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 pregnancy and placental localization on vascular responses to endogenous vasoconstrictor agents were studied in intramyometrial arteries dissected from myometrial biopsies. The tissues were taken from the lower uterine segment in patients subjected to hysterectomy (n = 8), and in pregnant patients undergoing caesarean section without (n = 8) and with low anterior placental insertion/placenta previa (n = 8). Isometric tension was recorded in vascular ring preparations mounted in organ baths and the contractile effects of angiotensin II, noradrenaline, vasopressin and the TxA2-mimic U46619 were studied. No differences in contractile responses between vessels from the three patient groups were found. When comparing vessels from all the pregnant patients with those from non-pregnant patients, vasopressin showed lower Emax values in preparations from the pregnant women, but otherwise no differences were found. The pD2 values (= -log EC50) ranked the agonists vasopressin greater than U46619 greater than or equal to angiotensin II greater than or equal to noradrenaline (U46619 greater than noradrenaline), while no major differences emerged for the Emax values. The results do not provide evidence that pregnancy and placental localization produce major changes in intramyometrial vascular responses to endogenous vasoconstrictor agents of suggested importance for regulation of human maternal placental resistance.
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PMID:Vascular responses in term pregnant and non-pregnant human uterus. 203 95

The purpose of this study was to determine the effects of converting enzyme inhibition on the contractile reactivity of porcine femoral and intramuscular resistance arteries. The arteries were dissected free of hind limb skeletal muscle from anaesthetized pigs (Micro-pig Yucatan, Charles River), and were mounted in organ chambers and in a myograph system for tension recording. Bradykinin induced an endothelium-dependent relaxation in both vessels which was potentiated by S 10211, a converting enzyme inhibitor, only in resistance arteries. Under basal conditions angiotensin II and angiotensin I did not contract resistance arteries although contraction could be obtained with other agents such as KCl, noradrenaline or vasopressin. If the tone was increased with noradrenaline, angiotensin II and angiotensin I produced an increase in tension. S 10211 inhibited the increase in tension induced by angiotensin I but not by angiotensin II in vessels with and without endothelium. These results suggest that (1) converting enzyme is present in the vascular wall of porcine resistance arteries, (2) this enzyme is not necessarily located on the endothelial cells and, (3) converting enzyme could influence the responsiveness to angiotensin I and bradykinin.
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PMID:Converting enzyme inhibition in isolated porcine resistance artery potentiates bradykinin relaxation. 207 51

Day-old chicks trained on a single-trial passive discrimination avoidance task using a concentrated chemical aversant, methyl anthranilate (MeA), have been shown to exhibit three stages of memory processing; short-, intermediate- and long-term. A similar learning task with the aversant diluted to 20% in ethanol leads to short-and intermediate-term memory, but no long-term memory. Subcutaneous administration of selected doses of the stress-related hormones, noradrenaline, ACTH and vasopressin in close temporal proximity to the training trial, produced long-term memory in chicks trained on the weakly reinforced task, mimicking the outcome of strongly reinforced learning and of retraining with the weakly reinforced task reported previously. These effects are shown to be associated with the production of a nonenergy-dependent phase of the intermediate memory stage, postulated to be necessary for long-term memory consolidation.
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PMID:Memory consolidation of weak training experiences by hormonal treatments. 209 77

Antibodies to oxytocin and noradrenalin were utilized in an immunocytochemical study of the caudal ventrolateral medulla of the rat brainstem. Noradrenalin was visualized by using antibodies to noradrenalin and by means of a silver-gold intensification of diaminobenzidine, whereas oxytocin could be demonstrated in the same section by using the diaminobenzidine precipitate as a marker. At the light microscopic level, oxytocin fibers were densely distributed around the A1 cell bodies. At the ultrastructural level, oxytocin-containing fibers were seen to terminate synaptically onto noradrenalin-containing neurons. Previous studies have shown that electrical stimulation of A1 neurons selectively activates vasopressin-secreting neurons in the supraoptic nucleus. Therefore, separate electrophysiological studies were set up, in which we observed that oxytocin infusions (100-200 pg) into the A1 area enhanced the activity of 16 out of 19 putative vasopressin-secreting neurons and elicited no response from any of 10 oxytocin-secreting neurons. This finding suggests that some of the parvicellular neurons in the paraventricular nucleus of the hypothalamus, from which the A1 neurons derive their oxytocin innervation, can activate the A1 cell group via this peptidergic neurotransmitter. One of the consequences of A1 neuronal activation is enhanced firing of hypothalamic supraoptic (and paraventricular) vasopressin-secreting neurons, and a consequent rise in plasma vasopressin.
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PMID:Oxytocin localization and function in the A1 noradrenergic cell group: ultrastructural and electrophysiological studies. 209 24

