factor (ANF) into the circulation. However, in mild essential hypertension, we have been unable to demonstrate an increase in plasma levels of ANF. To evaluate more precisely the lack of increase of ANF, we measured echocardiographically the diameters of the cardiac chambers and correlated these measurements with ANF values in normal subjects (n = 25), in patients with untreated essential hypertension (n = 20), and in patients with treated essential hypertension (n x 27). The plasma values of ANF were 21.9 +/- 2.8 pg/ml in the normal controls, 20.4 +/- 2.2 pg/ml in patients with untreated mild essential hypertension, and 32.6 +/- 2.8 pg/ml in patients with treated but uncontrolled essential hypertension (p less than 0.05). The plasma values of cGMP were 4.53 +/- 0.56 pmol/ml in the normal, 5.41 +/- 0.57 pmol/min in the patients with untreated essential hypertension, and 6.76 +/- 0.58 pmol/ml in treated essential hypertension (p less than 0.05). There were no significant differences in the size of the cardiac chambers between the three groups, except for the size of the right atrium, but there was a correlation between the ANF values and the size of the left atria (r = 0.29, p = 0.01, n = 72), as well as with the size of the intraventricular septum (IVS) in systole (r = 0.36, p = 0.002, n = 72). Since ANF levels are similar in mild untreated essential hypertension and normal volunteers, the ANF plasma levels could be a better reflection of the impact of the blood pressure on the myocardium than the level of blood pressure itself and indicate in patients the degree of cardiac impairment. On the other hand, there seems to be definitely an effect of treatment on the levels of ANF.
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PMID:Echocardiographic measurements and plasma levels of atrial natriuretic factor. 247 49


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