Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuroendocrine response after acute myocardial infarction (MI) results in activation of the sympathetic nervous system, the renin-angiotensin system, and vasopressin and atrial natriuretic peptide release. The net effect of this response is vasoconstriction, cardiac stimulation and regional flow redistribution that may have a favorable effect in some situations and a deleterious effect in others. The possible adverse effects of vasoconstriction were studied in a Veterans Administration Cooperative Study that evaluated a 48-hour infusion of sodium nitroprusside in the setting of acute MI. In the presence of mild, probably primarily diastolic left ventricular dysfunction, nitroprusside appeared to have an adverse effect on long-term survival. However, in the presence of more severe, probably predominantly systolic dysfunction, nitroprusside had a favorable effect on the prognosis. Therefore, the decision of whether to accept or inhibit neuroendocrine activation in acute MI probably depends on the severity of the disease and the timing of the therapeutic intervals.
Am J Cardiol 1990 May 22
PMID:Neuroendocrine activation after acute myocardial infarction. 214 9

We evaluated the effects of dopamine infusion (1.5 micrograms/Kg/min for 60 min) on secretion of atrial natriuretic factor before raised diuresis could affect extracellular fluid volume and hence peptide release. We investigated ten healthy subjects without cardiovascular, renal or endocrine disease and ten patients with congestive heart failure (New York Heart Association Classes III and IV). The study protocol required four 30 minute clearance periods: 1st basal, 2nd during placebo, 3rd and 4th during dopamine infusion. We measured diuresis, natriuresis, glomerular filtration rate, blood pressure, heart rate, central venous pressure and plasma concentrations of atrial natriuretic factor, noradrenaline, renin activity, aldosterone and antidiuretic hormone. Blood samples were drawn at the midpoint of each clearance period after measuring blood pressure, heart rate and central venous pressure. Atrial natriuretic factor was determined by radioimmunoassay after chromatographic extraction, noradrenaline was measured fluorometrically while plasma renin activity, aldosterone and antidiuretic hormone concentrations were obtained by radioimmunoassay. During dopamine infusion plasma atrial natriuretic factor plasma levels were significantly raised in healthy subjects while high basal values of the peptide in patients with congestive heart failure were significantly reduced; this trend was also evident for noradrenaline levels in both groups. Plasma renin activity, aldosterone and antidiuretic hormone values remained unchanged in healthy subjects, but plasma renin activity and aldosterone levels dropped significantly in congestive heart failure patients. Diuresis, natriuresis and glomerular filtration rate were significantly increased while blood pressure, heart rate and central venous pressure remained unchanged in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
G Ital Cardiol 1990 Mar
PMID:[Effects of dopamine infusion on the release of atrial natriuretic factor]. 214 May 54

The four major diagnostic criteria for the syndrome of congestive heart failure are left ventricular dysfunction, exercise intolerance, pulmonary congestion or edema and ventricular arrhythmias. Activation of norepinephrine, angiotensin II, vasopressin and atrial natriuretic peptide may be a key factor in the vasoconstriction and increased impedance to left ventricular ejection in heart failure. Interventions that interfere with these vasoconstrictor mechanisms should have a salutary effect on left ventricular performance. Treatment with angiotensin-converting enzyme (ACE) inhibitors, alpha-adrenoceptor blockers and vasopressin antagonists has resulted in hemodynamic benefits, but it has been more difficult to demonstrate long-term clinical effectiveness. Reductions in mortality have been demonstrated in patients with heart failure treated with vasodilators and ACE inhibitors. Improvement in the quality of life and prolongation of life are the only two appropriate goals in the management of heart failure. Further understanding of the role of angiotensin II and its interference by ACE inhibition in the tissue processes of heart failure is needed.
Am J Cardiol 1990 Oct 02
PMID:Mechanisms in heart failure and the role of angiotensin-converting enzyme inhibition. 222 Jun 1

The endothelium modulates coronary vascular tone by the release of endothelium-derived relaxing or contracting substances. The endothelium-derived relaxing factor has been identified as nitric oxide synthesized in endothelial cells from L-arginine. The endothelium can release other relaxing substances such as prostacyclin and a hyperpolarizing factor. Endothelin-1 is a potent vasoconstrictor peptide formed by endothelial cells, and is likely to be the physiologic antagonist of endothelium-derived relaxing factor. Other putative contracting factors include superoxide anions and products of arachidonic acid metabolism. Endothelium-derived relaxing factor is released spontaneously and in response to flow, platelet-derived products (that is, serotonin, thrombin and adenosine diphosphate) and certain autacoids (that is, acetylcholine, bradykinin, histamine, substance P, vasopressin, alpha-adrenergic agonists). A considerable heterogeneity of responses exists among vessels of different size from different anatomic origin and different species. Hypercholesterolemia, atherosclerosis, hypertension and myocardial ischemia or reperfusion, or both, impair endothelium-dependent relaxation. Under normal conditions, endothelium-derived relaxing factor appears to dominate the control of vascular tone of large and small coronary vessels, whereas in disease states, endothelium-derived contracting factors are released. Impairments of endothelial function may be important in the development of various forms of cardiovascular disease.
J Am Coll Cardiol 1990 Mar 01
PMID:Endothelial control of vascular tone in large and small coronary arteries. 240 18

