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)

Clonidine, an alpha 2-adrenergic agonist, induced a marked, dose-related increase of plasma IR-ANF in normally-hydrated rats. Maximal ANF release was observed at 10 min after injection of 50 micrograms clonidine, rising from 40.5 +/- 4.6 pg/ml (X +/- SEM) to 1064.4 +/- 22.4 pg/ml. This effect on plasma IR-ANF was partially blocked by pretreatment with 0.8 mg naloxone, whereas synthetic Arg8-vasopressin (AVP) did not inhibit clonidine's action. These findings indicate that increased ANF release may be involved in the mechanism of clonidine-induced diuresis. The clonidine's effect on ANF release may be mediated via activation of opioid receptors besides stimulation of alpha 2-adrenergic receptors.
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PMID:Plasma immunoreactive atrial natriuretic factor (IR-ANF) increases markedly after alpha 2-adrenergic stimulation with clonidine in normally-hydrated rats. 303 Mar 13

The binding characteristics of [3H]oxytocin [( 3H]OT) and [3H]lysine vasopressin [( 3H]LVP) to nonpregnant human myometrium were investigated. Binding of both radioligands was saturable, time dependent, and reversible. Whereas [3H]OT was found to bind to a single class of sites with high affinity [Kd, 1.5 +/- 0.4 (+/- SEM) nM] and low capacity [maximum binding (Bmax), 34 +/- 6 fmol/mg protein], [3H]LVP bound to two classes of sites, one with high affinity (Kd, 2.2 +/- 0.1 nM) and low capacity (Bmax, 198 +/- 7 fmol/mg protein) and another with low affinity (Kd, 655 +/- 209 nM) and high capacity (Bmax, 5794 +/- 1616 fmol/mg protein). The binding of the labeled peptides also displayed a marked difference in sensitivity to Mg2+ and guanine nucleotides. These differences in binding characteristics as well as the differences in potency of analogs in competing for [3H]OT and [3H]LVP binding indicate the presence of distinct receptors for OT and vasopressin in human myometrium. Pharmacological characterization of the high affinity binding sites for [3H]LVP indicated that these are of the V1 subtype. Although, as suggested by others, vasopressin and OT can bind to the same sites, the presence of distinct receptors for both peptides provides an explanation for the previously reported difference in myometrial responsiveness to OT and vasopressin.
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PMID:Oxytocin and vasopressin: distinct receptors in myometrium. 303 5

We studied the influence of a hypertonic saline infusion on the counterregulatory response to insulin-induced hypoglycemia in nine normal men. When given hypertonic saline, the men had less hypoglycemia in response to insulin, both acutely and in the recovery phase (P less than 0.01), and released 34% more glucagon (P less than 0.05) than when they were water loaded. The total integrated ACTH, cortisol, epinephrine, norepinephrine, and GH responses to hypoglycemia were similar after saline and water loading. After the saline load, the mean plasma vasopressin level rose from 11.0 +/- 2.2 (+/- SEM) to 20.9 +/- 2.9 pg/mL in response to insulin-induced hypoglycemia. In contrast, after the water load, vasopressin levels were undetectable (less than 2 pg/mL) and they increased only to 2.6 +/- 0.4 pg/mL with hypoglycemia. There was a significant positive correlation between basal plasma vasopressin and nadir glucose concentrations and a significant negative correlation between basal plasma vasopressin and the integrated fall in glucose after insulin administration (P less than 0.01 and P less than 0.025, respectively). The difference in the glycemic response to insulin may be related to the high vasopressin levels after saline loading, which could, either directly and/or through enhanced glucagon release, increase hepatic glucose production and thus limit the hypoglycemic response to insulin.
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PMID:Influence of infused hypertonic saline on the response to insulin-induced hypoglycemia in man. 303 50