Plasma concentrations of plasminogen activator activity (PAA) and factor VIII are partly controlled by circulating adrenaline and vasopressin. Acute rises in PAA and factor VIII occur during electroconvulsive therapy (ECT). To investigate the relationships between vasopressin (aVP), adrenaline and changes in PAA and factor VIII during ECT, 8 female and 2 male patients, median age 57 years (range 39-75) undergoing modified ECT had venous blood samples taken before and at 2 min, 15 min, 60 min and 24 h after cessation of seizure activity. AVP rose from 0.5 before ECT to 35.5 pg/ml at 2 min (P less than 0.005) and fell thereafter. PAA (10(6)/ECLT2) increased from 22 to 69 units (P less than 0.005) over the same time and fell to 13 units at 24 h (P less than 0.02). Tissue plasminogen activator activity (tPA) rose from 162 before to 1447 mIU/ml at 2 min. (P less than 0.005) and its inhibition activity fell from 8 to 3.75 IU/ml (P less than 0.005) over the same time and rose to 10.4 IU/ml after 24 h (P less than 0.02). There were no changes in adrenaline, noradrenaline, factor VIIIc, vWF or fibrinopeptides A and B beta 15-42. AVP correlated with tPA (rs = 0.64, P = 0.0022) and PAA (rs = 0.61, P = 0.004). These results support the hypothesis that aVP has a role in the regulation of fibrinolytic activity mediated by an increase in tPA. The absence of a factor VIII response may indicate that adrenaline is more important in the regulation of factor VIIIc and vWF.
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PMID:The effect of modified electroconvulsive therapy on vasopressin release and haemostasis in man. 212 14

We evaluated the effects of dopamine infusion (1.5 micrograms/Kg/min for 60 min) on secretion of atrial natriuretic factor before raised diuresis could affect extracellular fluid volume and hence peptide release. We investigated ten healthy subjects without cardiovascular, renal or endocrine disease and ten patients with congestive heart failure (New York Heart Association Classes III and IV). The study protocol required four 30 minute clearance periods: 1st basal, 2nd during placebo, 3rd and 4th during dopamine infusion. We measured diuresis, natriuresis, glomerular filtration rate, blood pressure, heart rate, central venous pressure and plasma concentrations of atrial natriuretic factor, noradrenaline, renin activity, aldosterone and antidiuretic hormone. Blood samples were drawn at the midpoint of each clearance period after measuring blood pressure, heart rate and central venous pressure. Atrial natriuretic factor was determined by radioimmunoassay after chromatographic extraction, noradrenaline was measured fluorometrically while plasma renin activity, aldosterone and antidiuretic hormone concentrations were obtained by radioimmunoassay. During dopamine infusion plasma atrial natriuretic factor plasma levels were significantly raised in healthy subjects while high basal values of the peptide in patients with congestive heart failure were significantly reduced; this trend was also evident for noradrenaline levels in both groups. Plasma renin activity, aldosterone and antidiuretic hormone values remained unchanged in healthy subjects, but plasma renin activity and aldosterone levels dropped significantly in congestive heart failure patients. Diuresis, natriuresis and glomerular filtration rate were significantly increased while blood pressure, heart rate and central venous pressure remained unchanged in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of dopamine infusion on the release of atrial natriuretic factor]. 214 May 54

The aim of the present study was to determine whether left atrial size--a likely indicator of atrial stretching--correlates with the plasma concentration of atrial natriuretic peptide and whether this relation is different in patients in sinus rhythm and in those with atrial fibrillation. Arterial plasma concentrations of immunoreactive atrial natriuretic peptide (ir-ANP), adrenaline, noradrenaline, aldosterone, and vasopressin were measured in 13 patients in sinus rhythm without apparent heart failure and in 13 patients in atrial fibrillation. The two groups were matched for left atrial diameter and the ratio of the left atrial diameter to the diameter of the aortic root (assessed by echocardiography). There were no significant differences in age, heart rate, blood pressure, or left ventricular end diastolic diameter between the two groups. Left atrial diameters varied from 33 to 60 mm. The mean (SD) plasma concentration of ir-ANP was significantly higher (35 (21) pmol/l) in the patients with atrial fibrillation than in those in sinus rhythm (12 (11) pmol/l). The concentration of plasma aldosterone was also higher in patients with atrial fibrillation (831 (366) v 523 (211) pmol/l). Concentrations of adrenaline, noradrenaline, and vasopressin were similar in both groups. None of the hormone concentrations correlated with left atrial dimensions. These results indicate that plasma concentrations of ir-ANP and aldosterone are highly sensitive indicators of changes in haemodynamic function during atrial fibrillation. They also underscore the difficulties of correlating echocardiographic assessment of patients with plasma concentrations of a vasoactive hormone.
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PMID:Raised plasma concentrations of atrial natriuretic peptide are independent of left atrial dimensions in patients with chronic atrial fibrillation. 214 16

