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)

Conditions like heart failure that augment the activity of neurohumoral mechanisms i.e. the renin-angiotensin systems, sympathetic nerve activity and vasopressin secretion are commonly associated with a decreased effective blood volume and a reduced renal perfusion. This leads to an increased dependence of renal hemodynamics on endogenous renal prostaglandin synthesis as a vasodilator and natriuretic counter-regulating system. We investigated the role of prostaglandins in renal functional control in an experimental setting of congestive heart failure by chronic inhibition of cyclooxygenase by indomethacin. In chronic moderate heart failure plasma levels of prostaglandin E2 and prostacyclin were unchanged whereas the urinary excretion of prostaglandin E2 was significantly increased, indicating an augmented synthesis within the kidney (Figures 1 to 3). After inhibition of prostaglandin synthesis we observed a profound increase of renal vascular resistance associated with a reduction of effective renal plasma flow and renal blood flow. This was mainly due to a constriction of the vas afferens of the glomerulum. This led to an impairment of renal function indicated by an increase of serum creatinine and blood urea nitrogen associated with a reduction of urinary flow and fluid retention (Figures 4 and 5). We also studied in a randomized, double-blind, placebo-controlled, parallel-group trial in 40 patients with congestive heart failure effects of acetylsalicylic acid (500 mg t.i.d.) on renal functional parameters. In patients with normal sodium intake acetylsalicylic acid reduced urinary prostaglandin E2 concentration by 37% which led to a reduction of daily urinary sodium excretion by 29% in comparison to placebo (Figure 6). These results clearly show the importance of vasodilator prostaglandins in the regulation of kidney function in heart failure where inhibition of cyclooxygenase results in profound deterioration of renal perfusion and kidney function and retention of fluid and sodium.
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PMID:[Role of prostaglandins in regulation of kidney function in heart failure]. 206 53

A vasoconstrictor-induced prostacyclin (PGI2) production in a perfused rat heart was found, suggesting a mitigating role of PGI2 on coronary vasoconstriction. Treatment of the heart with cyclooxygenase inhibitors (aspirin or indomethacin) decreased PGI2 production by more than 90% and paradoxically reduced the vasoconstriction response. The attenuating effect of cyclooxygenase blockade suggested that endogenous prostanoids contribute to serotonin-, vasopressin- or U46619-induced vasoconstriction. Two prostaglandin (PG) H2/thromboxane A2 (TXA2) receptor antagonists, i.e., 13-azaprostanoic acid (13-APA) and SQ 29,548 were used to investigate putative endogenous vasoconstrictor prostanoids on the exogenously induced vasoconstriction. Retrogradely perfused (5-6 ml/min) rat hearts were rendered guiescent, yet responsive to stimuli, by local injection of lidocaine to the atrioventricular node. Changes in coronary vascular resistance (i.e., perfusion pressure at constant flow) were monitored and the cardiac effluent was collected for analysis of 6-keto PGF1 alpha (the stable metabolite of PGI2) as well as PGF2 alpha by radioimmunoassay. Three vasoconstrictors, i.e., serotonin, vasopressin and the TXA2/PGH2 analog U46619, as well as authentic PGD2, PGE2 and PGF2 alpha were infused. PGD2, PGE2 and PGF2 alpha exerted a dose-related coronary vasoconstriction, as did U46619, serotonin and vasopressin. Treatment with 13-APA (100 microM) or SQ 29,548 (100 nM) almost abolished U46619-induced vasoconstriction. The addition of PGH2/TXA2 receptor antagonists also significantly reduced the pressor effect of exogenously administered PGs, serotonin and vasopressin, with the exception that SQ 29,548 did not significantly antagonize PGE2-induced vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endogenous vasoconstrictor prostanoids: role in serotonin and vasopressin-induced coronary vasoconstriction. 207 1

In rat aortic smooth muscle cells, vasopressin (AVP) induces prostacyclin (PGI2) production, probably as the consequence of phospholipase C activation. Our study analyzes the effects of phorbol 12-myristate 13-acetate (PMA)-induced protein kinase C (PKC) activation on AVP-induced inositol 1,4,5-trisphosphate formation, cytosolic free Ca2+ concentration [( Ca2+]c), and PGI2 production. PMA rapidly decreased PKC activity in the cytosol of smooth muscle cells, while increasing it transiently in the membranes with a maximum around 20 min. Prior exposure of the cells to PMA resulted in a transient inhibition of both AVP-induced inositol 1,4,5-trisphosphate formation and [Ca2+]c rise. This was inversely correlated with membraneous PKC activity and partially reversed by the PKC inhibitor staurosporine. In contrast, pretreating the cells with PMA markedly potentiated A23187 or AVP-induced PGI2 production. Under those conditions, AVP-induced PGI2 production did not correlate either with PMA-induced membranous PKC activity or with AVP-induced PLC activation. However, this potentiating effect of PMA was reversed by staurosporine and was not mimicked by the 4 alpha-phorbol, an inactive analogue of PMA. Thus, the possibility is raised that, while inhibiting AVP-induced PLC activation, PMA-induced PKC activation increases the Ca2+ sensitivity of the cellular signaling system leading to PGI2 production.
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PMID:Inhibitory and stimulatory effects of phorbol ester on vasopressin-induced cellular responses in cultured rat aortic smooth muscle cells. 211 56