The role of variation of venous return on baroreflex control of heart rate during lumbar epidural anesthesia was investigated in 12 unpremedicated patients. Group 1 patients (n = 6) received 8 ml of 0.5% plain bupivacaine in the epidural space (L3-4) (mean upper level of analgesia at T10). Group 2 patients (n = 6) received 8 ml of saline at the same level in the epidural space. Following the epidural injection, phenylephrine (PHE) and nitroglycerin (NTG) were employed to alter the stimulation of baroreceptor sites before and during application of lower body positive pressure (LBPP). Plasma bupivacaine, catecholamines, renin activity, and vasopressin were assayed. In contrast to saline, epidural bupivacaine induced a decrease in systolic arterial and right atrial pressures (-11 +/- 4 and -3.2 +/- 0.7 mmHg, respectively, mean +/- SEM) without change in heart rate, an increase in baroreflex slopes during PHE and NTG injections (+5.9 +/- 1.6 ms/mmHg and +2.8 +/- 0.9 ms/mmHg, respectively), and a decrease in plasma norepinephrine (-248 +/- 89 pg/ml). The application of LBPP restored hemodynamic and reflex variables to preepidural analgesia values, whereas plasma catecholamines decreased further. Plasma renin activity and vasopressin were not modified at any time in either groups. This study indicates that lumbar epidural anesthesia enhances cardiac vagal tone mainly through a decrease in venous return.
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PMID:Influence of venous return on baroreflex control of heart rate during lumbar epidural anesthesia in humans. 308 Sep 22

The role of circulating bradykinin in the regulation of cardiovascular homeostasis was studied in the normotensive conscious rat using a competitive antagonist of bradykinin at the receptor level. This antagonist (B4162) was administered intravenously as a bolus dose of 400 micrograms. This dose was shown to effectively block the hypotensive effect of exogenous bradykinin (2.5 micrograms) for at least 5 min. The bradykinin antagonist was administered at the end of an infusion of angiotensin II (1 ng/min, n = 5, or 12.5 ng/min, n = 6), of methoxamine (0.5 micrograms/min, n = 5, or 4 micrograms/min, n = 6), of lysine vasopressin (0.25 mUI/min, n = 11) or of saline (10 microliter/min, n = 7). The bradykinin antagonist did not change the mean arterial pressure of the control rats. The low doses of angiotensin II and of methoxamine did not have an effect on mean blood pressure. The bradykinin antagonist however increased mean blood pressure of these rats within 1 min by 10 +/- 2 (p less than 0.01, mean +/- SEM) and by 12 +/- 3 (p less than 0.01) mmHg, respectively. The large dose of angiotensin II raised mean blood pressure from 127 +/- 3.6 to 142 +/- 4.9 mmHg and that of methoxamine from 130 +/- 2 to 146 +/- 5 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Attenuation of the vasopressor effect of angiotensin II, vasopressin and alpha 1-adrenergic stimulation by bradykinin]. 311 81

Osmotic water permeability of the apical membrane of toad urinary epithelium is increased greatly by vasopressin (VP) and is associated with exocytic addition of granules and aggrephores at the apical surface. To determine the physiological role of granule exocytosis, we measured the osmotic water permeability and membrane fluidity of isolated granules, surface membranes and microsomes prepared from toad bladder in the presence and absence of VP. Pf was measured by stopped-flow light scattering and membrane fluidity was examined by diphenylhexatriene (DPH) fluorescence anisotropy. In response to a 75 mM inward sucrose gradient, granule size decreased with a single exponential time constant of 2.3 +/- 0.1 sec (SEM, seven preparations, 23 degrees C), corresponding to a Pf of 5 x 10(-4) cm/sec; the activation energy (Ea) for Pf was 17.6 +/- 0.8 kcal/mole. Under the same conditions, the volume of surface membrane vesicles decreased biexponentially with time constants of 0.13 and 1.9 sec; the fast component comprised approximately 70% of the signal. Granule, surface membrane and microsome time constants were unaffected by VP. However, in surface membranes, there was a small decrease (6 +/- 2%) in the fraction of surface membranes with fast time constant. DPH anisotropies were 0.253 (granules), 0.224 (surface membranes) and 0.190 (microsomes), and were unaffected by VP. We conclude: (1) granules have among the lowest water permeabilities of biological membranes, (2) granule water permeability is not altered by bladder pretreatment with VP, (3) granule membrane fluidity is remarkably lower than that of surface and microsomal membranes, and (4) rapid water transport occurs in surface membrane vesicles. The unique physical properties of the granule suggests that apical exocytic addition of granule membrane may be responsible for the low water permeability of the unstimulated apical membrane.
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PMID:Very low osmotic water permeability and membrane fluidity in isolated toad bladder granules. 314 39

