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 effect of Ca2+-mobilizing hormones, vasopressin, angiotensin II and the alpha-adrenergic agonist phenylephrine, on the metabolic flux through the tricarboxylic acid cycle was investigated in isolated perfused rat livers. All three Ca2+-mobilizing agonists stimulated 14CO2 production and gluconeogenesis in livers of 24-h-fasted rats perfused with [2-14C]pyruvate. Prazosin blocked the phenylephrine-elicited stimulation of 14CO2 and glucose production from [2-14C]pyruvate whereas the alpha 2-adrenergic agonist, BHT-933, did not affect the rates of 14CO2 and glucose production from [2-14C]pyruvate indicating that the phenylephrine-mediated response involved alpha 1-adrenergic receptors. Phenylephrine, vasopressin and angiotensin II stimulated 14CO2 production from [2-14C]acetate in livers derived from fed rats but not in livers of 24-h-fasted rats. In livers of 24-h-fasted rats, perfused with [2-14C]acetate, exogenously added pyruvate was required for an increase in the rate of 14CO2 production during phenylephrine infusion. This last observation suggests increased pyruvate carboxylation as one of the mechanisms involved in stimulation of tricarboxylic acid cycle activity by the Ca2+-mobilizing agonists, vasopressin, angiotensin II and phenylephrine.
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PMID:Hormonal regulation of the tricarboxylic acid cycle in the isolated perfused rat liver. 309 66

The effects of phenylephrine (alpha 1 +) and prazosin (alpha 1 -) on water intake, diuresis, food intake and blood pressure were compared in conscious normal and diabetic insipidus (DI) Long Evans rats. The two drugs did not change the values measured on 24 hours in the two groups of animals (tables I and II). Phenylephrine induced a diuretic response in both normal and DI rats during the two first hours. Water intake was decreased in normal rats and increased in DI animals (fig. 1). Prazosin induced an antidiuretic effect in the two groups of animals, an increase in water intake in normal rats and a decrease in water intake in DI animals (fig. 2). Blood pressure was not changed in the two groups of animals two hours after injection. The comparison between the different results shows that the first changes induced by phenylephrine or prazosin were changes in diuresis. Since the two drugs act in a same way on the diuresis of normal and vasopressin--deprived rats, it is concluded that the neurohypophysial peptide is not involved in the variations of urinary volume induced by the alpha 1-adrenergic drugs.
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PMID:[Role of alpha 1 adrenergic receptors in water balance in the rat]. 631 53

In order to investigate the role of central alpha 1- and alpha 2-adrenoceptors in the control of vasopressin (ADH) release and the cardiovascular system, norepinephrine (NE) (1.4 microgram/kg), methoxamine (1.4 microgram/kg), yohimbine (60 micrograms/kg), and prazosin (40 micrograms/kg) were administered via the cerebral ventricles in urethane-chloralose-anesthetized dogs after morphine sedation (n = 42). In the control study 0.9% saline was administered. NE resulted in a significant fall in blood pressure, heart rate, and ADH release. Methoxamine tended to activate the cardiovascular system, but did not affect the release of ADH significantly. Prazosin decreased blood pressure significantly with a significant rise in heart rate and ADH release. Pretreatment with prazosin did not block significantly the effect of NE on blood pressure, heart rate, and ADH release. Yohimbine did not affect the cardiovascular system and ADH release significantly. Pretreatment with yohimbine completely blocked the effect of NE on ADH release, and brought about a slight rise in blood pressure and heart rate. In none of the experiments could changes in ADH release be attributed to changes in plasma osmolality. These results indicate that central alpha 1-adrenoceptors might act to activate the cardiovascular system, but have no effects on ADH release in anesthetized dogs. On the other hand, central alpha 2-adrenoceptors might act to reduce ADH release and to depress the cardiovascular system.
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PMID:The role of central alpha 1- and alpha 2-adrenoceptors in the regulation of vasopressin release and the cardiovascular system. 632 45

