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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Alpha-human atrial natriuretic polypeptide (alpha-hANP) was applied to 16 clinical patients, 6 patients with essential hypertension, 7 patients with congestive heart failure and 3 patients with cirrhosis. Following intravenous bolus injection of 400 micrograms of synthetic alpha-hANP, a hypotensive effect of very rapid onset was found, which was more potent in the hypertensive patients than in the normotensive cases. Cardiac functions were improved significantly with a similar time course as the depressor response in the cases of heart failure or hypertension. Hemodynamic observations showed a marked increase in cardiac output, cardiac index, stroke volume, ejection fraction and ejection rate, and a concomitant decrease of the pressure in the right side of the heart and pulmonary circulation in these subjects. In addition, the renal response to alpha-hANP induced obvious increases in urine volume, electrolytes and creatinine excretions in all the subjects. Finally, plasma levels of aldosterone, Arg-vasopressin and noradrenaline were also altered by alpha-hANP. No significant side effects were registered. The above result confirms the therapeutic actions of alpha-hANP in human subjects and opens the possibility to research alpha-hANP as a powerful pharmacological tool as well as potential new medicine for human disorders.
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PMID:Therapeutic actions of alpha-human atrial natriuretic polypeptide in 16 clinical cases. 295 43

In essential hypertension ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by the organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Even the young hypertensive heart of normal size with no angiographic abnormalities appears to be prone to ischemia, because the coronary reserve is seriously limited even in the absence of coronary stenosis. Unlike ventricular distensibility, myocardial compliance may be normal even in the presence of pronounced myocardial hypertrophy. As myocardial compliance decreases, systolic wall stress increases and ventricular function is reduced. The hypertensive heart, the most common form of an irregular hypertrophy of the ventricular wall, is found in 14% of such cases. Analysis of the degree of hypertrophy shows that the hypertrophy can be inappropriately high (high mass-to-volume ratio, reduced wall stress), appropriate, or inappropriately low (normal mass-to-volume ratio, increased wall stress). Coronary reserve is reduced even in hypertensive hypertrophy without evidence of coronary artery disease. MVO2 per mass unit was directly correlated with systolic wall stress per cross-sectional area of the left ventricular wall. It is concluded that the appropriateness of left ventricular hypertrophy, as a result of mass-to-volume ratio and stress, is a major determinant of left ventricular performance, of coronary blood flow, and of myocardial oxygen consumption. Pharmacotherapeutical means of reversing cardiac hypertrophy (prazosin, clonidine, enalapril, and nifedipine) were analyzed in concentrically, as well as eccentrically, hypertrophied left ventricles. Regression of cardiac hypertrophy, i.e. therapeutic intervention on a critical precursor of hypertensive congestive heart failure, can be obtained by various antihypertensive agents. Prazosin, calcium channel blockers and angiotensin-converting enzyme inhibitors as well as a combined treatment regimen using alpha-receptor blockers together with diuretics and vasodilators can all induce regression of hypertrophy associated with an improvement in left ventricular function. Moreover, an improved coronary reserve may reduce the ischemic risk of the hypertrophied myocardium. However, not all antihypertensive drugs seem equally effective in bringing about coronary regression of left ventricular hypertrophy. No regression or little regression has been found with diuretic monotherapy despite a satisfactory reduction in blood pressure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Comparative analysis of cardiac function, geometry, energetics and coronary reserve in hypertensive heart disease. 296 4