Plasma levels of both atrial natriuretic factor (ANF) and vasoconstrictor neurohormones are often increased in patients with congestive heart failure (CHF). It has been speculated that ANF is a counterregulatory hormone that influences regional blood flow and sodium balance in human patients by either direct vasorelaxation or by inhibiting the release of other vasoconstrictor neurohormones. The exact relation of increased ANF levels to regional vascular resistance and vasoconstrictor neurohormones has not previously been documented. Thus, we examined the relation between plasma ANF levels, levels of vasoconstrictor neurohormones, and forearm, splanchnic and renal blood flow in 20 normal subjects and in 17 patients with chronic CHF. The plasma ANF level was directly correlated with the plasma norepinephrine concentration (r = 0.83, p less than 0.01), plasma epinephrine concentration (r = 0.46, p less than 0.01), plasma renin activity (r = 0.50, p less than 0.01), plasma angiotensin II concentration (r = 0.79, p less than 0.01) and plasma vasopressin concentrations (r = 0.65, p less than 0.01). Positive correlations existed between plasma ANF levels and the calculated vascular resistances, i.e., between ANF and forearm vascular resistance (r = 0.41, p less than 0.05), splanchnic vascular resistance (r = 0.74, p less than 0.01) and renal vascular resistance (r = 0.66, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1989 Jan 15
PMID:Relation of atrial natriuretic factor to vasoconstrictor hormones and regional blood flow in congestive heart failure. 252 Dec 70

The aim of this paper was to study atrial natriuretic factor, plasma renin activity and antidiuretic hormone values during paroxysmal atrial arrhythmias with different ventricular rates before and after pharmacological cardioversion and during chronic atrial flutter-fibrillation. The study was carried out: 1) during acute arrhythmias (atrial flutter-fibrillation or supraventricular tachycardia) and after restoration of normal sinus rhythm in 2 patients without heart disease, in 13 with chronic heart disease and in 6 with acute myocardial infarction; 2) during chronic atrial flutter-fibrillation in 5 patients with chronic ischemic heart disease, without congestive heart failure. Atrial natriuretic factor, aldosterone, plasma renin activity and antidiuretic hormone values were measured by radio-immunoassay. During paroxysmal atrial arrhythmias atrial natriuretic factor levels were higher than normal in all patients, particularly in those with supraventricular tachycardia. Most of the aldosterone measurements were above the normal range. As far as plasma renin activity and antidiuretic hormone values are concerned, levels higher than the normal range were found in the patients with severe hemodynamic impairment. Central venous pressure was above normal in all patients except in the 2 without heart disease, and there was a positive correlation between atrial natriuretic factor and central venous pressure values. After restoration of normal sinus rhythm atrial natriuretic factor values returned to normal except in acute myocardial infarction patients, in 1 chronic ischemic heart disease patient with congestive heart failure and in 3 patients with mitral valve disease. In all patients with chronic atrial flutter-fibrillation and in 5 patients with acute atrial flutter-fibrillation and low rate, above normal atrial natriuretic factor values were found with normal central venous pressure values. Atrial distension due to high central venous pressure values, lack of atrial contraction and rhythmic detension of the atrial stretch receptors, may be considered the major stimuli responsible for atrial natriuretic factor release during acute paroxysmal atrial arrhythmias and atrial flutter-fibrillation with low ventricular rate, respectively.
G Ital Cardiol 1989 May
PMID:[Atrial natriuretic factor in acute atrial hyperkinetic arrhythmia and chronic atrial fibrillo-flutter]. 252 75

The present study analyzes the hemodynamics of intracardiac occlusive periods during balloon mitral or aortic valvuloplasty and compares them with immediate plasma levels of atrial natriuretic factor (ANF), vasopressin and renin activity. Forty-nine patients were studied; 33 of them had mitral stenosis and 16 had aortic stenosis. The mean age was 52 +/- 17 years. During dilations pressures were monitored from the ascending aorta and left atrium. Plasma levels of ANF, vasopressin and renin were serially determined at baseline, after diagnostic procedures, within 15 to 30 seconds after the first 2 occlusive dilations, and 1 and 7 hours later. There were no significant changes in plasma renin throughout the study stages. ANF and vasopressin significantly increased after the dilations. These hormonal changes were related to the significant hemodynamic changes observed during intracardiac occlusion. The left atrial pressure correlated directly and significantly (r = 0.54, p less than 0.001) with plasma ANF levels throughout the conditions. On the other hand, the plasma vasopressin also correlated (r = 0.76, p less than 0.001) with systemic pressure in an exponential fashion. These findings show that abrupt releases of ANF and vasopressin occur immediately after intracardiac occlusive periods as a response to the acute and transient hemodynamic changes observed.
Am J Cardiol 1989 Sep 01
PMID:Abrupt homeostatic responses to transient intracardiac occlusion during balloon valvuloplasty. 252 81

