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 antihypertensive effect of inhibitors of the angiotensin I-converting enzyme (ACE = kininase II) results from their vasodilatory and natriuretic effects as well as their effect on baroreceptor function. In addition to the inhibition of systemic and local angiotensin II formation, other local hormonal systems may also be involved in this effect at multiple target sites. Thus, potentiation of the vasodilator and natriuretic kinin system following inhibition of kininase II is thought to contribute to the persistent hypotensive effect of ACE inhibitors despite normalization of circulating ACE activity. Although increased plasma bradykinin levels cannot be detected, we found that the enhanced kinin-dependent local vascular prostacyclin production can be blunted in vitro by aprotinin, a kallikrein inhibitor. ACE inhibition may affect the atrial natriuretic peptide (ANP) system as the renin-angiotensin system and ANP appear to play antagonistic roles at the peripheral and central nervous system levels. Inhibition of kallikrein or of kininase II were both shown to modulate the natriuretic and vasorelaxant effects of ANP. In hypertensive subjects, we found that ACE inhibition with blood pressure normalization reduces basal and stimulated plasma ANP and blunts the renal sodium excretion in response to saline loading. In contrast, we did not observe effects of acute ACE inhibition in healthy sodium-depleted volunteers on plasma vasopressin under basal conditions or in response to passive tilt. Finally, we investigated the interaction of ACE inhibition with substance P, a powerful endogenous diuretic and natriuretic peptide that may have a transmitter function in the baroreceptor reflex arch.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinin- and non-kinin-mediated interactions of converting enzyme inhibitors with vasoactive hormones. 169 69

Iloprost (ZK 36374; a stable prostacyclin analogue) increases basal as well as potassium-evoked vasopressin and oxytocin secretion from rat neurointermediate lobes in vitro. This finding suggests a possible regulatory role of endogenous prostacyclin in the release of neurohypophysial hormones.
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PMID:Effect of a prostacyclin analogue on the vasopressin and oxytocin secretion in vitro. 172

In accordance with the results of examining 40 children with nephrotic and mixed glomerulonephritis, it has been established that in the pathogenesis of the nephrotic syndrome of paramount importance is imbalance of the output of renal prostanoids, manifesting in the predominance of the vasopressor and proaggregate fraction--thromboxane A2 and in the deficiency of its antagonist prostacyclin that exerts a protective action on glomerular filtration. Sodium and water retention in patients with the nephrotic syndrome favours an increase of the content of antidiuretic hormone and plasma renin activity.
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PMID:[Endogenous vasoactive factors in children with nephrotic syndrome]. 175 19

Dexamethasone 21-acetate (DMS 21-A) time- and dose-dependently suppressed bradykinin-stimulated prostacyclin synthesis in porcine aortic endothelial cells. The suppression was more prominent in the presence of pertussis toxin, which by itself could enhance bradykinin-induced prostacyclin synthesis. The DMS 21-A treatment diminished prostacyclin synthesis also in response to vasopressin. In contrast, it did not affect prostacyclin synthesis in response to arachidonic acid or A23187. Melittin-induced prostacyclin synthesis was reduced only at low doses (1-7 x 10(-7) M). The suppression of bradykinin-induced prostacyclin synthesis by DMS 21-A was completely blocked by cycloheximide. DMS 21-A had no effect on the cellular level of lipocortin I protein, but increased the anti-phospholipase A2 activity in EDTA extracts of the cells. These results suggest that the DMS 21-A treatment induces phospholipase A2 inhibitor protein(s) other than lipocortin I and reduces prostacyclin production in response to limited stimuli.
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PMID:Glucocorticoid treatment reduces prostacyclin synthesis in response to limited stimuli. 182 73

A study of neurohumoral and functional determinants of the advance of Ischemic heart disease in 39 patients with unstable stenocardia with positive results of loading tests (transesophageal electrocardiostimulation and veloergometry) allowed to reveal a significant reduction of the coronary reserve and regional dysfunction of the myocardium that interrelated with changes of the prostacyclin/thromboxane balance, increase of vasopressin with unchanged angiotensin II value and increased marker of the functional state of thrombocytes--beta-thromboglobulin. These changes may be one of the leading links in the pathogenesis of destabilization.
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PMID:[Neurohumoral and functional determinants of destabilization in patients with acute forms of ischemic heart disease]. 183 6

In chronic heart failure, neurohumoral mechanisms play an important role in the regulation of cardiac performance directly, by influencing systolic and diastolic function of the myocardium, and indirectly, by modulating pre- and afterload. The important vasoconstrictor, fluid and sodium retaining factors are the renin-angiotensin-aldosterone system, sympathetic nerve activity and vasopressin; the vasodilator, volume and sodium eliminating factors are atrial natriuretic peptide, vasodilator prostaglandins, such as prostacyclin and prostaglandin E2, dopamine, bradykinin and, possibly, endothelium-derived relaxing factor and vasoactive intestinal peptide. There is evidence from experimental and clinical studies that sympathetic nerve activity is stimulated in the early phase of the disease, as is the secretion of atrial natriuretic peptide, which increases in proportion to an increased preload. In early or mild heart failure, atrial natriuretic peptide suppresses the activity of the renin-angiotensin-aldosterone system, may prevent an increase in peripheral vascular resistance and preserves renal blood flow. In more severe heart failure, the renin-angiotensin-aldosterone system is activated, leading to an increase of peripheral and renal vascular resistance and fluid and sodium retention. This is associated with an increased production of vasodilator prostaglandins. In severe heart failure, mostly in connection with hyponatraemia, a non-osmolar inappropriately high secretion of vasopressin can be demonstrated. These findings suggest that early therapeutic intervention to suppress unfavourable neurohumoral mechanisms or to support protective factors, such as atrial natriuretic peptide, may be of particular importance in the treatment of congestive heart failure, delaying progression of the disease, which would improve survival.
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PMID:Hormones in heart failure--regulation and counterregulation. 183 97

