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)

We have exposed primary dispersed hypothalamic cultures from 14-day-old fetal Sprague-Dawley rats to substances known to either elevate adenosine 3',5'-cyclic monophosphate (cAMP) levels or increase vasopressin (VP) secretion. The levels of VP in the medium collected from the cultures were determined by radioimmunoassay, and the number of neurophysin (NP)-positive cells after immunohistochemistry was counted. cAMP-elevating agents, 3-isobutyl-1-methylxanthine (200 microM) and forskolin (25 microM), in combination (I-F) maintained NP synthesis and VP secretion in 19-day cultures. I-F replacement by K+ (28 mM), isoproterenol (10 microM), glutamate (10 microM), or bicuculline (10 microM) during the last week of culture resulted in maintenance of NP expression and transient stimulation of VP secretion, but these agents did not induce NP expression independently of I-F treatment. In contrast, exposure to the dopamine D1 agonist SKF-38393 (10 microM) significantly increased NP expression independently and after replacement of I-F. Dopamine D1A receptors were detected by immunofluorescence on NP-expressing cells, providing a morphological basis for this response. These results suggest a role for D1A receptors in the regulation of VP gene expression.
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PMID:Neurophysin expression is stimulated by dopamine D1 agonist in dispersed hypothalamic cultures. 877 72

The modulation of the production of prostacyclin and thromboxane from cat and cat aortic tissue slices by different vasoactive agents has been studied in order to reveal whether the release of these main two vasoactive prostanoids goes in parallel or may be controlled independently. Norepinephrine, isoproterenol, phentolamine, propranolol, angiotensin II, vasopressin, bradykinin, thrombin, verapamil, gallopamil, dopamine or methionin enkephalin were added to the incubation medium and 6-keto-PGF1 alpha (the stable metabolite of prostacyclin) and TxB2 (the stable metabolite of thromboxane) were determined in the supernatant by radioimmunoassay. The ratio of the release of prostacyclin and thromboxane was computed. Norepinephrine increased both prostacyclin and thromboxane release. Isoproterenol increased the ratio of prostacyclin and thromboxane released in cat aortic tissue slices. Phentolamine and propranolol had no effects. Angiotensin II induced a slight but statistically insignificant increase in the ratio of the two prostanoids released. Vasopressin increased thromboxane release only. Bradykinin stimulated the prostacyclin while thrombin stimulated the thromboxane release. Verapamil decreased both prostacyclin and thromboxane production. Gallopamil decreased prostacyclin release and increased thromboxane release from vessel wall slices in a certain concentration range causing a characteristic dose dependent minimum in the ratio of prostacyclin and thromboxane release. Dopamine separately increased prostacyclin release while enkephalin had no significant effect. The data obtained show that in vascular tissue some unidentified yet cytophysiological mechanisms might exist which specifically control the activities of the prostacyclin synthase and thromboxane synthase enzymes.
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PMID:Prostacyclin and thromboxane production of rat and cat arterial tissue is altered independently by several vasoactive substances. 890 22

1. Systemic administration of a dopamine D2 receptor agonist, such as quinpirole, causes a centrally mediated rise in blood pressure (BP) with a maximum at 1-2 min after injection. At 30 min after injection, when BP has returned to baseline, further treatment with these drugs has little effect on BP. Moreover, the antihypertensive effects of sympathoinhibitory drugs, such as clonidine and rilmenidine, is markedly inhibited. Increased circulating levels of vasopressin contribute to the initial rise in BP, but return to baseline thereafter. Differential changes in sympathetic vasomotor tone may be involved in the apparent desensitization induced by quinpirole. 2. Stimulation of the region of origin of the mesolimbic dopamine (DA) system in the brain, the ventral tegmental area, causes a long-lasting increase in BP. In this model, circulating levels of vasopressin are moderately increased through a non-dopaminergic mechanism. Dopaminergic stimulation causes a functional potentiation of the effect of vasopressin, resulting in an increase in BP. 3. Spontaneously hypertensive rats (SHR) display several changes in central dopaminergic responses. Dopamine levels in the brain are normal, while resting DA activity appears reduced. Partial depletion of forebrain DA levels, particularly in the nigrostriatal system, causes an inhibition of the development of hypertension and normalizes deficient functional responses to dopaminergic drugs in the SHR. 4. These results show that brain DA is involved in several aspects of cardiovascular regulation and may be involved in the development of hypertension. The widespread involvement of brain DA systems in behavioural, hormonal and cardiovascular mechanisms suggests that these systems play an important role in the integration of stress and environmental stimuli with homeostatic mechanisms in the body.
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PMID:Pressor responses to brain dopaminergic stimulation. 931 86

