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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The increased neuroendocrine activity in patients with congestive heart failure appears to be a generalized attempt to maintain blood pressure at the expense of reduced cardiac performance and salt and water retention. It is likely that baroreceptor dysfunction contributes to increased sympathetic nervous system activity in patients with congestive heart failure. The usual tonic inhibitory messages emanating from baro- and mechanoreceptors in the great vessels and heart fail to adjust sympathetic traffic from the brain to the periphery, leading to uninhibited sympathetic tone. Arginine vasopressin and plasma renin activity may be increased secondarily; however, plasma renin activity activation could also be induced by a low-salt diet and diuretic use. Preliminary baseline data indicate that patients with left ventricular dysfunction (ejection fraction less than or equal to 35%) but no or very mild symptoms of heart failure have increased plasma levels of norepinephrine, atrial natriuretic factor and arginine vasopressin, while plasma renin activity is normal, suggesting that neuroendocrine activity contributes to the pathogenesis of congestive heart failure. Neurohormones such as angiotensin II may alter gene expression, leading to changes in the shape and size of the cell. Remodeling of the heart and blood vessels is associated with both heart failure and hypertension. Angiotensin-converting enzyme inhibitors have been demonstrated to retard or reverse the remodeling process under certain experimental conditions. Studies are currently under way to test this possibility in patients.
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PMID:Neuroendocrine activity in congestive heart failure. 222 Jun 3

Arginine vasopressin (AVP) is known to be increased in patients and experimental animals with chronic cardiac failure (CCF). The importance of an increase in biosynthesis of AVP in the hypothalamus has, however, not heretofore been investigated and is the purpose of the present study. CCF secondary to infarction of myocardial tissue was induced by ligation of the left anterior descending coronary artery and sham operated animals served as controls. Four weeks later hypothalamic AVP mRNA was determined by solution hybridization using sense and anti-sense strand RNA. The blood pressure was lower in CCF than sham animals (131.2 +/- 3.1 vs. 112.8 +/- 4.0 mm Hg, P less than 0.05) and the total heart, and right and left ventricle weights were significantly higher in CCF rats. Plasma AVP was higher in CCF (sham 6.78 +/- 0.30; CCF 11.46 +/- 0.64 pg/ml, P less than 0.001) and plasma atrial natriuretic peptide was also higher in CCF than sham animals (205 +/- 36 vs. 554 +/- 56 pg/ml, P less than 0.001). The AVP mRNA in hypothalamus was significantly higher in CCF than sham animals (55.5 +/- 3.7 vs. 95.9 +/- 4.0 pg/micrograms total RNA, P less than 0.001). There was no difference in beta-actin mRNA in the hypothalamus of sham and CCF rats, indicating that the AVP-mRNA increase was specific in CCF. These results therefore demonstrate that increased AVP biosynthesis in the hypothalamus, in addition to release of the hormone from the posterior pituitary, may occur in CCF.
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PMID:Arginine vasopressin gene expression in chronic cardiac failure in rats. 226 64

Acute myocardial infarction is associated with complex neuroendocrine changes, including release of arginine vasopressin, norepinephrine, and epinephrine, and activation of the renin-angiotensin system. Arginine vasopressin levels are maximal on admission, and subsequently fall even in patients in whom left ventricular failure develops. Plasma levels of norepinephrine and epinephrine are at their highest on admission and return to the normal range in patients with uncomplicated infarction, but they remain significantly elevated in patients in whom left ventricular failure or late ventricular arrhythmias develop. In contrast to catecholamines and arginine vasopressin, plasma renin and angiotensin levels are within normal limits on admission in patients without complications but increase by the third day. Patients with left ventricular failure already have increased plasma levels of renin and angiotensin on admission, but further marked and persistent increases occur over the following days. All of the aforementioned hormones may interact to cause systemic or coronary vasoconstriction, which may have short-term adverse hemodynamic consequences. Furthermore, increased afterload may result in infarct expansion and left ventricular dilatation, which will impair left ventricular function still further. Interruption of the cycle of vasoconstriction and worsening left ventricular failure by angiotensin converting enzyme inhibitors may reduce the incidence of heart failure after myocardial infarction.
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PMID:Neuroendocrine changes in acute myocardial infarction. 306

