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 potential role of adrenaline, both circulating and in the central nervous system, in the maintenance of high blood pressure was examined in stroke-prone spontaneously hypertensive rats (SHRSP). alpha-Monofluoromethyldopa, a long-lasting inhibitor of dopa decarboxylase, was used to induce rapid depletion of central and peripheral catecholamine stores. Subsequent inhibition of phenylethanolamine-N-methyltransferase (PNMT) allowed the gradual restoration of dopamine and noradrenaline but not adrenaline, resulting in a greater relative depletion of adrenaline. Adrenaline was almost totally depleted in the circulation and peripheral tissues. The resting level of blood pressure, however, was unaffected, excepting after administration of a vasopressin (AVP) antagonist. Moreover, there was no reduction in the magnitude of acute pressor responses to electrical stimulation of the rostral ventrolateral medulla oblongata (C1 area), despite extensive loss of adrenaline from the brainstem and spinal cord. The results suggest that adrenaline contributes to the resting level of blood pressure but that its loss can be offset by the pressor activity of AVP. Thus neither central nor peripheral adrenaline stores appear to be essential for the maintenance of hypertension or for centrally-evoked vasoconstriction in adult SHRSP.
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PMID:Effects of depleting central and peripheral adrenaline stores on blood pressure in stroke-prone spontaneously hypertensive rats. 194 21

Primary monolayer cultures of rat epididymal cells have been shown to secrete chloride and bicarbonate when stimulated with beta-adrenergic agents, humoral agents and vasoactive peptides. The intracellular messengers mediating the secretory response are unknown. In this study intracellular AMP, Ca2+ and inositol phosphates were measured in epididymal monolayers at rest and upon stimulation with various secretory agonists. Adrenaline, forskolin, lysylbradykinin, prostaglandin, endothelin, angiotensin II, antidiuretic hormone and vasoactive intestinal peptide at concentrations that stimulate anion secretion caused a rise in intracellular cyclic AMP. The increase in cyclic AMP by adrenaline was blocked by propranolol but not by phentolamine. Studies of the concentration-effect relationships showed that for adrenaline and endothelin the EC50 for stimulation of cyclic AMP was higher than that for stimulation of anion secretion. None of these agonists affects intracellular Ca2+ concentration and inositol phosphate contents in epididymal monolayers. Ca2+ ionophores A21387, ionomycin and erythrosin B (with irradiation with white light), at concentrations that stimulate anion secretion, also stimulated a rise in intracellular cyclic AMP and concomitantly increased intracellular Ca2+. The increase in cyclic AMP was dependent on extracellular Ca2+. It is not known whether the secretory response to Ca2+ ionophores was mediated by an increase in cell Ca2+ per se, or cyclic AMP. However, it can be concluded that cyclic AMP is the second messenger which mediates the secretory responses to physiological stimuli.
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PMID:Secretory agonists stimulate a rise in intracellular cyclic AMP but not Ca2+ and inositol phosphates in cultured rat epididymal epithelium. 197 25

Lysine vasopressin was injected (0.25 IU/100 g body wt) intraperitoneally only once to unilaterally splanchnic denervated pigeons. Adrenomedullary catecholamine (CA) content was measured spectrofluorometrically 0.5, 4, 12, 24, 72, 144 and 216 h after administration. The findings revealed that in innervated glands, vasopressin caused 59-74% decrease of norepinephrine (NE) 4 and 24 h after administration while in denervated glands it resulted in 18-65% release of NE 0.5 to 144 h after injection. This indicates that the splanchnic nerve prevents early phase (up to 0.5 h) of vasopressin-induced release of NE. Vasopressin also caused decrease of Epinephrine (E) from both the innervated (68-73%) and denervated (69-74%) glands 0.5 and 4 h after injection indicating that the splanchnic nerve has no effect on vasopressin-induced release of E. Accelerated resynthesis of NE exceeding the control value (44-94%) was encountered 144 and 216 h after injection as compared to a slower increase (14%) in denervated glands 216 h after injection. Higher rate of resynthesis of E was encountered in the innervated glands 12 and 72 h after treatment. The findings clearly point out that the splanchnic nerve accelerates resynthesis of both NE and E induced by vasopressin.
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PMID:Neural modulation of lysine vasopressin-induced changes of catecholamines in the adrenal medulla of the pigeon. 204 87

