Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

About one third of patients receiving dialysis for end stage renal failure have chronic fluid overload despite advice to restrict their oral fluid intake. To investigate the potential of an angiotensin converting enzyme inhibitor in reducing the urge to drink and consequent gain in weight, a double blind, placebo controlled crossover trial of enalapril was conducted in 25 patients receiving dialysis who had fluid overload. The trial comprised a baseline period of four weeks; two periods of treatment, each of four weeks, during which patients received either placebo or enalapril 5 mg twice each week; and a follow up period of four weeks. Five patients withdrew from the trial, one because of an adverse drug reaction to enalapril. A range of biochemical and behavioural variables was measured during the baseline period, at the completion of periods 1 and 2, and during follow up. These variables included gain in weight between dialysis sessions; blood pressure; plasma concentrations of sodium, angiotensin II, and vasopressin; plasma renin and angiotensin converting enzyme activities; osmolality; and estimations of thirst, intake of fluid, and control of drinking. Enalapril caused a significant reduction in gain in weight between dialysis sessions, thirst, and oral intake of fluid in parallel with significantly increased renin activity, significantly decreased angiotensin converting enzyme activity, and decreased concentrations of angiotensin II. Gain in weight and angiotensin converting enzyme activity returned to baseline values once patients stopped taking enalapril. These results suggest that enalapril may act on the renin-angiotensin system and reduce intake of fluid by inhibiting angiotensin converting enzyme.
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PMID:Controlled trial of enalapril in patients with chronic fluid overload undergoing dialysis. 283

Plasma levels of immunoreactive alpha human atrial natriuretic peptide (IR-ANP) were measured in nine patients with chronic renal failure before and after removal of 1.3-3.7 litres of fluid by ultrafiltration and again during volume repletion with intravenous sodium chloride solution (150 mmol/l: saline). Baseline levels of IR-ANP were elevated but fell by 22% during ultrafiltration. Saline infusion induced a rapid and steep rise in IR-ANP levels which were 150% of baseline while body weight was still 2% below baseline. Changes in plasma renin, angiotensin II, aldosterone and vasopressin during the study were slight compared with the change in IR-ANP, but noradrenaline levels rose threefold during ultrafiltration. There was a significant positive relationship between arterial pressure and IR-ANP levels before and after ultrafiltration. These results lend support to the suggestion that atrial peptides are of physiological importance, especially in states of chronic fluid overload such as chronic renal failure.
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PMID:Exaggerated responsiveness of immunoreactive atrial natriuretic peptide to saline infusion in chronic renal failure. 294 53

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

Inasmuch as atrial natriuretic factor (ANF) is apparently involved causally in the renal response to acute hypervolemia, it became of interest to study cellular mechanisms of release and renal tubular action. To study release mechanisms, freshly excised rat heart atria were incubated in vitro. Activation of the cellular adenylate cyclase system by either beta-adrenergic stimulation or the vasopressin analog deamino-8-D-arginine vasopressin did not result in ANF release. By contrast, activation of the polyphosphoinositide system by alpha-adrenergic stimulation or stimulation of the V1-type vasopressin receptors, and by a calcium ionophore or active phorbol ester, significantly increased natriuretic activity in the medium and reduced it in tissue. It is concluded, therefore, that activation of this latter system is the mechanism for ANF secretion from atrial myocytes. To test the effect of ANF on tubular transport in the medullary collecting duct, microcatheterization was used in rats before and during i.v. infusion of synthetic atrial peptide (23 amino acids). It was found that tubular delivery of salt to this part of the nephron was increased, and that reabsorption in the duct itself was reduced. In control experiments, increased delivery was associated with proportionately increased reabsorption, which demonstrated glomerulotubular balance in the nephron segment under normal conditions. The natriuretic effect of ANF, therefore, was not caused solely by enhanced tubular load, but included specific inhibition of duct sodium reabsorption as an essential feature of the renal response.
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PMID:Mechanisms of release and renal tubular action of atrial natriuretic factor. 301 20

In 83 diabetic patients (23 of them were insulin-dependent) and 34 healthy subjects the influence of water immersion (WI) for 2 hrs on plasma renin activity (PRA), plasma aldosterone and vasopressin (AVP) level was examined. In both examined groups WI exerted a suppressive effect on PRA, plasma aldosterone and AVP level. In this respect only quantitative but not qualitative differences between diabetics and normals were observed. Presence of moderately advanced diabetic nephropathy and autonomic neuropathy influenced only slightly WI induced alterations of the renin-aldosterone system and AVP secretion. In all diabetic patients a defective volumetric mechanism of both the renin-aldosterone system and AVP secretion was stated. In addition in diabetic patients with late diabetic complications a defective osmotic mechanism of AVP secretion was observed. These findings suggest participation also of factors other than hypervolemia and decrease of the plasma osmolality in the mechanism of the observed WI induced suppression of the renin-angiotensin system and AVP secretion in diabetic patients.
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PMID:[Effect of water immersion on plasma renin activity, vasopressin and aldosterone level in diabetics]. 331 Apr 25