Arginine vasopressin (AVP) regulation was studied in 42 patients with severe heart failure (CHF) and 10 patients without CHF during cardiac catheterization. Plasma AVP levels were elevated in CHF compared with non-CHF patients (2.98 +/- 2.48 vs. 1.01 +/- 0.44 pg/ml, P less than 0.01). In non-CHF patients, osmotic loading with angiographic contrast caused increases in plasma osmolality (283 +/- 4 to 290 +/- 5 mosmol/l, P less than 0.05) and AVP (1.01 +/- 0.44 to 1.79 +/- 0.20 pg/ml, P less than 0.001). In 10 CHF patients, similar osmotic loading produced an increase in plasma osmolality (275 +/- 13 to 288 +/- 17 mosmol/l, P less than 0.05) and an exaggerated rise in plasma AVP (3.61 +/- 3.17 to 16.30 +/- 12.17 pg/ml, P less than 0.001). The increase in plasma AVP per unit increase in osmolality was greater (P less than 0.01) in the CHF patients (1.36 +/- 1.25 pg . mosmol-1 . 1(-1)) than in non-CHF patients (0.18 +/- 0.17). To determine whether improved cardiac performance would lower AVP levels, 18 CHF patients received the experimental agent MDL 17,043, with improved cardiac index (1.9 +/- 0.4 to 3.3 +/- 0.7 1 . min-1 . m-2, P less than 0.001). Plasma AVP levels did not change significantly (1.99 +/- 0.74 to 2.81 +/- 2.06 pg/ml), but significant inverse correlations were found between changes in plasma AVP and changes in mean (r = -0.53) and systolic (r = -0.65) arterial pressure after MDL 17,043 infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma vasopressin response to osmotic and hemodynamic stimuli in heart failure. 315 13

Arginine vasopressin is elevated in congestive heart failure. To determine the effect of arginine vasopressin upon systemic hemodynamics and regional blood flows, we administered the specific inhibitor of the vascular action of vasopressin [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)-tyrosine]-arginine vasopressin [d(CH2)5Tyr(Me)AVP] to 15 dogs with chronic right-heart failure produced by tricuspid avulsion and progressive pulmonary artery constriction. The animals exhibited increased plasma arginine vasopressin and norepinephrine levels. Vasopressin inhibition increased cardiac output and left ventricular dP/dt and dP/dt/P, and it decreased total peripheral vascular resistance, whereas mean aortic pressure did not change significantly. Simultaneously, blood flow increased to skeletal muscle, kidneys, skin, and right and left ventricular myocardium. Plasma catecholamines also increased. Pretreatment with propranolol and prazosin abolished the increases in cardiac output and left ventricular function produced by vasopressin inhibition. Pretreatment also led to a decrease in mean aortic pressure after vasopressor inhibition. In contrast, administration of d(CH)2)5Tyr(Me)AVP to 11 sham-operated animals or administration of normal saline to nine sham-operated and eight heart-failure dogs was without effect either in the absence or in the presence of adrenergic receptor blockade. Thus, arginine vasopressin participates in the control of the circulation in right-sided congestive heart failure, with both a direct constrictor action on blood vessels and an indirect action by inhibition of the sympathetic nervous system.
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PMID:Short-term hemodynamic effects of vasopressin V1-receptor inhibition in chronic right-sided congestive heart failure. 318 Mar 81

Arginine vasopressin levels in 17 neonates with cardiac disease were compared with control levels in 10 healthy newborn infants. Infants with congestive heart failure who were free of left ventricular outflow tract obstruction had a mean level of 80 +/- 18 pg/ml, which was significantly greater than the mean control level (p less than 0.001). Infants with congestive heart failure and left ventricular outflow tract obstruction had a mean vasopressin level of 3 +/- 0.7 pg/ml, which was lower than the mean control level of 6 +/- 0.7 pg/ml (p less than 0.05). The data suggest that impaired forward flow to high pressure sinoaortic and ventricular baroreceptors is necessary for vasopressin release in congestive heart failure. In left ventricular outflow tract obstruction with heart failure these receptors may be impaired or absent, leading to decreased vasopressin release. Low plasma arginine vasopressin may adversely affect circulatory homeostasis.
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PMID:Variable arginine vasopressin levels in neonatal congestive heart failure. 334 66

