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)

The mechanism of hyponatremia associated with pneumonia has been debated. In particular, the responsibility of inappropriate antidiuretic hormone secretion has been questioned. We have shown that inappropriate antidiuretic hormone secretion is a nearly constant finding during pneumonia and is roughly proportional to the extent of pneumonia. Nevertheless, it must be emphasized that extracellular fluid volume may be increased, diminished or normal during pneumonia, depending on the underlying condition (congestive heart failure, cirrhosis) or on the importance of extrarenal losses (sweats, fever). Careful clinical and laboratory assessment of extracellular fluid volume should enable adequate therapy.
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PMID:[Hyponatremia of acute pulmonary infections]. 226 57

Central alpha-adrenoceptor agonists (methyldopa, clonidine, guanabenz) decrease sympathetic outflow and renin and vasopressin secretion as well as increase parasympathetic activity. These drugs are commonly employed as antihypertensives. Two other conditions, chronic heart failure and ischemic heart disease, may also benefit from central alpha-adrenergic stimulation. In both acute and chronic heart failure, central alpha-adrenoceptor agonists reduced cardiac work load by decreasing heart rate, systemic arterial pressure and reducing venous tone. Also, plasma catecholamines were decreased. Exercise at comparable work loads was achieved at a lower pressure-rate product and effort capacity was sometimes increased. Central alpha-adrenoceptor agonists increased effort capacity in patients with ischemic heart disease and angina pectoris. Again, the benefits are thought to be decreased heart rate, systemic arterial blood pressure and rate-pressure products during exercise; catecholamines are reduced in these patients as well. Central alpha-adrenoceptor agonists offer another avenue of approach to alter neurohumoral factors in congestive heart failure and ischemic heart disease and thereby produce beneficial hemodynamic response.
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PMID:Central alpha-adrenergic agonists in chronic heart failure and ischemic heart disease. 241 48

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 should be more specific in action than the presently available and very successful converting enzyme inhibitors.
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PMID:Circulatory basis for the use of angiotensin converting enzyme inhibitors in hypertension and cardiac failure. 242 88

The effects of human alpha-natriuretic peptide (alpha-ANP) were investigated in seven patients with severe congestive heart failure by incremental bolus injections and by a continuous infusion for 30 min. alpha-ANP was measured in plasma before and after administration. We found a significant inverse correlation between basal levels of alpha-ANP and cardiac output. The administration of alpha-ANP resulted in a fall of peripheral vascular resistance, an increase in cardiac output, a relatively small decrease in blood pressure, and almost no change in pulmonary arterial pressure. alpha-ANP inhibits aldosterone and cortisol secretion and enhances diuresis and urinary sodium and potassium excretion. Plasma adrenocorticotropic hormone was reduced in two of the patients after the continuous infusion. Plasma renin concentration, norepinephrine, vasopressin, and plasma levels of 6-keto prostaglandin F1-alpha and prostaglandin E2 were unchanged. A small but significant decrease of serum potassium was observed.
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PMID:Human atrial natriuretic peptide: plasma levels, hemodynamic, hormonal, and renal effects in patients with severe congestive heart failure. 243 34

In hypoosmolar hyponatremia, vasopressin is commonly observed to be less than maximally suppressed. This is attributed to the presence of nonosmolar vasopressin stimuli. However, the exact relationship of nonsuppressed antidiuretic hormone to specific circulatory parameters is controversial. Therefore, in the present study, we examined this question in 100 hypoosmolar hyponatremic patients in the Department of Medicine. Despite plasma hypoosmolality, vasopressin was found to be measurable in 92% of patients. Seventy patients suffered from edematous disorders (congestive heart failure, cirrhosis) or volume contraction per se; in these patients we observed unequivocal, though indirect, evidence of advanced circulatory alterations. These were associated with hyponatremia and nonsuppressed vasopressin. However, the latter could not be related directly to a specific circulatory parameter such as mean arterial blood pressure, creatinine clearance, plasma renin activity (PRA), norepinephrine, or aldosterone. However, patients with nondetectable vasopressin (n = 8) differed significantly from those with high vasopressin concentrations (n = 8: PADH greater than 9 pg/ml); in the latter, pulse rate (104 +/- 3 vs. 82 +/- 5 beats/min), plasma urea concentration (90 +/- 5 vs. 32 +/- 5 mg/dl), plasma urate concentration (7.2 +/- 0.8 vs. 3.6 +/- 0.8 mg/dl), and PRA (36 +/- 7 vs. 9.5 +/- 4.6 ng AI/ml/h) were all significantly higher than in the former. It is concluded that, in hyponatremia, the relationship between circulatory impairment and vasopressin is complex.
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PMID:Vasopressin in hyponatremia: what stimuli? 243 81

The hemodynamic and hormonal changes produced by adriamycin-induced cardiomyopathic congestive heart failure in rabbits were studied. Adriamycin cardiomyopathy in rabbits led to ventricular dilatation, pleural and pericardial effusions, hepatic congestion, and ascites. These pathological changes were associated with the maintenance of a normal blood pressure but a lowered cardiac output and increased total peripheral resistance. Plasma renin activity and plasma norepinephrine were increased twofold in rabbits with congestive cardiac failure. However, plasma vasopressin and osmolality were normal, whereas an increased vascular sensitivity to the infusion of exogenous vasopressin was demonstrated. Despite the normal levels of plasma vasopressin, administration of a specific vascular vasopressin antagonist led to a fall in blood pressure, a significant increase in cardiac output, and a decrease in total peripheral resistance. No such hemodynamic changes occurred on infusing normal rabbits with the vascular vasopressin antagonist, nor did any significant hemodynamic changes occur on injecting vehicle in rabbits with heart failure. These results suggest that in adriamycin-induced cardiomyopathic heart failure in rabbits, there is activation of the renin-angiotensin system and the sympathetic nervous system together with an increased sensitivity to vasopressin. These three hormonal systems help to maintain blood pressure by increasing total peripheral resistance in this experimental model of heart failure.
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PMID:Role of vasopressin in experimental congestive cardiac failure. 243 82