1. The effect of an intracisternal injection of 20 micrograms kg-1 of acetylcholine was studied on systolic and diastolic blood pressures, heart rate, and plasma levels of noradrenaline, adrenaline, vasopressin, plasma renin activity and atrial natriuretic factor in chloralose-anaesthetized dogs, 8 of which were normal and 7 with diabetes insipidus (deprived of vasopressin secretion by surgical lesion of the hypothalamoneurohypophysial system). 2. Acetylcholine significantly increased systolic and diastolic blood pressures in both groups of animals. However, the rise in blood pressure was significantly shorter lived in the dogs with diabetes insipidus. 3. Acetylcholine significantly increased plasma levels of noradrenaline but not adrenaline in control animals and in dogs with diabetes insipidus. Noradrenaline and adrenaline responses after acetylcholine were not different in the two groups of animals. 4. Acetylcholine induced a significant increase in vasopressin plasma levels only in control animals while in dogs with diabetes insipidus vasopressin remained at nearly undetectable levels. 5. Acetylcholine significantly increased atrial natriuretic factor plasma levels only in control dogs. 6. Although plasma renin activity increased in both groups of animals after the i.c. injection of acetylcholine, this change was not significant in any group. 7. These results suggest that, in the anaesthetized dog, the central injection of acetylcholine induces a rise in blood pressure through both an increase in sympathetic outflow and a release of vasopressin.
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PMID:Cardiovascular effects of central injection of acetylcholine in anaesthetized dogs: a role for vasopressin release. 214 57

Atrial natriuretic peptide, ANP(99-126), is derived from cardiac atrial tissue and has potent effects on salt and water homeostasis, including the inhibition of aldosterone and vasopressin release. Recent studies have also suggested that it may suppress the pituitary-adrenal axis. In addition, N-truncated forms of ANP, such as ANP(103-126), have been identified within the central nervous system, with a prominent hypothalamic localization in the paraventricular nucleus. We have therefore investigated whether ANP(99-126) and ANP(103-126) are able to modulate the release of the principal ACTH-releasing factor, corticotrophin-releasing factor-41 (CRF-41), from the rat hypothalamus in vitro. The static incubation system has been previously described in detail. Male Wistar rats were decapitated between 09.00 and 09.30 h, their hypothalami rapidly removed, and four half-hypothalami incubated for 20-min intervals following a period of stabilization. The effect of the ANP peptides on the basal (B) and KCl (28 mmol/l)-stimulated (S) release of immunoreactive CRF-41 was studied by means of successive incubations in the absence (B1, S1) and presence (B2, S2) of the peptides. The ratios B2:B1 and S2:S1 were compared with parallel control incubations by ANOVA. Neither form of ANP had any effect on the basal release of CRF-41. ANP(99-126) caused a dose-dependent inhibition of CRF-41 release in the concentration range 1-100 nmol (P less than 0.01). ANP(103-126) also suppressed the release of CRF-41 in the concentration range 100 pmol/l-100 nmol/l (P less than 0.01), with a minimum S2:S1 ratio at 10 nmol/l, and a decrease in effect at 100 nmol/l. Finally, the stimulation of CRF-41 release induced by noradrenaline (10 nmol/l and 1 mumol/l) was non-competitively antagonized by 100 nmol ANP(99-126)/l and 10 nmol ANP(103-126)/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic peptides inhibit the release of corticotrophin-releasing factor-41 from the rat hypothalamus in vitro. 214 72

1. Administration of bradykinin caused dose-dependent vasoconstriction in rat isolated perfused mesenteric arteries precontracted with noradrenaline. 2. The vasoconstrictor response was not mediated by BK1-bradykinin receptors. 3. Inhibition of cyclo-oxygenase with indomethacin, aspirin or meclofenamate abolished the vasoconstrictor effect of bradykinin, showing that a member of the arachidonic acid cascade may be involved. 4. Inhibitors of thromboxane synthesis (imidazole and UK 38485) did not affect or only reduced the bradykinin-induced vasoconstriction. 5. The endoperoxide H2/thromboxane A2 receptor antagonist SQ 29548 significantly reduced the vasoconstrictor effect of bradykinin, but did not affect the vasoconstrictor response to noradrenaline, adrenaline, vasopressin, 5-hydroxytryptamine or prostaglandins. 6. The eicosanoid(s) that mediate bradykinin-induced vasoconstriction appear to be synthesized outside the arterial endothelium. 7. The data suggest that the vasoconstrictor effect of bradykinin in the rat isolated mesenteric artery is mediated by vasoconstrictor arachidonic acid metabolites including the cyclic endoperoxides and/or the thromboxanes.
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PMID:Bradykinin-induced vasoconstriction of rat mesenteric arteries precontracted with noradrenaline. 214 65


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