The recovery of pancreatic islet cells from cadaveric donors for allotransplantation may depend on the functional condition of the pancreas of the donor prior to organ harvesting. We examined donor hemodynamic and biochemical parameters and their effects on the subsequent yield of islet cells after harvesting. All pancreata were flushed and preserved in University of Wisconsin (UW) solution and digested using automated method within 8 hours. In the first analysis, digestions were divided into high-yield (> 2000 IEQ/g pancreas), and low-yield (< 2000 IEQ/g) groups and donor variables were averaged for each group. Donors whose pancreata yielded > 2000 IEQ/g received significantly greater amounts of Dopamine (14.43 micrograms/kg/min vs 9.35 mg/kg/min, p = 0.05). The daily urine output between groups was also significantly different. Maximum systolic blood pressure (SBP), minimum systolic blood pressure, use of vasopressin, length of hospitalization, and maximum base deficit were compared between the two groups. Less severe hypoglycemia (lowest blood glucose 143 mg/dL vs 107 mg/dL, p = 0.02) and lower amylase levels (36.2 U vs 80.7, p = 0.07 were noted in the high-yield group. A trend towards higher islet yields was associated with lowest hourly urine output > 60 (2040 IEQ/g vs 1649 IEQ/g p = 0.09), maximum SBP > 200 (2097 vs 1673, p = 0.07, and surprisingly, lowest SBP below 80 (2013 vs 1742, p < 0.1). Amount of fluids administered prior to procurement had no influence on islet yield. In conclusion, hemodynamic variables such as urine output, systolic blood pressure, and degree of pressor support were modestly associated with successful islet isolation. The preliminary data suggest that better multifactor donor analysis is imperative for standardization and monitoring of multiorgan donors. The association of higher blood glucose levels with successful isolation may also be related to resuscitation with dextrose-containing fluids.
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PMID:The effect of clinical and biochemical donor parameters on pancreatic islet isolation yield from cadaveric organ donors. 986 41

Patients undergoing surgery for idiopathic scoliosis were studied to determine the incidence and aetiology of oliguria during the perioperative period and to evaluate the efficacy of low dose dopamine in preventing its occurrence. Thirty patients, aged 6-18 years undergoing elective surgery were studied. Anaesthesia was standardized. Patients were randomized to receive either dopamine infusion (3 micrograms.kg-1.min-1) (Group A) (n = 15) or dextrose infusion (control) (Group B) (n = 15). Serum and urinary electrolytes and osmolalities and serum antidiuretic hormone (ADH) concentrations were measured. Urine output and haemodynamic parameters were recorded. Intraoperative oliguria occurred in 7% of patients in Group A and 47% in Group B (P < 0.05). Postoperative oliguria occurred in 20% of patients in Group A and 47% in Group B (P > 0.05). Urine and serum biochemical analysis revealed a statistically significant decrease in serum sodium and osmolality (P < 0.005) and an increase in urinary sodium and osmolality in both groups. Serum ADH concentrations were increased in both groups (P < 0.05), returning to baseline 18 h postoperatively. We conclude that oliguria during corrective spinal surgery occurs in association with excess ADH secretion as opposed to perioperative hypovolaemia. Dopamine increases urine output in the perioperative period but does not prevent the release of ADH and its subsequent biochemical effects.
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PMID:Oliguria during corrective spinal surgery for idiopathic scoliosis: the role of antidiuretic hormone. 1059 54

