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)

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

Congestive heart failure (CHF) is not only reflected by such mechanical problems as forward- and backward failure, but it is also associated with a complex pattern of compensatory neuro-endocrine mechanisms, e.g., enhanced activity of both the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS); enhanced release of vasopressin from the pituitary gland; enhanced release of the atrial natriuretic factor (ANF) from the cardiac atria. These neuro-endocrine mechanisms not only operate as such but also display a complex pattern of mutual interactions. These mechanisms, though potentially beneficial short-term, may also be harmful when persisting during progression of the disease. For this reason they offer potential targets in the treatment of CHF besides the classical measures aimed directly at improving cardiac contractility. The following groups of drugs are discussed as therapeutic measures that suppress the aforementioned detrimental compensatory mechanisms: various types of vasodilator drugs; diuretics; beta 1-adrenoceptor blocking agents in low dosage; saralasin; ACE-inhibitors. So far, the enhanced release of vasopressin and ANF have not offered realistic new therapeutic targets in CHF, although their pathophysiologic issue is highly relevant.
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PMID:Compensatory changes of sympathetic tone, the renin-angiotensin-aldosterone system, vasopressin, and ANF as potential therapeutic targets in congestive heart failure. 297 94

We studied the effects of alpha-human atrial natriuretic factor (alpha-h-ANF) on diuresis, glomerular filtration rate (GFR), natriuresis, atrial blood pressure (BP), heart rate (HR) and plasmatic levels of aldosterone, renin activity (PRA), antidiuretic hormone (ADH) in 21 patients with congestive heart failure (CHF), (NYHA, class IV) and 15 healthy volunteers. Three different doses (25, 50 and 100 micrograms) of alpha-h-ANF were administered; each subject received only one dose. Protocol was as follows: 2 periods of 30 minutes each before alpha-h-ANF administration; 2 periods of 15 minutes and 3 of 30 minutes each after it. Aldosterone, PRA, ADH and plasmatic level of ANF were measured by radioimmunoassay. In patients with CHF 25 and 50 micrograms of alpha-h-ANF produced a significant increase in diuresis, GFR, and natriuresis but no modification of BP. On the contrary BP decreased significantly after 100 micrograms of alpha-h-ANF, without changes in renal function. In healthy volunteers the effects of alpha-h-ANF appeared simultaneously and to same degree after each dose. Both in patients and healthy subjects alpha-h-ANF administration had little effect on aldosterone, renin and ADH secretion. The effects of alpha-h-ANF in patients with CHF may be caused by a lowered receptor sensitivity due to a high level of ANF and to their different haemodynamic status.
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PMID:[Hemodynamic and renal effects of synthetic atrial natriuretic factor (alpha-h-ANF) in patients with congestive heart failure]. 297 92

The activation of the renin-angiotensin system that occurs during the development of congestive heart failure (CHF) may be accompanied by continued secretion of vasopressin (AVP) in response to non-osmotic stimuli. Increased supine plasma AVP levels (by radio-immunoassay) were found in 31 patients with moderate to severe CHF (11.49 +/- 1.00 pg/ml s.e.m.) 24 h after the last diuretic dose, which correlated with plasma renin activity (PRA) (r = 0.37, P less than 0.05). However, acute inhibition of converting enzyme with captopril did not decrease plasma AVP levels (14.9 +/- 3.9 versus 14.0 +/- 2.8 pg/ml, n = 8). Indeed, in six out of eight patients, plasma AVP actually increased following captopril - presumably secondary to haemodynamic changes. Readministration of captopril after 4 months of captopril treatment, 12 h after the last dose, again did not change AVP levels (9.58 +/- 1.2 versus 13.1 +/- 1.9 pg/ml), whereas changes in haemodynamics, PRA and angiotensin II were as expected and similar to the first test. These results suggest that the acute haemodynamic action of captopril in CHF is not mediated via suppression of vasopressin, although in some patients with non-osmotic vasopressin, excess activation of the renin-angiotensin-aldosterone system might constitute a factor.
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PMID:Plasma vasopressin as influenced by acute and chronic blockade of the renin-angiotensin system. 300 1

The response to ramipril, 10 and 20 mg on consecutive days, in 9 patients with severe (New York Heart Association functional class III or IV) chronic congestive heart failure was measured. Hemodynamic cannulae were placed more than 2 days before ramipril administration to ensure a stable baseline. Dietary sodium (40 mmol daily) and potassium (80 mmol daily) were constant before and during the study, and maintenance doses of digoxin and furosemide (80 to 1,000 mg daily) were continued unchanged. Ramipril induced pronounced, sustained decreases in angiotensin converting enzyme activity, angiotensin II and aldosterone levels, and a reciprocal increase in plasma renin activity. Plasma catecholamines, antidiuretic hormone and cortisol levels were not altered. Urinary sodium and potassium excretion diminished, plasma sodium decreased and plasma potassium increased. Plasma urea and creatinine levels increased. Ramipril treatment resulted in a decrease in systemic arterial pressure that was sustained for 24 hours, a decrease in heart rate and an increase in cardiac index, but little change in pulmonary artery pressure or right atrial pressure. Three patients were drowsy after ramipril administration, and 1 patient had a marked, temporary reduction in urine output. It was concluded that ramipril is a potent, long-acting angiotensin converting-enzyme inhibitor that is likely to be beneficial in patients with severe cardiac failure.
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PMID:Acute hemodynamic, hormonal and electrolyte effects of ramipril in severe congestive heart failure. 303 25

