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 effects of chronic constriction of the thoracic inferior vena cava (TIVCC) on plasma atrial natriuretic factor (pANF) were studied in conscious dogs (n = 5). TIVCC decreased left and right atrial pressure and led to a decrease in pANF concentration from 199 +/- 12 to 104 +/- 14 pg/ml while plasma renin and vasopressin concentrations increased. These hormonal changes were associated with a significant fall in sodium excretion to less than 5 meg/day. pANF remained suppressed during chronic TIVCC as the dogs expanded their extracellular fluid volume and developed ascites. Acute release of TIVCC resulted in abrupt increases in left and right atrial pressure but only a modest rise in pANF from 96 +/- 16 to 185 +/- 45 pg/ml. The magnitude of the rise in pANF (twofold) contrasted sharply with the eightfold increase in sodium excretion that occurred over the first 24 hours. Our data suggest that decrease in atrial pressure below normal results in a decline in pANF, which, acting in concert with the activated renin-angiotensin system and vasopressin, may contribute to sodium retention. On the other hand, during acute release of TIVCC, which markedly increased atrial pressure and sodium excretion, pANF only returned to control levels. These data suggest that ANF release may be attenuated during chronic reduction in atrial pressure and also raise a question concerning the magnitude of the primary role of ANF in this natriuretic response.
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PMID:Plasma atrial natriuretic factor during chronic thoracic inferior vena caval constriction. 296 84

Since its discovery, ANF has provided multitudinous opportunities to explore its relationship to various biologic functions. Hundreds of publications investigating various aspects of this newly discovered hormone system have appeared. ANF exhibits a plethora of direct and indirect biologic activities that oppose the hypervolemic and hypernatremic effects exerted by the renin-aldosterone-angiotensin system. Additionally, ANF and ANF receptors are present in the central and peripheral nervous system, and ANF administered in the brain exerts striking effects relating to vasopressin and water consumption. It thus appears that ANF functions as a neurotransmitter or neuromodulator in consort with its direct peripheral actions. One may anticipate that continued research will uncover more interesting biology and elucidate the interplay between ANF and various control systems responsible for volume and electrolyte homeostasis.
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PMID:Structure and biologic properties of the atrial natriuretic peptides. 296 60

ANF immunoreactivity is present in specific, discrete brain nuclear groups; distinct, ANF-containing axonal projections have been mapped. The major concentration of ANF neurons resides along the walls of the third ventricle, in the anteroventral periventricular region. These cells project to neuroendocrine centers in the septum, medial preoptic area, paraventricular nuclei, and median eminence and to the periventricular thalamic nucleus. A second group of neurons project from the lateral hypothalamic area at least partly to the spinal cord. The third major group of ANF neurons projects from the region of the visceral centers in the pons and brain stem to the mesencephalic interpeduncular nucleus and the hypothalamus. Brain ANF is stored and released as the 24- and 25-amino-acid form, in contrast to plasma, where the 28-amino-acid form predominates, and the atria, where the larger prohormone is the stored form. The control of release of brain ANF appears to differ from that from the heart, as demonstrated during dehydration studies in the rat. CNS effects of ANF are predicted by the presence of specific ANF-binding sites and by the ability of iontophoretically applied ANF to alter single neuron excitability in a dose-related fashion. The major actions of ANF within the brain are well coordinated with its actions in the periphery and seem appropriate to its function as a controller of fluid volume and electrolyte composition. Thus, ANF's ability to oppose the action of vasopressin in the kidney is matched centrally by its potent inhibitory effect on vasopressin release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor and the central nervous system. 296 63

Pharmacological strategies have been employed to manipulate the response to atriopeptin (AP-28; ANF 99-126) in rats. These approaches include: heparin infusion which blocks the natriuresis-diuresis produced by exogenous AP infusion or by acute volume expansion; and autoimmune rats with endogenous antibody that blocks the natriuresis-diuresis produced by administration of exogenous AP or by acute volume expansion in anesthetized rats. Administration of the pressor analog 1-deamino-arg8-vasopressin (dAVP) to rats produces an elevation in systemic and right atrial blood pressure and markedly increases atriopeptin blood levels. The dAVP also produces a delayed natriuresis-diuresis which is effectively blunted in the autoimmune or heparin treated rats. The above approaches provide tools, in the absence of a specific receptor antagonist, with which to validate the intrinsic involvement of AP in physiological, pharmacological, or pathophysiological events.
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PMID:Strategies for the in vivo inhibition of endogenous atriopeptin. 297 57