The role of the sympathetic nervous system, angiotensin II and vasopressin in limiting the hypotensive effect of prazosin (0.25 mg i.v.) was investigated in conscious normotensive rats. Within 45 min, mean blood pressure fell from 120 +/- 1 to 98 +/- 1 mm Hg (mean +/- S.E.M., P less than .001) while pulse rate rose from 463 +/- 9 to 500 +/- 9 beats/min (P less than .01). The blood pressure response to prazosin tended to be most pronounced in the rats with the smallest increase in heart rate (r = 0.58, P less than .001). Plasma norepinephrine and epinephrine levels were higher in prazosin-treated rats than in the controls (P less than .001). In the animals receiving prazosin, plasma renin activity was 4 times (P less than .001) and plasma vasopressin 7 times (P less than .01) higher than in the controls. Blockade of angiotensin II with saralasin (10 micrograms/min) further decreased blood pressure of the prazosin-treated rats by 22 +/- 4 mm Hg (P less than .001). In contrast, dPVDAVP (25 micrograms), a vasopressin antagonist, had no effect. Prazosin decreased the pressor response to methoxamine (10 micrograms) by 80% (P less than .001) but not to angiotensin II (60 ng). However, prazosin enhanced the reflex bradycardia induced by angiotensin II (P less than .001). These data demonstrate that both the sympathetic and the renin angiotensin system are markedly stimulated by prazosin; they both appear to limit its acute hypotensive action. In contrast, although plasma vasopressin is also increased, its pressor action is effectively buffered, probably due to enhanced baroreflex sensitivity.
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PMID:Blood pressure dependency on vasopressin and angiotensin II in prazosin-treated conscious normotensive rats. 634 43

In advanced heart failure, severe edema develops associated with hyponatremia. In 20 patients with severe congestive heart failure, we studied plasma antidiuretic hormone (ADH) concentrations related to hemodynamics and plasma osmolality. Prazosin was used to test the acute response to changes in atrial receptors and hemofiltration to test the response to changes in volume receptors. One group of the patients had inappropriately high ADH values (14.5 +/- 8.8 pg/ml) in relation to their plasma osmolality, which was well below normal values (276 +/- 23 mosmol/kg water) with no apparent osmoregulatory control. The other group showed a normal relationship of ADH and plasma osmolality (3.9 +/- 1.0 pg/ml; 289 +/- 8 mosmol/kg water), Only in the normal regulating group did lowering of left atrium pressure by prazosin result in a rise in ADH related to the decrease in pressure. Inappropriately high ADH secretion could be reversed by hemofiltration. This suggests that the syndrome of "dilutional hypo-osmolality" in severe congestive heart failure may be caused by an inappropriately high ADH secretion in which the osmoreceptor system is dominated by nonosmolar stimuli; however, it cannot be ruled out that associated hemodynamic effects in the kidney or other intrarenal or hormonal factors contribute to this mechanism.
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PMID:Antidiuretic hormone in congestive heart failure. 705 22

Isolated rat hindlimbs were perfused at 37 degrees C and constant physiological pressure (80 +/- 0.5 mmHg) while the flow rate that was allowed to freely self-adjust was monitored. Under these conditions, evidence was obtained for both alpha- and beta-adrenergic stimulation of oxygen consumption (VO2) in contrast to constant-flow perfusion, which has only convincingly shown alpha-adrenergic stimulation of VO2 in response to adrenergic agents. Addition of norepinephrine (NE; 1-33 nM) led to an increase in VO2 with a maximum of 29% above the basal value at 3.3 nM, even though the flow rate decreased. Phenylephrine (3.3-33 nM) and vasopressin (10-100 pM) also showed similar, but lesser in magnitude, vasoconstriction-associated stimulatory effects on VO2. Prazosin (an alpha 1-antagonist) completely reversed the NE-mediated decrease in flow rate and significantly blocked the increased VO2. In contrast, isoproterenol (10-1,000 nM) increased both flow rate (30%) and VO2 (32%). The isoproterenol-stimulated VO2 was not blocked by the beta 1-, beta 2-antagonist propranolol (10 microM), although the increased flow was reversed. In the presence of propranolol (1 or 10 microM), BRL-35135A (a beta 3-agonist) also stimulated VO2 (18%) without significant change in flow rate. These results lend further support to the role of the alpha 1-adrenoceptor in muscle VO2. In addition there is evidence for the presence of a functional beta 3-adrenoceptor as an additional subtype responsible for NE-mediated thermogenesis in the rat hindlimb.
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PMID:Constant-pressure perfusion of rat hindlimb shows alpha- and beta-adrenergic stimulation of oxygen consumption. 749 49