Acute physical stresses such as major surgery, insulin-induced hypoglycaemia and exercise are associated with acute increases in circulating concentrations of factor VIII and increases in fibrinolytic activity. The mechanisms involved in producing these responses are partly under hormonal control and there is evidence that the neurohormones adrenaline and arginine vasopressin mediate some of the changes. Adrenaline infusions in man produce increases in both factor VIII and fibrinolysis and the rise in factor VIII is blocked by pretreatment with propranolol. Receptor blockade with propranolol also prevents the rise in factor VIII associated with hypoglycaemia to support the view that adrenaline is an important mediator under these circumstances. The pituitary antidiuretic hormone, arginine vasopressin, produces similar changes in haemostasis at plasma concentrations above those required for its renal effects, but within the range commonly seen during certain physical stresses. However, studies in clinical models that produce increases in vasopressin without a concomitant increase in adrenaline concentrations show enhanced fibrinolysis but no change in factor VIII. Thus it seems that adrenaline and vasopressin have a role in the regulation of haemostasis associated with stress, although the role of vasopressin in the regulation of factor VIII is open to question.
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PMID:Hormonal regulation of the acute haemostatic response to stress. 210 14

Prolactin (PRL) responds to several stimuli that elicit release of adrenocorticotropin (ACTH), but does not increase in response to hemorrhage in fetal animals. To determine whether PRL increases after hemorrhage in older animals, 11 immature female swine were prepared chronically under halothane and conditioned behaviorally to lie in a sling. They were bled 14 ml/kg over 5 min. PRL, ACTH, cortisol (F), lysine vasopressin (LVP), and pressure renin activity (PRA) were measured by radioimmunoassay. Epinephrine (EPI) and norepinephrine (NE) were separated by high-performance liquid chromatography. Arterial PRL increased at 0.75 and 1 h (P less than 0.01) and paralleled ACTH and F that peaked at 0.75 h (P less than 0.05 and P less than 0.01, respectively). All three hormones recovered significantly by 4 h. In contrast, PRA and LVP peaked transiently at 0.25 h after hemorrhage and recovered by 1.5 h (P less than 0.05, in each case). EPI and NE did not change significantly. In individual pigs, ACTH and F each showed correlations (Spearman) with PRL that were positive in 10 pigs and significant in six and five pigs, respectively. The pig with the smallest ACTH change (8.4 pg/ml peak) showed no increase in PRL. Peaks in PRL were simultaneous with (five pigs) or delayed by 15 min (four pigs) or 30 min (one pig) from peaks in ACTH. Significant correlations of PRL with PRA and with LVP occurred in only two pigs and in one pig, respectively. A common pathway may contribute to other independent mechanisms controlling the release of ACTH and PRL after hemorrhage.
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PMID:Response of prolactin to hemorrhage is similar to that of adrenocorticotropin in swine. 215 59