In chronic heart failure, neurohumoral mechanisms play an important role in the regulation of cardiac performance by direct influences on systolic and diastolic function of the myocardium, and indirectly, by modulation of pre- and afterload. Important vasoconstrictor, fluid- and sodium-retaining factors are the renin-angiotensin-aldosterone system, sympathetic nerve activity, and vasopressin; vasodilator, volume, and sodium-eliminating factors are atrial natriuretic peptide, vasodilator prostaglandins like prostacyclin and prostaglandin E2, dopamine, bradykinin, and possibly, endothelial derived relaxing factor (EDRF). There is evidence from experimental and clinical studies that the sympathetic nerve activity is stimulated in the early phase of the disease, as well as is the secretion of atrial natriuretic peptide which increases in relation to a rise in preload. In early or mild heart failure, atrial natriuretic peptide suppresses the activity of the renin-angiotensin-aldosterone system, which may prevent an increase in peripheral vascular resistance and preserve renal blood flow. In more severe heart failure, the renin-angiotensin-aldosterone system is activated, leading to an increase of peripheral and renal vascular resistance and fluid and sodium retention. This is associated with an increased production of vasodilator prostaglandins. In severe heart failure, mostly in connection with hyponatremia, a nonosmolar, inappropriately high secretion of vasopressin can be demonstrated. These findings suggest that early interventions in order to suppress unfavorable neurohumoral mechanisms or to support protective factors like atrial natriuretic peptide may be of particular importance in the treatment of congestive heart failure with the aim of a retardation of the progression of the disease, which would result in an improvement of survival.
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PMID:Role of neuroendocrine mechanisms in the pathogenesis of heart failure. 183 44

Preincubation of rat liver cells (the C-9 cell line) for 25 min with phenylarsine oxide at levels ranging from 0.06 to 0.6 microM amplifies prostaglandin I2 production when subsequently stimulated by platelet activating factor, lysine vasopressin, bradykinin, thapsigargin, and the Ca2+ ionophore, A-23187, but not that stimulated by exogenous arachidonic acid. The amplification is decreased after preincubation for 25 min with 1.8 microM phenylarsine oxide. Preincubation of mouse lymphoma cells (the WEHI-3 cell line) with phenylarsine oxide at levels ranging from 0.06 to 1.8 microM for 60 min does not affect prostaglandin E2 levels but inhibits leukotriene B4 and C4 production stimulated by the Ca(2+)-ionophore, A-23187. Amplification of prostaglandin production by phenylarsine oxide is reversed 100 times more effectively by 2,3-dimercaptopropanol than by 2-mercaptoethanol. Deesterification of lipids appears to be regulated positively in rat liver cells and leukotriene production negatively in mouse lymphoma cells by phosphorylation of tyrosine.
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PMID:Regulation of arachidonic acid metabolism by phenylarsine oxide. 185 23

Sodium vanadate (11 microM) amplified the PGI2 production of rat liver cells (the C-9 cell line) incubated with thrombin, platelet activating factor, lysine-vasopressin, the Ca2(+)-ionophore A-23187, interleukin-1 beta, 12-tetradecanoylphorbol-13-acetate, teleocidin, epidermal growth factor, palytoxin, thapsigargin and colchicine but not that stimulated by exogenous arachidonic acid. Sodium vanadate (2.2 microM) also amplified PGF2 alpha production of dog kidney cells (the MDCK cell line) incubated with norepinephrine and, at 0.4 microM, PGI2 production of bovine aorta smooth muscle cells stimulated by serotonin. Sodium vanadate (55 microM) did not affect production of PGE2 and PGF2 alpha in rat basophil leukemia cells (the RBL-1 cell line) stimulated by the Ca2(+)-ionophore A-23187, but did inhibit synthesis of peptide-containing leukotrienes and 12-hydroxyeicosatetraenoic acid. When used with cultured cells at micromolar concentrations, vanadate is known to inhibit protein tyrosine-phosphate phosphatases. These results suggest that in some cells deesterification of lipids is positively regulated, at least in part, by phosphorylation of tyrosine whereas in leukocytes, lipoxygenase activities are negatively regulated, at least in part, by phosphorylation of tyrosine.
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PMID:Actions of vanadate on arachidonic acid metabolism by cells in culture. 202 Jul 48

Cigarette smoking is associated with an increased risk and extent of advanced atherosclerotic vascular disease in peripheral as well as coronary arteries. The likelihood of claudication, amputation, stroke, abdominal aortic aneurysm, and failure of vascular reconstruction is higher in smokers than nonsmokers. Smoking exerts its deleterious effects through many interactive mechanisms. Nicotine and carbon monoxide produce acute cardiovascular consequences, including altered myocardial performance, tachycardia, hypertension, and vasoconstriction. Smoking injures blood vessel walls by damaging endothelial cells, thus increasing permeability to lipids and other blood components. Among metabolic and biochemical changes induced by smoking are elevated plasma, free fatty acids, elevated vasopressin, and a thrombogenic balance of prostacyclin and thromboxane A2. Chronic smoking is associated with a tendency for increased serum cholesterol, reduced high density lipoprotein, and other lipid effects that contribute to atherosclerosis. In addition to rheologic and hematologic changes from increased erythrocytes, leukocytes, and fibrinogen, smokers have alterations in platelet aggregation and survival that produce thrombosis. Considering the ubiquitous repercussions of this menace, vascular surgeons should play an active role in motivating their patients to quit smoking.
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PMID:The peripheral vascular consequences of smoking. 206 25


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