Fluid excess can cause hyporeninemia and hypoaldosteronemia in hemodialysis patients. In six patients on CAPD, plasma renin activity (PRA) and plasma aldosterone (PA) were elevated to levels of : PRA 10.2 +/- 2.9 nl (1-5 ng/ml/h), and PA: 47.4 +/- 16.2 (normal 5-20 ng/dl). In 4 patients, data posthemodialysis and later during CAPD revealed that PRA increased from 0.9 +/- 0.3 to 14.1 +/- 4.6 and PA increased from 3.4 +/- 0.3 to 67.4 +/- 24.9 on CAPD (p less than 0.05). Mean arterial pressure was lower on CAPD and serum glucose was higher. No significant difference was seen in weight, hematocrit, BUN, or potassium, however. Plasma volume was not decreased in five CAPD patients: 3619 +/- 358 ml (predicted 3083 +/- 201 ml). Elevated catecholamine levels were seen in CAPD patients: norepinephrine 868.0 +/- 104.1 (normal 358.4 +/- 41.5 pg/ml), epinephrine 386.3 +/- 49.2 (normal 58.3 +/- 10.6 pg/ml). Plasma vasopressin levels were elevated to the range usually seen with hyperosmolality. In eight patients who lost or gained weight on CAPD, levels of PRA and PA changed as expected, but catecholamine levels did not correlate with weight changes. The data suggest that in CAPD patients, PRA and PA may be elevated in association with augmented sympathetic stimulation and elevated vasopressin levels. Serial observations demonstrated that PRA and PA can respond appropriately to changes in body weight, while catecholamine and vasopressin levels seem to be influenced by other factors.
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PMID:Increased levels of plasma renin, aldosterone, catecholamines and vasopressin in chronic ambulatory peritoneal dialysis (CAPD) patients. 331 3

The aim of this work was to study the influence of beta-adrenoreceptor blockade on the adaptation to exercise of one of the hormonal systems (arginine vasopressin) involved in the regulation of blood volume and pressure in spontaneously hypertensive rats (SHR). Systolic blood pressure (SBP) was measured in SHR and WKY rats during 11 wk of swim training. At the end of the training program we determined post-exercise values of plasma arginine-vasopressin (pAVP), osmolality (pOsm), K+ (pK+), Na+ (pNa+), hemoglobin (Hgb), and hematocrit (Hct) in SHR and WKY rats. The following groups were studied: control (C), propranolol treated (PC), swim trained (S), and propranolol-treated and swim-treated (PS). SBP was significantly reduced by swim training or propranolol, bu these beneficial effects on SBP were attenuated when propranolol and swim training were combined. pNa+ and pOsm were significantly reduced by training alone in SHR. This reduction of pNa+ and, consequently, of pOsmol without any modification of other parameters could suggest an Na+ loss. In contrast, the SHR group treated with propranolol alone showed a significant reduction in Hct, suggesting an increased plasma volume without Na+ loss. PS SHR showed a significant reduction of Hgb, Hct, proteins, pNa+, and pOsmol, probably as a consequence of the additive effects of swimming- and propranolol-induced hypervolemia with Na+ loss. The slight and nonsignificant reduction in pAVP observed with either training or propranolol treatment alone became much more pronounced and statistically significant when the 2 treatments were combined. WKY rats showed a much smaller response to exercise and beta-adrenoreceptor blockade than SHR. We conclude that the hypervolemia suggested in PS SHR could be a possible cause of attenuation of the beneficial effects of either swimming or propranolol on SBP.
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PMID:Effects of propranolol and swim-training on blood pressure, plasma electrolytes, and vasopressin in spontaneously hypertensive and normotensive rats. 367 62

We have studied the postoperative diuresis patterns in 116 patients following the removal of a pituitary adenoma using the trans-sphenoidal approach. We observed a normal diuresis (ND) in 55 patients and a hypotonic polyuria (HP) in 61 patients, consisting of water elimination (WE = 45 cases) and transient diabetes insipidus (DI = 16 cases). We investigated the problem of predicting these patterns from eight pre-operative factors by applying stepwise logistic discriminant analysis. We demonstrated that DI was significantly associated with a posterior localization of the adenoma in the pituitary gland and that WE was more frequently observed in cases of suprasellar expansion, in young patients, and in prolactin secreting tumors. Finally, we discuss the pathogenic role of these factors in the occurrence of HP, taking into account inhibition of vasopressin secretion and possible fluid overload.
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PMID:Study of hypotonic polyuria after trans-sphenoidal pituitary adenomectomy. 370 Aug 41

This manuscript emphasizes the physiology of fluid-electrolyte-hormonal responses during the prolonged inactivity of bed rest and water immersion. An understanding of the total mechanism of adaptation (deconditioning) should provide more insight into the conditioning process. Findings that need to be confirmed during bed rest and immersion are: 1) the volume and tissues of origin of fluid shifted to the thorax and head; 2) interstitial fluid pressure changes in muscle and subcutaneous tissue, particularly during immersion; and 3) the composition of the incoming presumably interstitial fluid that contributes to the early hypervolemia. Better resolution of the time course and source of the diuretic fluid is needed. Important data will be forthcoming when hypotheses are tested involving the probable action of the emerging diuretic and natriuretic hormones, between themselves and among vasopressin and aldosterone, on diuresis and blood pressure control.
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PMID:Physiology of fluid and electrolyte responses during inactivity: water immersion and bed rest. 670 76

Experiments were carried out in the anesthetized monkey to determine the influence of acute hypervolemia on plasma vasopressin (ADH) concentration. The administration of an isotonic-isooncotic high molecular weight dextran infusion in two steps, each in an amount equal to 15% of the estimated blood volume, produced substantial elevations of left ventricular end diastolic pressure (17.1 cm H2O); however, no consistent change in mean plasma ADH concentration or mean arterial pressure occurred. The results support the position that in the primate, arterial blood pressure rather than blood volume is the major modulator of ADH secretion when blood volume is increased isoosmotically.
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PMID:Failure of acute intravascular volume expansion to alter plasma vasopressin in the nonhuman primate, Macaca fascicularis. 676 88


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