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

ANF is a newly discovered peptide hormone that has significant implications for critical care physicians. This hormone, released from the heart, is especially responsive to fluid challenges as well as to many of the drugs commonly used in the ICU, including pressor and anesthetic agents. It has potent arterial vasodilating effects in pharmacologic doses and may be an important natural vasodilating agent, especially in the renal vascular bed. In patients on dopamine, it may potentiate the renal vasodilating effect and may provide an effective therapy for developing acute renal failure. Children with congenital heart disease and patients with CHF have elevated levels that clearly alter the aldosterone-angiotensin II system and may help us to understand and treat these conditions more effectively. Additionally, ANF may be a marker for adequacy of treatment in these disease states. The potential uses for ANF include diuresis in patients with fluid overload and diuretic resistance, treatment of CHF, and as a short-acting vasodilator. In the ICU, many therapies affect cardiac pressures and volume regulation. Positive-pressure ventilation may decrease the release of ANF by decreasing venous return and thus contribute to water retention. Drugs used in the ICU may directly affect ANF levels and markedly affect the homeostasis of fluid and electrolyte balance. This hormone system interacts intimately with renin, angiotensin II, and aldosterone. These interactions may play a significant role in the development of essential hypertension. Although not addressed in this article, the treatment and understanding of essential hypertension may be significantly advanced by understanding these relationships. It is clear that ANF acts as a hormone with complex interactions between the heart, volume status, electrolyte balance, renin-angiotensin II-aldosterone, vasopressin, and vascular tone. Although currently no definitive picture exists for these complex interactions, this is an exciting new hormone with significant implications for patient management in the ICU. As research continues, the picture will become clearer and our understanding of this new hormone more precise.
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PMID:Atrial natriuretic factor in the pediatric intensive care unit. 297 48

An explosion of research over the last seven years has led to the discovery and characterization of a peptide, originating in the heart's atria, that possesses impressive vasorelaxant and natriuretic properties. Although the several atrial peptides that have been isolated by researchers working in different laboratories vary in length, all contain the same core sequence. Cardionatrin I, a 28-amino acid peptide, is the likely active circulating hormone. In the atrial peptide's action on vascular smooth muscle, it appears especially to counter the effects of angiotensin II. The peptide's effects on renal hemodynamics and sodium excretion include a marked increase in glomerular filtration rate. Atrial hormone also induces impressive natriuresis in experimental animals, for which an increase in glomerular filtration rate may be a necessary component. Atrial hormone has been found to reduce arterial blood pressure in both animals and humans. In experimental animals, the peptide appears to lower blood pressure by different mechanisms in high- and low-renin forms of hypertension, and to lower pressure to a greater degree and with lower doses in the former as compared with the latter. In patients with essential hypertension, primary aldosteronism, congestive heart failure, renal failure, and perhaps ascitic cirrhosis, plasma ANH levels tend to be higher than they are in normotensive individuals. Atrial hormone causes marked and sustained suppression of renal renin secretion and, thus, of plasma renin levels. In addition, atrial hormone blocks aldosterone secretion and opposes the vasoconstrictive effects of angiotensin II and the sodium-retaining action of aldosterone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic hormone: a regulator of blood pressure and volume homeostasis. 297 65

Arterial hypertension is by definition a haemodynamic disorder. At least 3 different subsets of cardiovascular pathophysiological features can be identified in so-called essential hypertension: The young lean patient characterised by an elevated cardiac output and renal blood flow, elevated plasma renin activity and circulating catecholamine levels, as well as symptoms and signs of hyperadrenergic hypertension. The elderly patient characterised by a low cardiac output often with left ventricular hypertrophy, elevated total peripheral resistance, nephrosclerosis, and symptoms and signs of target organ disease. The obese patient (and to a lesser degree the black patient) characterised by expanded fluid volume state, elevated cardiac output, a normal to low total peripheral resistance, and symptoms and signs of volume overload. To initiate antihypertensive therapy, the drug of choice in the young patient is a beta-adrenergic receptor blocker; in the elderly it is a haemodynamic vasodilator (anti-adrenergic drug, slow channel calcium blocker, or converting enzyme (ACE) inhibitor), and in black or obese patients it remains a thiazide diuretic. Enalapril, a new ACE inhibitor is indicated as a first-step agent in the great majority of hypertensive patients in whom the elevated arterial pressure should be reduced by a decrease in total peripheral resistance, without compromising systemic or regional blood flow. In contrast to other antihypertensive agents, enalapril will lower preload and afterload to the left ventricle while improving systemic and regional flow in elderly patients with latent or manifest congestive heart failure.
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PMID:Cardiovascular pathophysiology of essential hypertension: a clue to therapy. 299 85