The role of prostaglandins (PG) has been evoked in the mechanism of action of indapamide. Indeed, PG can act in the regulation of the blood pressure (BP) at different levels: vasodilatation, diuretic, natriuretic, antagonism of angiotensin II and vasopressin (VP), action on adrenergic system. To confirm this hypothesis, we studied the action of certain eicosanoids inhibitors on the antihypertensive action of indapamide in the SHR rat, anaesthetized with pentobarbital (40 mg/kg i.p.). Indapamide (3 mg/kg i.p.) induces significant decrease on BP over 60 min. Mepacrine (5 mg/kg i.p.), phospholipase A2 inhibitor, indomethacin (5 mg/kg i.p), cyclo-oxygenase inhibitor, and tranylcypromine (0,1 mg/kg i.p.), prostacyclin synthase inhibitor, antagonize the antihypertensive action of indapamide. In order to eliminate the importance of VP, we used Brattleboro rats (genetically depleted in VP): indapamide (3 mg/kg i.p.) maintains its hypotensive activity. To eliminate the role of kidney in PG synthesis, we have used cyclo-oxygenase extrarenal inhibitor (sulindac) and the bilateral nephrectomy. Sulindac (1,25 mg/kg i.p.) and the bilateral nephrectomy do not remove the hypotensive action of indapamide. These results, demonstrating the PG extrarenal role and probably that of PGI2, localized in the vascular wall, could explain part of the antihypertensive mechanism of indapamide.
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PMID:[Role of prostaglandins in the mechanism of action of indapamide]. 212 58

The antihypertensive action of angiotensin-converting enzyme (ACE) inhibitors may be related to inhibition of systemic and local vascular angiotensin-II formation, to a potentiation of the local vascular kinin system with secondary stimulation of prostacyclin synthesis, and also to their effects on the central nervous system as well as on renal hemodynamics and excretory function. More detailed studies in patients with severe hypertension, previously not adequately controlled by conventional therapy with a diuretic, a beta-blocking agent and a vasodilator dihydralazine, showed that addition of the ACE inhibitor ramipril normalized systolic and diastolic blood pressure (BP) without hypotensive episodes or reflex tachycardia. ACE inhibition caused a change in the baroreceptor set point as we had previously demonstrated in healthy subjects, but baroreceptor sensitivity was not affected and the pressure response to exogenous norepinephrine remained unchanged by ACE inhibition. Despite the significant reduction in BP in our patients, endogenous creatinine clearance remained unaltered. Furthermore, the decrease in BP is accompanied by an initial natriuresis probably contributing to the BP-lowering effect of ACE inhibitors. Decreased proximal tubular reabsorption may include enhanced urate clearance reflected by a decrease in serum urate concentration which we observed despite continuous diuretic treatment. ACE inhibition also prevents secondary aldosteronism and thereby avoids renal potassium loss. In our patients this resulted in a 10% decrease in urinary potassium excretion and a small rise in serum potassium concentration. Redistribution of intrarenal blood flow with increased medullary flow, in addition, will antagonize the hydroosmotic effect of vasopressin, thus resulting in a rise in free-water clearance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiotensin-converting enzyme inhibition in patients with essential hypertension. 225 20

Prostanoid excretion with urine in children suffering from glomerulonephritis indicates that in the kidneys the output of prostacycline decreases and that of thromboxan rises. In glomerulonephritis children prostacycline and prostaglandin E promote the maintenance of glomerular filtration, which is evidenced by the reduction of their output in the stage of chronic renal failure. The growth of renin and antidiuretic hormone synthesis in children suffering from nephrotic glomerulonephritis is not accompanied by the increase of the output of prostaglandin E, their renal antagonist, and may be one of the reasons of the development of the edematous syndrome.
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PMID:[Renal prostaglandins in glomerulonephritis in children]. 225 97