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

The effects of lysine-vasopressin (VP) and pepsanurin (PU) on the diuretic-saluretic action of ANF were investigated. Anaesthetized female rats under constant intravenous perfusion with isotonic glucose solution (0.6 ml/h/100 g body weight) were used. Blood pressure was recorded continuously and in the urine collected every 20 min, volume, NA and K excretion were measured. In each rat two intravenous boluses of either 2.5 ug synthetic rat atriopeptin II or an equivalent amount of a semipurified rat atrial extract were assayed. Thirty min before the ANF second bolus, an i.v. injection of lysine-vasopressin was given. Doses of 0.1, 1, 5, 10 and 50 mU were used. PU in the dose of 0.5 ml, obtained from 20 ml of human plasma was administered intraperitoneally, 40-60 min before the second bolus of ANF. The smaller doses of VP did not inhibit the urinary response to ANF, and the higher one (50 mU) produced a significant facilitation of ANF effect. Contrariwise, PU produced a considerable inhibition on water, NA and K excretion promoted by ANF.
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PMID:Atrial natriuretic factors (ANF) and antidiuretic agents. 297 32

Effect of elevation of blood atrial natriuretic peptide (rat 1-28 ANF) level on pressor responses and bradycardia elicited by vasopressin (AVP) was compared in conscious normotensive (WKY) and spontaneously hypertensive (SHR) rats 14-16 weeks old, instrumented with arterial and venous catheters 1-2 days prior to the experiment. Blood pressure and heart rate were determined before and after i.v. injection of 2.5, 5.0 and 10.0 ng of AVP under control conditions (infusion of saline) and during infusion of ANF at a rate of 0.3 micrograms kg-1 min-1. Administration of ANF did not influence pressor responsiveness to AVP (determined as a maximum increase of systolic blood pressure) neither in WKY nor in SHR, however, it elongated the pressor response to the lowest dose of AVP in WKY. Atrial natriuretic factor significantly enhanced bradycardic responsiveness to AVP (determined as a maximum decrease of HR) in WKY but not in SHR. Reduction of heart rate in relation to the corresponding elevation of the systolic pressure (delta HR/delta SP) was also significantly greater in WKY but not in SHR. This effect was significant when blood pressure increases elicited by AVP did not exceed 40 mmHg. The results suggest that ANF potentiates reflex bradycardia elicited by AVP. This action may be a mechanism buffering blood pressure increases in response to AVP. Absence of this effect in SHR may be related to the impairment of the reflex control of blood pressure in this strain.
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PMID:Atrial natriuretic factor enhances vasopressin-induced bradycardia in normotensive (WKY) but not in spontaneously hypertensive (SHR) rats. 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 effect of intracerebroventricular (i.c.v.) treatment of rat atrial natriuretic factor III (ANF III; 0.5 microgram) was measured on the arginine-8-vasopressin (AVP) and oxytocin (OXT) contents of rat hypothalamic and limbic brain areas as well as those in the plasma. The hormone concentrations were determined by radioimmunoassay (RIA). The administration of ANF III in conscious euhydrated rats resulted in a significant reduction of both AVP and OXT contents in the hippocampus. Ether anesthesia interfered with the effect of ANF III, since in anesthetized rats ANF III reduced the levels of AVP and OXT in the septal regions, too. ANF III had no effect on the basal plasma AVP and OXT concentrations, however, the peptide inhibited the plasma AVP and OXT elevation induced by hyperosmosis (intraperitoneal injection of 2.5% NaCl). The results suggest that ANF III may be important in the control of the activity of both the peripheral (hypothalamo-neurohypophyseal) and the central (brain) AVP-ergic and OXT-ergic systems.
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PMID:The effect of atrial natriuretic factor on arginine-8-vasopressin and oxytocin levels in various brain regions and plasma. 297 24

Clonidine, an alpha 2-adrenergic agonist, induced a marked, dose-related increase of plasma IR-ANF in normally-hydrated rats. Maximal ANF release was observed at 10 min after injection of 50 micrograms clonidine, rising from 40.5 +/- 4.6 pg/ml (X +/- SEM) to 1064.4 +/- 22.4 pg/ml. This effect on plasma IR-ANF was partially blocked by pretreatment with 0.8 mg naloxone, whereas synthetic Arg8-vasopressin (AVP) did not inhibit clonidine's action. These findings indicate that increased ANF release may be involved in the mechanism of clonidine-induced diuresis. The clonidine's effect on ANF release may be mediated via activation of opioid receptors besides stimulation of alpha 2-adrenergic receptors.
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PMID:Plasma immunoreactive atrial natriuretic factor (IR-ANF) increases markedly after alpha 2-adrenergic stimulation with clonidine in normally-hydrated rats. 303 Mar 13


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