The aim of this study was to pursue the roles of the catecholamine receptors in the anteroventral third ventricular region (AV3V), a cerebral site engaged in various stress responses, in prostaglandin (PG) E2-evoked vasopressin (AVP) release and cardiovascular action. Experiments were conducted in conscious rats in which cerebral and vascular cannulae had been implanted chronically. Local infusion (0.5 microliter, 1 min) of dopamine (150 nmol), a D1-dopaminergic agonist SKF 38393 (17 nmol) and an alpha-adrenergic agonist phenylephrine (150 nmol), as well as PGE2 (7 nmol), into the AV3V enhanced plasma AVP 5 min later, without affecting plasma osmolality and electrolytes. In contrast to the increases in both arterial pressure and heart rate observed when PGE2 was applied, dopamine and SKF 38393 did not affect these variables, and phenylephrine elevated only arterial pressure. The AV3V infusion of a beta-agonist isoproterenol (100 nmol) did not change plasma AVP, although it decreased arterial pressure and increased heart rate. The increase in plasma AVP by dopamine was not blocked by the preinfusion of the D2-antagonist sulpiride (13 nmol) into the AV3V 10 min before, but was abolished by that of the D1-antagonist SCH-23390 (8 nmol). The effects of phenylephrine on both plasma AVP and the blood pressure were prevented by the preadministration of the alpha-antagonist phenoxybenzamine (13 nmol). However, the pretreatments with phenoxybenzamine, sulpiride or SCH 23390 did not inhibit the responses of AVP, arterial pressure and heart rate caused by PGE2. These antagonists were without significant effect on AVP and other variables when given alone. The infusion sites of PGE2 and the other drugs identified histologically included the AV3V structures such as the organum vasculosum laminae terminalis or its vicinity, median preoptic nucleus, medial preoptic nucleus and periventricular hypothalamic nucleus. Dopamine or phenylephrine administered into the cerebral ventricle at the same dose as used in the AV3V application did not exert a significant effect on plasma AVP, arterial pressure and heart rate. These results suggest that catecholamine receptors in the AV3V may not be involved in the AVP-secreting, tachycardiac and pressor responses evoked by topical action of PGE2 on this area, despite their ability to influence hormone release and cardiovascular function.
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PMID:Negligible role of catecholaminergic receptors in the anteroventral third ventricular region in mediating vasopressin-releasing and cardiovascular actions of prostaglandin E2. 1063 27

Dopamine modulates cardiovascular function by actions in the central and peripheral nervous system, by altering the secretion/release of prolactin, pro-opiomelanocortin, vasopressin, aldosterone, and renin, and by directly affecting renal function. Dopamine produced by the renal proximal tubule exerts an autocrine/paracrine action via two classes of dopamine receptors, D1-like (D1 and D5) and D2-like (D2, D3, and D4), that are differentially expressed along the nephron. The autocrine/paracrine function of dopamine, manifested by tubular rather than by haemodynamic mechanisms, becomes most evident during extracellular fluid volume expansion. This renal autocrine/paracrine function is lost in essential hypertension and in some animal models of genetic hypertension. The molecular basis for the dopaminergic dysfunction in hypertension may involve an abnormal post-translational modification of dopamine receptors.
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PMID:D1 dopamine receptor signalling defect in spontaneous hypertension. 1069 8