1. The inflow of Mn2+ across the plasma membranes of isolated hepatocytes was monitored by measuring the quenching of the fluorescence of intracellular quin2, by atomic absorption spectroscopy and by the uptake of 54Mn2+. The inflow of other divalent metal ions was measured using quin2. 2. Under ionic conditions which resembled those present in the cytoplasmic space, Mn2+, Zn2+, Co2+, Ni2+ and Cd2+ each quenched the fluorescence of a solution of Ca2(+)-quin2. 3. The addition of Mn2+, Zn2+, Co2+, Ni2+ or Cd2+ to cells loaded with quin2 caused a time-dependent decrease in the fluorescence of intracellular quin2. Plots of the rate of decrease in fluorescence as a function of the concentration of Mn2+ reached a plateau at 100 microM-Mn2+. 4. The rate of decrease in fluorescence induced by Mn2+ was stimulated by 20% in the presence of vasopressin. The effect of vasopressin was completely inhibited by 200 microM-verapamil. Adrenaline, angiotensin II and glucagon also stimulated the rate of decrease in the fluorescence of intracellular quin2 induced by Mn2+. 5. The rate of decrease in fluorescence induced by Zn2+, Co2+, Ni2+ or Cd2+ was stimulated by between 20 and 190% in the presence of vasopressin or angiotensin II. 6. The rates of uptake of Mn2+ measured by atomic absorption spectroscopy or by using 54Mn2+ were inhibited by about 20% by 1.3 mM-Ca2+o and stimulated by 30% by vasopressin. 7. Plots of Mn2+ uptake, measured by atomic absorption spectroscopy or with 54Mn2+, as a function of the extracellular concentration of Mn2+ were biphasic over the range 0.05-1.0 mM added Mn2+ and did not reach a plateau at 1.0 mM-Mn2+. 8. It is concluded that (i) hepatocytes possess both a basal and a receptor-activated divalent cation inflow system, each of which has a broad specificity for metal ions, and (ii) the receptor-activated divalent cation inflow system is the receptor-operated Ca2+ channel.
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PMID:The liver cell plasma membrane Ca2+ inflow systems exhibit a broad specificity for divalent metal ions. 216 60

1. Endothelin (ET), vasopressin (VP) and angiotensin II (AII) all stimulate aldosterone production in adrenal glomerulosa cells but the response to AII is greater than that to either ET or VP. 2. Total inositol phosphate responses to AII and ET were similar but the response to VP was lower. 3. Cytosolic free Ca2+ responses to AII were higher than to either of the other peptides. 4. Metabolism of 145IP3 was different under stimulation by the three different peptides. 5. Adrenal glomerulosa cells can distinguish between three different agonists which stimulate phosphatidylinositol turnover and produce a selective response to each peptide.
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PMID:Mechanisms involved in the stimulation of aldosterone production by angiotensin II, vasopressin and endothelin. 218 8

Heart rate (HR), mean arterial pressure (MAP), indices of sympathetic and parasympathetic activity (plasma concentrations of adrenaline, noradrenaline and pancreatic polypeptide, PP), vasopressin (VP) and aldosterone (ALDO) were measured in six pigs during continuous bleeding resulting in hypovolaemic shock, from which five survived. Three stages of haemorrhage could be defined. Stage I. Resting MAP was 85 +/- 6 mmHg and increased to 96 +/- 5 mmHg with a blood loss of 275 (range 250-300) (10 (9-12)% of the estimated blood volume) concomitant with an increase in HR from 105 +/- 5 to 113 +/- 6 beats min-1 (P less than 0.05). Stage II. After a blood loss of 375 (300-500) ml (15 (13-16)%) MAP fell to 62 +/- 9 mmHg and HR to 95 +/- 5 beats min-1 (P less than 0.05). Stage III. A blood loss of 1113 (825-1450) ml (44 (30-52)%) resulted in a MAP of 50 +/- 4 mmHg and an increase in HR to 206 +/- 3 beats min-1 (P less than 0.05). Adrenaline increased from 0.3 +/- 0.1 to 0.8 +/- 0.3 (stage II) and 3.6 +/- 1.1 nmol l-1 (stage III) (P less than 0.05); noradrenaline from 0.4 +/- 0.1 to 1.5 +/- 0.4 (stage II) and 5.9 +/- 1.7 nmol l-1 (stage III) (P less than 0.05); PP from 6.2 +/- 1.6 to 13.3 +/- 2.3 (stage II) and 20.9 +/- 7.8 pmol l-1 (stage III) (P less than 0.05). VP changed only marginally, but ALDO increased from 496 +/- 54 to 623 +/- 76 pmol l-1 (stage III) (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular and endocrine responses to haemorrhage in the pig. 231 78