1. A hormonal-sympathetic reflex model for long-term control of arterial pressure is presented. It is hypothesized that the hormonal-sympathetic reflex regulates arterial pressure during chronic dietary salt loading by decreasing sympathetic tone. This sympathetic response is mediated by an increase in plasma vasopressin (AVP) and a decrease in plasma angiotensin (AngII). 2. Three new models of neurogenic salt-dependent hypertension are presented. All models are theoretically based on an impaired hormonal-sympathetic reflex. 3. In the first model, sympathetic responsiveness is 'clamped' by long-term alpha-adrenergic blockade with prazosin. Prazosin treated rats exhibit marked salt-dependent hypertension despite normal suppression of the renin-angiotensin system. 4. In the second model, the ability of the central nervous system to respond to salt-induced changes in AVP and AngII concentrations was prevented by long-term administration of antagonists selective for the AVP-V1 and AT1. This 'clamp' of the afferent hormonal signal resulted in salt-dependent hypertension identical in magnitude to that observed in prazosin treated rats. 5. In the third model, the long-term arterial pressure responses to increasing dietary salt were examined in sino-aortic denervated (SAD) rats. SAD rats exhibited salt-dependent hypertension, of lesser magnitude than that observed with 'clamped' afferent and efferent pathways of the hormonal-sympathetic reflex. 6. A primary role for hormonal 'error signals' is presented and the impact this perspective has on past and future investigations of central mechanisms of long-term arterial pressure regulation is discussed.
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PMID:Hormones as long-term error signals for the sympathetic nervous system: importance of a new perspective. 904 15

In rats, the daily changes in hepatic lipase (HL) activity in the liver follow the diurnal rhythm of the catecholamines. To study the underlying mechanism, the effect of adrenaline on maturation and secretion of HL was determined in freshly isolated rat hepatocytes. Adrenaline (10 microM) acutely inhibited the secretion of HL. This effect was abolished by 0.1 microM prazosin, but not by 1 microM propranolol, indicating the involvement of the alpha1-adrenergic pathway. Prazosin was at least 1000-fold more potent than WB4101, a selective alpha1A-antagonist. Adrenaline had no effect on HL secretion in hepatocytes pretreated with chloroethylclonidine, an irreversible alpha1B-selective antagonist. Inhibition of HL was not induced by 10 microM methoxamine, a alpha1A-selective agonist. Thus, adrenaline inhibited HL secretion through activation of the alpha1-adrenoceptors subtype B, which have been shown to signal through Ca2+ as well as cAMP. A similar reduction in HL secretion was induced by the Ca2+-mobilizing hormones angiotensin II (100 nM) and vasopressin (12 nM), the Ca2+ ionophore A23187 (2 microM), and by thapsigargin (1 microM), which inhibits the ER Ca2+-ATPase pump. HL secretion was unaffected by elevating cAMP with 10 microM forskolin or 1 microM 8-Br-cAMP. These results suggest that the alpha1B-adrenergic effects on HL expression are mainly mediated through elevation of intracellular Ca2+. Chelation of extracellular Ca2+ and subsequent lowering of intracellular Ca2+ with EGTA also inhibited HL secretion. In pulse-chase experiments, adrenaline was shown to inhibit the maturation of HL from the 53 kDa, Endo H-sensitive precursor to the Endo H-resistant, catalytically active protein of 58 kDa. In addition, adrenaline induced intracellular degradation of newly synthesized HL. Similar post-translational effects, both qualitatively and quantitatively, were observed with A23187, thapsigargin and EGTA. We conclude that the inhibition of HL maturation and increase in intracellular degradation induced by catecholamines, A23187, thapsigargin and EGTA is evoked by changes in Ca2+ homoeostasis, possibly through lowering ER Ca2+.
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PMID:Maturation and secretion of rat hepatic lipase is inhibited by alpha1B-adrenergic stimulation through changes in Ca2+ homoeostasis: thapsigargin and EGTA both mimic the effect of adrenaline. 948 Aug 78


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