Atrial natriuretic peptides (ANP) exert vasodilating and natriuretic actions. The present study was undertaken to test the effect of low dose infusions of synthetic ANP on hemodynamic and humoral variables of patients with severe heart failure. Eight patients, aged 26 to 71 years, with severe congestive heart failure due to ischemic heart disease or idiopathic dilated cardiomyopathy were included in the study. Synthetic human (3-28) ANP was infused at doses ranging from 0.5 to 2 micrograms/min for up to 3 h. Pulmonary capillary wedge pressure fell from 24 +/- 1 to 16 +/- 2 mm Hg (mean +/- SEM) (p less than 0.01) and cardiac index tended to rise from 2 +/- 0.2 to 2.3 +/- 0.2 L/min/m2 (NS), while blood pressure and heart rate did not change. One patient experienced a marked drop in pulmonary capillary wedge and arterial blood pressure that necessitated the administration of saline. ANP infusion did not alter plasma renin activity or plasma aldosterone, norepinephrine, or vasopressin levels. It decreased plasma epinephrine levels from 0.472 +/- 0.077 to 0.267 +/- 0.024 nmol/L (p less than 0.05). Plasma ANP levels were markedly elevated in all patients before initiating the infusion. They had no predictive value for the hemodynamic response to exogenous ANP. No correlation was observed between the hemodynamic effects of ANP and those induced by the subsequently administered converting enzyme inhibitor captopril, which seemed to improve cardiac function more consistently.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Infusion of atrial natriuretic peptide to patients with congestive heart failure. 246 56

PGI2, or prostacyclin, and PGE2 are major derivatives of arachidonic acid. Arachidonic acid is converted by the cyclooxygenase enzyme to intermediate prostaglandin endoperoxides which are then enzymatically converted to PGI2 and PGE2 as well as to thromboxane A2 and PGF2 alpha. Aspirin and other nonsteroidal anti-inflammatory drugs inhibit the cyclooxygenase enzyme thereby reducing the amount of PGE2 and PGI2 produced. In the kidney, major stimuli of prostaglandin synthesis include vasoconstrictor hormones such as angiotensin II, vasopressin, endothelin and norepinephrine. Renal PGI2 and PGE2 synthesis is also increased after renal ischemia, immune injury to the kidney, and with renal parenchymal disease. Renal prostaglandin production also increases with severe arteriosclerotic cardiovascular disease, congestive heart failure, and severe hepatic disease. The increment of renal prostaglandin synthesis is important since PGI2 and PGE2 act as modulators of renal ischemia and vasoconstriction. The modulatory action leads to a negative feedback loop through which PGE2 and PGI2 and renal blood vessels in glomeruli reduce the vasoconstrictor action of the agonist, such as angiotensin II or norepinephrine. Nonsteroidal anti-inflammatory drugs can have nephrotoxic effects if they are used in clinical situations in which renal prostaglandin synthesis has increased compensatorily. In other words, the administration of indomethacin or other prostaglandin inhibitory drugs will reduce renal blood flow and glomerular filtration rate in patients with congestive heart failure, significant hepatic disease, or renal ischemia and vasoconstriction. PGI2 and PGE2 may have additional beneficial effects within the kidney in addition to being vasodilatory.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostaglandin I2 and the kidney. 251 64

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)
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PMID:Relation of atrial natriuretic factor to vasoconstrictor hormones and regional blood flow in congestive heart failure. 252 Dec 70

Atrial natriuretic factor (ANF) is a humoral agent isolated in recent years from cardiac atrial tissue, and produced by atrial cardiocytes as a peptide precursor containing 152 amino acids. In secretory atrial granules, it is stored in reserve form as a prohormone and released into circulation as a 28-amino acid peptide from the C-terminal portion of the peptide precursor representing the active circulating hormone. ANF possesses potent natriuretic, myorelaxant, vasodilatory and blood pressure-lowering properties. Besides, it inhibits renin, aldosterone and vasopressin secretion. It is present also in the CNS and its function is closely related to the sympathetics nerves. By its direct renal and vascular effect, renin-angiotensin-aldosterone system and vasopressin inhibition and, by its neuromodulatory action on the central and sympathetic nerves, ANF plays an important role in electrolyte, volume and pressure homeostasis. The development of a radioimmunoassay for ANF determination in the plasma of rats and man enabled us to follow up its changes under various experimental conditions (water deprivation, increased or decreased salt intake, effect of anaesthetics, ontogenetic changes in ANF concentration during development of hypertension in the spontaneously hypertensive rat) and in clinical studies (effect of ECV expansion in controls, arterial hypertension, liver cirrhosis as well as ANF changes in congestive heart failure or chronic renal failure). These findings of ours have supported the concept that ANF represents an important adaptive and corrective mechanism mobilized during intravascular volume and blood pressure changes in an effort to normalize these. ANF is expected to find use also in the treatment of oedema, arterial hypertension and acute renal failure.
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PMID:Atrial natriuretic factor and its role in the regulation of electrolyte, volume and pressure homeostasis. 252 70


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