The aim of this paper was to study plasma atrial natriuretic factor, renin activity, aldosterone and antidiuretic hormone in low-output heart failure syndromes such as cardiogenic shock, hypovolemic shock and hypotension with bradycardia syndrome. A total of 30 patients were investigated: 10 with cardiogenic shock due to acute myocardial infarction of the anterior wall (systolic and diastolic blood pressure 56.0 +/- 3.7/40.5 +/- 2.0 mmHg; heart rate 119.7 +/- 1.2 beats/min; central venous pressure 16.2 +/- 0.6 cmH2O) (I group), 10 with hypovolemic shock induced by melena in peptic ulcer (systolic and diastolic blood pressure 74.5 +/- 1.5/57.5 +/- 1.7 mmHg; heart rate 111.0 +/- 1.4; central venous pressure 6.3 +/- 0.5 cmH2O) (II group), 10 with hypotension with bradycardia syndrome which occurred in patients during acute myocardial infarction of the inferior wall (systolic and diastolic blood pressure 71.9 +/- 2.0/58.0 +/- 2.6 mmHg; heart rate 52.0 +/- 2.2 beats/min; central venous pressure 4.6 +/- 0.4 cmH2O) (III group). Plasma atrial natriuretic factor values were measured using radioimmunoassay after chromatographic pre-extraction; plasma renin activity, aldosterone and antidiuretic hormone values were calculated using radioimmunoassay. Circulating atrial natriuretic factor was significantly (p less than 0.01) higher in patients with cardiogenic shock (102.4 +/- 7.4 pg/ml) than in healthy volunteers (8.4 +/- 0.3 pg/ml). In the former there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the IInd and IIIrd groups of patients were in the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
G Ital Cardiol 1989 Aug
PMID:[Atrial natriuretic factor in cardiogenic shock, in hypovolemic shock and in the bradycardia-hypotension syndrome following acute myocardial infarction]. 253 Jan 27

Ca2+-mobilizing receptor-induced inositol phospholipid hydrolysis has been studied in cultured endothelial cells (EC) from human aorta, pulmonary artery, and umbilical vein. It was shown that in EC the release of inositol phosphates can be stimulated by histamine, thrombin, serotonin, acetylcholine, carbachol, bradykinin, vasopressin, angiotensin II, platelet-activating factor (PAF), the thromboxane A2 mimetic, U46619, and prostaglandin E2. The most effective agonists were thrombin, histamine, and PAF, producing two- to five-fold increases in inositol phosphate level, and a 50-90% elevation of the level of inositol trisphosphate within 5 min. Effects of other agonists were smaller, although significant. Incubation of EC with histamine or PAF for 1 h resulted in a four- to eight-fold decrease of beta-adrenoreceptor density in the plasma membranes. The activity of isoproterenol-stimulated adenylate cyclase was depressed, and the degree of stimulation by isoproterenol was reduced. Similar effects were obtained after treatment of EC with the protein kinase C activator 4 beta-phorbol 12 beta-myristate 13 alpha-acetate, suggesting a role of protein kinase C in receptor desensitization. It is concluded, that stimulation of inositol phospholipid hydrolysis, and, consequently, activation of protein kinase can cause receptor imbalance in human vascular endothelium. This mechanism may play a pivotal role in the pathogenesis of cardiovascular and pulmonary diseases.
J Mol Cell Cardiol 1989 Feb
PMID:Regulation of phosphoinositide turnover in endothelium from human pulmonary artery, aorta and umbilical vein. Antagonistic action on the beta-adrenoceptor coupled adenylate cyclase system. 254 21

In addition to hypertension and hypercholesterolemia, the third major risk factor in vascular diseases such as atherosclerosis and acute thrombosis is nicotinism, particularly that involving the smoking of cigarettes. Each cigarette smoked, with inhalation, is followed by increases in blood pressure and heart rate due to release of catecholamines and vasopressin. In addition, nicotine intake modifies the metabolism of certain drugs, such as beta-blockers, diminishing their antihypertensive action and hence nullifying the therapeutic benefit. Hypertension in smokers therefore constitutes a real "model" for the pharmacologic study of certain antihypertensives. Clearly the essential aim with any hypertensive subject is discontinuance of smoking, which is difficult to achieve with heavy smokers since genuine drug dependence is involved. There is no "miracle" treatment. It is necessary in each case to study the characteristics of dependence, which is both psychologic and pharmacologic (nicotine being the principal drug). Appropriate, and hence more effective therapies can then be proposed in light of the results obtained.
Ann Cardiol Angeiol (Paris) 1989 Dec 15
PMID:[How to prevent vascular risk related to smoking: an aid to discontinue smoking]. 262 4


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