Enalapril maleate is a new angiotensin converting enzyme inhibitor marketed in the U.S. by Merck Sharp and Dohme. It has been demonstrated to actively interfere with the renin-angiotensin-aldosterone system. This is reflected by both hemodynamic (decreased blood pressure) and humoral (increased plasma renin, angiotensin I, and decreased angiotensin II) responses to enalapril therapy. Activity in the kallikrein-bradykinin system is still controversial. Enalapril maleate is a prodrug which is quickly absorbed, hydrolyzed by the liver to the active metabolite enalaprilic acid, and excreted 33 percent in the bile and 61 percent in the urine. The therapeutic dosage range is 10-40 mg/d, maximum of 40 mg, given once or twice daily. The onset and duration of action are dose related. Vertigo and headache have been the most commonly reported side effects. Clinical comparison of enalapril to hydrochlorothiazide, beta-adrenergic blockers, and captopril find it efficacious in the treatment of essential hypertension. Efficacy in treating congestive heart failure and hypertension secondary to renal artery stenosis has also been demonstrated for both angiotensin converting enzyme inhibitors. The overall efficacy and safety of enalapril and captopril appear equivalent when used at low doses in patients with uncomplicated hypertension.
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PMID:Enalapril: a new angiotensin converting enzyme inhibitor. 300 62

The renin-angiotensin system has a range of physiological actions concerned with the control of the circulation. Angiotensin II has both an immediate and a delayed pressor effect, it stimulates the secretion of aldosterone and antidiuretic hormone, promotes thirst, stimulates the sympathetic nervous system at various sites while inhibiting vagal tone, and has a range of direct effects on the kidney. Several aspects of this range of actions can become deranged in a number of forms of hypertension as well as in congestive cardiac failure. Hence much effort has been directed in recent years to the development of agents designed to interfere with the renin-angiotensin system and to apply these clinically in the treatment of hypertension and congestive cardiac failure. Orally active converting enzyme inhibitors are of proven benefit not only in renovascular hypertension, but also, when combined with loop diuretics, in the treatment of intractable hypertension as well as, both alone and in combination with thiazide diuretics, in the treatment of essential hypertension. In congestive cardiac failure controlled trials have shown that converting enzyme inhibitors can improve exercise tolerance while diminishing lassitude, correct potassium deficiency and limit ventricular arrhythmias. Energetic efforts are being made to develop orally active inhibitors of the enzyme renin itself, since these would be more specific in action than the presently available and very successful converting enzyme inhibitors.
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PMID:The clinical use of angiotensin converting enzyme inhibitors in hypertension and cardiac failure. 303 14

An elevated total peripheral resistance is the haemodynamic hallmark of both arterial hypertension and congestive heart failure. In essential hypertension it is the main pathogenetic abnormality, whereas in congestive heart failure it is the result of vasoconstriction serving to compensate for the fall in cardiac output and arterial pressure. Any drug that lowers total peripheral resistance can, therefore, potentially favourably influence established hypertension as well as unload the left ventricle in congestive failure. In essential hypertension, urapidil lowers arterial pressure acutely by a fall in total peripheral resistance with a small compensatory increase in cardiac output. Concomitantly, renal and splanchnic blood flow increase and the resistance in these vascular beds falls. In congestive heart failure, the acute administration of urapidil increases cardiac index and lowers mean pulmonary artery wedge pressure and systemic vascular resistance by about 30%. At the same time, a mild fall in mean arterial pressure is observed. Long term non-invasive studies document that these acute haemodynamic effects remain preserved in both arterial hypertension and congestive heart failure. Urapidil seems, therefore, to be a promising agent for the treatment of haemodynamic disorders that are characterised by an elevation of total peripheral resistance, such as established essential hypertension and congestive heart failure.
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PMID:Haemodynamic effects of urapidil in arterial hypertension and congestive heart failure. 304 61


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