Arginine vasopressin, a potent vasoconstrictor and regulator of body water, is frequently increased in the plasma of patients with congestive heart failure. Other neurohumoral control networks, such as the sympathetic nervous system and the renin-angiotensin system, also demonstrate increased activity in congestive heart failure, but fail to respond normally to physiologic stress, such as orthostatic tilt. To assess the response of plasma vasopressin to orthostasis in heart failure, vasopressin was measured before and at 10 and 45 minutes during passive upright tilt in 15 patients with congestive heart failure and their response was compared with that in 9 normal control subjects. Arginine vasopressin was measured by radioimmunoassay. In the normal subjects, plasma arginine vasopressin was 5.3 +/- 2.3 pg/ml at control, was unchanged at 10 minutes, but significantly increased to 7.0 +/- 2.5 pg/ml at 45 minutes (p less than 0.05). In contrast, patients with congestive heart failure showed no significant changes in arginine vasopressin levels from the control levels of 11.6 +/- 5.5 pg/ml. Both plasma norepinephrine and renin activity increased in the normal subjects, but failed to increase from higher baselines in patients with congestive heart failure. Thus, plasma arginine vasopressin, like plasma norepinephrine and renin activity, does not increase in response to upright tilt in patients with congestive heart failure. The explanation is not evident but could involve either abnormalities in reflex control of plasma vasopressin in congestive heart failure or in clearance of the hormone during orthostasis.
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PMID:Impaired response of plasma vasopressin to orthostatic stress in patients with congestive heart failure. 635 40

Chronic heart failure is a complex clinical syndrome characterized by many neuroendocrine manifestations by which the organism responds to the reduced cardiac output--the reduced minute volume. In order to ensure the blood flow to vitally important organs in several regions of the circulation vasoconstriction occurs. The plasma noradrenaline (NA) level rises and this correlates with the stage of chronic heart failure. In chronic heart failure the renin production in the kidney and vascular wall rises and thus also the angiotensin II (AG II) formation is increased. AG II is an affective direct arterial constrictor which facilitates NA release from terminal nerve endings and stimulates aldosterone secretion. AG II conditions also myocardial hypertrophy. Arginine vasopressin (AVP) is usually also elevated in chronic heart failure. In vasoconstriction associated with chronic heart failure participates also endothelin, an effective vasoconstrictor substance which modulates the renin-angiotensin-aldosterone system and has also an antinatriuretic effect. As a compensating response to the increased formation of vasoconstrictor substance during chronic heart failure endogenous vasodilatating and natriuretic substances are formed. Another vasodilatating factor is the atrial natriuretic factor (ANF) which is secreted by atrial myocytes as a result of atrial distension, hypernatremia or tachycardia. ANF inhibits renin, aldosterone and AVP formation. The ANF level correlates closely with the grade of chronic heart failure. With advancing heart failure also down regulation of receptors for ANF occurs. Dopamine, a natural precursor of NA, is also a vasodilatating substance and is secreted during stimulation of the sympathetic nerve. In chronic heart failure the formation of vasoconstrictor substances predominates above vasodilating ones.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Neuroendocrine changes in chronic heart failure]. 809 65

Neurohormonal imbalances clearly contribute to the pathophysiology of chronic congestive heart failure. Agents that interfere with the generation or effects of angiotensin II and aldosterone, or which block the effects of excess sympathetic drive, all favorably affect mortality. Arginine vasopressin, through its V(1A) and V(2) receptor-mediated effects, could theoretically also contribute to progression of left ventricular dysfunction and heart failure by aggravating systolic and diastolic wall stress, and by directly stimulating myocardial hypertrophy. Arginine vasopressin levels are increased in congestive heart failure patients; acutely, both V(1A) and V(2) antagonists produce beneficial hemodynamic responses in both clinical and experimental congestive heart failure. Experimental studies also indicate beneficial effects of V(1A) and V(2) antagonists (alone or in combination) on hemodynamics and possibly ventricular remodeling after myocardial injury. Currently, there are no long-term studies of any type of arginine vasopressin antagonist in human heart failure, but both the theoretical rationale and preclinical data would appear to justify such efforts.
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PMID:Congestive heart failure: potential role of arginine vasopressin antagonists in the therapy of heart failure. 1236 87

Despite diuretics being used to relieve the fluid retention/congestion associated with heart failure (HF), patients with HF are commonly hospitalised due to progressive volume retention with an increase in body weight and the deterioration of symptoms. Arginine vasopressin acts at vasopressin V2 receptors in the kidney as an antidiuretic. Tolvaptan is an orally-active selective V2-receptor antagonist. In the Acute and Chronic Therapeutic Impact of a Vasopressin antagonist in Congestive Heart Failure trial of patients hospitalised with HF, tolvaptan 30 mg/day increased urine volume and induced a weight loss of 3.3 kg at discharge (placebo; 1.9 kg). In post hoc analyses, mortality was lower with tolvaptan in patients with renal impairment and severe congestion, compared to placebo. Thus, it seems that tolvaptan is an advancement in the treatment of severely decompensated HF.
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PMID:Is vasopressin-receptor antagonism an advancement in the treatment of heart failure? 1511 14


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