The relationship between portal tributary blood flow (PBF) and hepatic arterial blood flow (HAF) was studied in awake, unrestrained rats with the radiolabeled microsphere technique. Six distinct patterns of response emerged. In group A (PBF+, HAF 0), ethanol, acetate, glucagon, prostacyclin, and a mixed diet increased PBF without a change in HAF; in group B (PBF+, HAF+), adenosine and histamine increased both PBF and HAF; in group C (PBF 0, HAF+), isoflurane and triiodothyronine did not change PBF but increased HAF; and in group D (PBF-, HAF+), halothane and vasopressin decreased PBF and increased HAF. Acute partial portal vein ligation decreased PBF (56%) and increased HAF (436%). Hypoxia (7.5% O2) decreased PBF (28%) and increased HAF (110%). In group E (PBF+, HAF-), acute hepatic artery ligation increased PBF (35%) and reduced HAF (74%), while in group F (PBF-, HAF-), thyroidectomy reduced PBF and HAF (36 and 47%, respectively). All blood flow responses were accompanied by the expected changes in both portal tributary and hepatic arterial vascular resistances. The data suggest that the portal and hepatic arterial vascular territories have regulatory mechanisms that allow for independent changes.
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PMID:Relationship between portal venous and hepatic arterial blood flows: spectrum of response. 226 Jun 56

Plasma levels of glucagon, secretin, norepinephrine, arginine-vasopressin, and prostaglandin biosynthesis in the gastric mucosa were determined in cirrhotic patients with gastric vascular ectasia associated with hypoacidity, in cirrhotics without this lesion, and in healthy controls. Plasma concentrations of glucagon, secretin, and norepinephrine were similar in cirrhotics with gastric vascular ectasia and cirrhotics without this lesion, these concentrations being significantly higher (p less than 0.05) than in healthy controls. However, there was no significant difference between plasma levels of arginine-vasopressin in patients with cirrhosis (with or without gastric vascular ectasia) and those in healthy controls. The biosynthesis of prostaglandin E2 in the antrum of the gastric mucosa was significantly higher in cirrhotics with gastric vascular ectasia than in cirrhotics without this lesion (p less than 0.05) and healthy controls (p less than 0.005). Prostaglandin E2 in the corpus was significantly higher (p less than 0.05) in cirrhotics with gastric vascular ectasia than in healthy controls. The biosynthesis of 6-keto PGF1 alpha (a stable metabolite of prostacyclin) and PGF2 alpha in the corpus and antrum of gastric mucosa was not significantly different in cirrhotics with gastric vascular ectasia, cirrhotics without this lesion and healthy controls. Since prostaglandin E2 has a vasodilator and acid-inhibitory effect, we speculate that high content of this prostanoid in the gastric mucosa may play a role in the pathogenesis of ectatic capillaries and acid inhibition present in some cirrhotic patients.
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PMID:Increased gastric PGE2 biosynthesis in cirrhotic patients with gastric vascular ectasia. 230 36

A total of 119 patients with myocardial infarction hospitalized within 24 hrs from the disease onset were examined. He-Ne laser irradiation of the blood (daily 40 min sessions for 3-5 days) was carried out in 45 patients (Group 1). The rest 74 patients (Group 2) were administered common therapy. A number of biologically active substances were radioimmunoassayed in the blood of 12 Group 1 and 11 Group 2 patients on days 1, 3, and 7 of the disease. The pain syndrome was alleviated in Group 1 patients, in contrast to Group 2 patients, and the frequencies of ventricular arrhythmias, of heart failures, and of the condition recurrences were reduced, as was the mortality rate. Laser therapy resulted in reduction of the activities of the hypophyseoadrenocortical and aldosteron-renin-angiotensin systems. Besides blood levels of dilatants and proaggregants (PGF2 alpha, vasopressin, angiotensin II) reduced in these patients, whereas vasodilating and antiaggregation hormones (PGE, PGI2) levels increased and the PGI2/TxB2 ratio improved.
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PMID:[The use of low-intensity laser irradiation of the blood in myocardial infarction]. 236 94

The experiment on white rats has revealed that water-soluble antioxidant-emoxipin, having obvious membrane modulating effect, does not influence the rate of watering and congestion of the lungs, the speed of reabsorption of fluid from lung tissue, the permeability of the capillary-alveolar barrier both in the blood-tissue direction and vice versa. Preliminary introduction of emoxipin increased the amount of edema fluid in the lungs when noradrenaline, centrogenic and especially vasopressin pulmonary edema developed, but in did not influence the development of vagotomic pulmonary edema. Stimulation of adenylcyclase or introduction of prostacyclin slowed down the development of centrogenic and vasopressin edema of the lungs. On the basis of these data it can be concluded that the intensification of pulmonary edema after emoxipin introduction is connected with its antioxidant activity.
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PMID:[Effects of a membrane modulator derived from 3-hydroxypyridine class on the development of pulmonary edema]. 239 93


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