The emergence of diuretic drugs and angiotensin converting enzyme (ACE) inhibitors ranks amongst the major therapeutic advances of modern medicine. The discovery of these drug groups arose largely by chance, yet each has dramatically influenced the treatment of congestive cardiac failure and arterial hypertension. The central role which diuretics have had in the management of both oedema and hypertension hinges on their ability to induce a net renal excretion of solute and water by selective interference with either active or passive ion transport processes in different segments of the nephron. Irrespective of sites of action, the continued antihypertensive action of diuretics is characterized by a reduction in plasma volume and extracellular fluid (ECF) volume that lasts for as long as the diuretic is given. The mechanism of this effect remains unclear but may involve autoregulatory reactions that leave cardiac output unaltered but maintain a sustained reduction in total peripheral resistance. ACE inhibitors also lower blood pressure by decreasing total peripheral resistance, leaving cardiac output, plasma volume and ECF volume unchanged. The detailed way these haemodynamic changes are achieved remains unknown but inhibition of converting enzyme present not only in the kidney but also in many extrarenal tissue sites, appears important. In both hypertension and cardiac failure, however, the kidney acts as a key target organ for ACE inhibitors. The increased renal vascular resistance and inappropriate renal salt excretion are reversed with enhanced renal blood flow and saluresis. Both angiotensin II (AII) and vasopressin-mediated contraction of glomerular mesangial cells is inhibited, making glomerular filtration more efficient. Reduced aldosterone secondary to blockade of AII formation contributes to saluresis whilst encouraging positive potassium balance. ACE inhibition also impairs breakdown of kinins which may contribute to intrarenal and peripheral vasodilation either on their own or via release of prostaglandins and other vasoactive substances. The hypotensive actions of diuretics are potentiated by ACE inhibition primarily through blockade of AII formation and prevention of secondary aldosteronism. In combination, these drugs permit low doses to be used because of their synergistic effects. Caution has to be exercised whenever ACE inhibition is used, without and especially with diuretics, in the management of renovascular hypertension and other low-perfusion states. In these circumstances, AII plays an important autoregulatory role in preserving glomerular filtration through an increase in post-glomerular resistance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evolution of diuretics and ACE inhibitors, their renal and antihypertensive actions--parallels and contrasts. 303 17

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

Because hyponatremia is frequently associated with preceding diuretic treatment and unrestricted fluid intake--conditions which have not been addressed sufficiently in published literature--we studied the pathophysiology and the clinical setting of such hyponatremia in a large group of internal medicine patients. We observed: a) Of an initial 310 patients with chemical hyponatremia only 204 (64%) had an associated plasma hypoosmolality. Since a normal plasma osmolality excludes a disturbance of water metabolism only the 204 patients with hypoosmolar hyponatremia were included in the study. This data shows that plasma osmolality is an essential measurement in any evaluation of hyponatremia. b) In 204 consecutive patients with hypoosmolar hyponatremia the electrolyte disturbance was related to advanced congestive cardiac failure in 25%, decompensated liver cirrhosis in 18%, volume contraction in 28%, syndrome of inappropriate antidiuretic hormone secretion in 19% and renal insufficiency in 4%. c) Plasma vasopressin was measurable in 90% of the 204 patients. It is known that radioimmunoassays to measure vasopressin fail to reliably detect low concentrations of circulating vasopressin (less than 0.5 pg/ml). It may therefore be stated that hypoosmolar hyponatremia was generally characterized by a failure of antidiuretic hormone suppression. d) Mean daily fluid intake of hyponatremic patients was 2.35 +/- 0.15 l. In the presence of stimulated vasopressin this large a fluid intake is bound to worsen the severity of hyponatremia. e) Of 204 patients 126 were treated with diuretics at the time of study. In these patients hyponatremia worsened during such treatments and was associated with evidence of prerenal azotemia. However there were no significant differences between diuretic-treated and -untreated patients with respect to plasma vasopressin stimulation and amount of fluid intake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of diuretics, hormonal derangements, and clinical setting of hyponatremia in medical patients. 305 Feb 65

The effect of captopril on renal function, central hemodynamics and the hormonal status was studied in 14 patients with chronic congestive heart failure in single administration of the drug at a dose of 25 mg and during short-term course therapy at a daily dose of 75 mg for 7 days. Captopril single administration was shown to cause an increase in natriuresis by 121% and diuresis by 120%. Correlation analysis showed that the natriuretic effect of captopril resulted from a decrease in tubular sodium reabsorption which, in its turn, was determined by a decrease in the production of angiotensin II and changes of pritubular circulation. Seven-day course therapy was accompanied by the patients' improved general status, improved indices of hemodynamics, and better tolerance to physical exercise. At the same time diuresis and renal excretion of sodium were above the basal level by 113 and 86%, respectively. It can be assumed that this natriuretic effect was determined by the suppression of angiotensin II, aldosterone and probably norepinephrine and vasopressin production. The analysis has shown that a favorable captopril renal effect is not mediated through improved central hemodynamics but results from changes of the hormonal and neurohumoral status.
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PMID:[Renal effects of captopril in chronic heart failure]. 306 12

Congestive heart failure is a very complex clinical syndrome characterized by a number of important extracardiac features. In an attempt to maintain circulatory homeostasis, there is activation of a number of vasopressor/Na+ retentive forces. Plasma levels of angiotensin, norepinephrine and vasopressin rise, likely contributing to heightened peripheral resistance and antidiuresis. These forces appear to be offset to some extent by vasodilator/Na+ excretion activity in the form of increased prostaglandins, atrial natriuretic factor, and dopamine. There is a complex interplay between these neurohumoral systems in heart failure which is just beginning to be understood.
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PMID:Extracardiac features of heart failure: catecholamines and hormonal changes. 306 12


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