The effects of intrathecally administered arginine-vasopressin (AVP) and substance P (SP) on adrenal medullary secretion of epinephrine were examined in anesthetized Sprague-Dawley rats. Plasma epinephrine levels were measured in blood samples taken directly from the adrenal vein using a novel micropuncture technique. The blood samples (20-30 microliter in volume) were taken before, and 2 min, 15 min and 30 min after intrathecal injections of AVP, SP or vehicle only. Plasma was assayed for epinephrine using high pressure liquid chromatography. Adrenal venous epinephrine levels were not significantly altered by the intrathecal administration of AVP, thereby suggesting that adrenal epinephrine secretion is not involved in the cardiovascular responses previously reported to occur following similar doses of intrathecal AVP. Intrathecal SP administration, while causing blood pressure responses similar to those produced by AVP, resulted in significant increases in adrenal vein epinephrine. This finding suggests that activation of adrenal secretion of epinephrine may contribute to SP-initiated blood pressure changes.
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PMID:The effects of intrathecal administration of arginine-vasopressin and substance P on blood pressure and adrenal secretion of epinephrine in rats. 242 66

Jakobs, Bauer & Watanabe [(1985) Eur. J. Biochem. 151, 425-430] reported that treatment of platelets with phorbol 12-myristate 13-acetate (PMA) prevented GTP- and agonist-induced inhibition of adenylate cyclase in membranes from the platelets. This was attributed to the phosphorylation of the inhibitory guanine nucleotide-binding protein (Gi) by protein kinase C. In the present study, the effects of PMA on cyclic [3H]AMP formation and protein phosphorylation were studied in intact human platelets labelled with [3H]adenine and [32P]Pi. Incubation mixtures contained indomethacin to block prostaglandin synthesis, phosphocreatine and creatine kinase to remove ADP released from the platelets, and 3-isobutyl-1-methylxanthine to inhibit cyclic AMP phosphodiesterases. Under these conditions, PMA partially inhibited the initial formation of cyclic [3H]AMP induced by prostaglandin E1 (PGE1), but later enhanced cyclic [3H]AMP accumulation by blocking the slow decrease in activation of adenylate cyclase that follows addition of PGE1. PMA had more marked and exclusively inhibitory effects on cyclic [3H]AMP formation induced by prostaglandin D2 and also inhibited the action of forskolin. Adrenaline, high thrombin concentrations and, in the absence of phosphocreatine and creatine kinase, ADP inhibited cyclic [3H]AMP formation induced by PGE1. The actions of adrenaline and thrombin were attenuated by PMA, but that of ADP was little affected, suggesting differences in the mechanisms by which these agonists inhibit adenylate cyclase. sn-1,2-Dioctanoylglycerol (diC8) had effects similar to those of PMA. The actions of increasing concentrations of PMA or diC8 on the modulation of cyclic [3H]AMP formation by PGE1 or adrenaline correlated with intracellular protein kinase C activity, as determined by 32P incorporation into the 47 kDa substrate of the enzyme. Parallel increases in phosphorylation of 20 kDa and 39-41 kDa proteins were also observed. Platelet-activating factor, [Arg8]vasopressin and low thrombin concentrations, all of which inhibit adenylate cyclase in isolated platelet membranes, did not affect cyclic [3H]AMP formation in intact platelets. However, the activation of protein kinase C by these agonists was insufficient to account for their failure to inhibit cyclic [3H]AMP formation. Moreover, high thrombin concentrations simultaneously activated protein kinase C and inhibited cyclic [3H]AMP formation. The results show that, in the intact platelet, the predominant effects of activation of protein kinase C on adenylate cyclase activity are inhibitory, suggesting actions additional to inactivation of Gi.
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PMID:Effects of activation of protein kinase C on the agonist-induced stimulation and inhibition of cyclic AMP formation in intact human platelets. 244 6


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