During the past decade, it has become evident that dopamine plays an important role in the regulation of fluid and electrolyte balance and blood pressure. Dopamine exerts its actions through two families of dopamine receptors, designated D1-like and D2-like, which are identical in the brain and in peripheral tissues. The two D1-like receptors--D1 and D5 receptors--expressed in mammals are linked to stimulation of adenylyl cyclase. The three D2-like receptors--D2, D3, and D4,--are linked to inhibition of adenylyl cyclase. Dopamine affects fluid and electrolyte balance by regulation of renal excretion of electrolytes and water through actions on renal hemodynamics and tubular epithelial transport and by modulation of the secretion and/or action of vasopressin, renin, aldosterone, catecholamines, and endothelin B receptors (ETB) receptors. It also affects fluid and sodium intake by way of "appetite" centers in the brain and alterations of gastrointestinal tract transport. The production of dopamine in neural and non-neural tissues and the presence of receptors in these tissues suggest that dopamine can act in an autocrine or paracrine fashion. This renal autocrine-paracrine function, which becomes most evident during extracellular fluid volume expansion, is lost in essential hypertension and in some animal models of genetic hypertension. This deficit may be caused by abnormalities in renal dopamine production and polymorphisms or abnormal post-translational modification and regulation of dopamine receptor subtypes.
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PMID:Renal dopamine and sodium homeostasis. 1098 Nov 46

The neural control of the subcommissural organ (SCO) has been partially characterized. The best known input is an important serotonergic innervation in the SCO of several mammals. In the rat, this innervation comes from raphe nuclei and appears to exert an inhibitory effect on the SCO activity. A GABAergic innervation has also been shown in the SCO of the rat and frog Rana perezi. In the rat, GABA and the enzyme glutamate decarboxylase are involved in the SCO innervation. GABA is taken up by some secretory ependymocytes and nerve terminals, coexisting with serotonin in a population of synaptic terminals. Dopamine, noradrenaline, and different neuropeptides such as LH-RH, vasopressin, vasotocin, oxytocin, mesotocin, substance P, alpha-neoendorphin, and galanin are also involved in SCO innervation. In the bovine SCO, an important number of fibers containing tyrosine hydroxylase are present, indicating that in this species dopamine and/or noradrenaline-containing fibers are an important neural input. In Rana perezi, a GABAergic innervation of pineal origin could explain the influence of light on the SCO secretory activity in frogs. A general conclusion is that the SCO cells receive neural inputs from different neurotransmitter systems. In addition, the possibility that neurotransmitters and neuropeptides present in the cerebrospinal fluid may also affect the SCO activity, is discussed.
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PMID:Neural input and neural control of the subcommissural organ. 1124 62

We compared the effects of dopamine and norepinephrine on vasopressin (AVP)-stimulated increases in osmotic water permeability (Pf) and cAMP accumulation in the rat inner medullary collecting duct (IMCD). Both dopamine and norepinephrine inhibited AVP-induced Pf and cAMP accumulation in a concentration-dependent manner; however, norepinephrine was approximately 100-fold more potent than dopamine. The effects of dopamine on Pf were antagonized by the selective alpha(2)-adrenoceptor antagonist, rauwolscine (10 nM--1 microM). Clozapine (10 microM), a dopamine D(4) receptor antagonist with significant activity at adrenergic receptors, partially attenuated both dopamine and norepinephrine-induced decreases in AVP-stimulated Pf. Dopamine-induced inhibition of AVP-dependent cAMP levels was antagonized by the alpha(2)-adrenoceptor antagonists, rauwolscine, idazoxan, and yohimbine, but not by the dopamine receptor antagonists, spiperone, SCH-23390, or raclopride. Clozapine (1--10 microM) inhibited the effects of both dopamine and norepinephrine on AVP-stimulated cAMP levels. We conclude that the inhibitory effects of dopamine on AVP-induced Pf and cAMP accumulation in the rat IMCD are mediated via alpha(2)-adrenoceptors.
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PMID:Dopamine inhibits vasopressin action in the rat inner medullary collecting duct via alpha(2)-adrenoceptors. 1150 96


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