Osmoregulation of vasopressin release and thirst was studied in the mid-follicular and mid-luteal phases of the menstrual cycle of five patients with cyclical oedema defined by peripheral oedema and weight gain (greater than 3.0 kg) manifest in two consecutive luteal phases. Results are compared to those already obtained in eight healthy women. In the patients, basal plasma osmolality in the mid-luteal phase was significantly lower than in the mid-follicular periods (patients, 283 +/- 1, 287 +/- 1 mOsmol/kg, respectively, mean +/- SEM, P less than 0.05; controls, 282 +/- 1, 286 +/- 1 mOsmol/kg, respectively, P less than 0.05). Plasma osmolality (pOsm) and plasma arginine vasopressin (pAVP) were measured during hypertonic (850 mmol/l) saline infusion in both phases of the cycle; linear regression analyses of these data gave the following mean regression equations, (i) mid-follicular, pAVP = 0.55 (pOsm - 285), r = 0.94 and (ii) mid-luteal, pAVP = 0.42 (pOsm - 281), r = 0.93. The abscissal intercept was significantly different (P less than 0.025). Osmotic threshold for severe thirst onset was lower in the mid-luteal phase compared to the mid-follicular value (296 +/- 1, 299 +/- 1 mOsmol/kg, respectively, P less than 0.01). Basal data and results of thirst onset and theoretical threshold for vasopressin release in response to osmotic stimulation obtained in the patients were similar to healthy control women. We conclude that osmoregulation in cyclical oedema is normal.
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PMID:Osmoregulation of vasopressin secretion and thirst in cyclical oedema. 325 60

[Arg8]-Vasopressin (AVP) has been shown to exert characteristic central physiological actions in the ventral septal area of the rat brain. This study reports the characterization of receptors for AVP in synaptic plasma membranes prepared from the ventral septal area, the lateral septum, and the hippocampus. Binding of [3H]AVP was temperature and time dependent, linearly related to protein concentration, saturable, and specific. Scatchard plot analysis suggested the presence of a population of binding sites in the three brain areas with dissociation constants and maximal binding capacities, respectively, of 1.06 +/- 0.39 nM and 24.0 +/- 7.01 fmol/mg of protein (mean +/- SEM; n = 3 for the ventral septal area, 0.92 +/- 0.13 nM and 47.0 +/- 4.96 fmol/mg of protein (n = 3) for the lateral septum, and 0.91 +/- 0.14 nM and 25 +/- 5.02 fmol/mg of protein (n = 3) for the hippocampus. In all three brain regions, the rank order of potencies of several vasopressin analogs, unrelated peptides, and other compounds for competitive displacement of ligand indicated a receptor with properties resembling those of the V1-like receptor for AVP. These data document the presence of a high-affinity, V1-like vasopressin receptor in the rat ventral septal area for which the pharmacological properties are similar to those previously reported in physiological studies.
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PMID:Subcellular localization and characterization of vasopressin binding sites in the ventral septal area, lateral septum, and hippocampus of the rat brain. 333 62

1. The specific antidiuretic agonist [4-valine, 8-D-arginine]vasopressin (VDAVP) was administered intravenously to seven conscious dogs at a rate of 10 ng min-1 kg-1. Cardiac output (aortic electromagnetic flowmeter), mean arterial pressure and regional blood flows (radioactive microspheres) were measured before and after 30 min of infusion. 2. Mean arterial pressure fell from 89.9 +/- 4.5 (mean +/- SEM) to 82.3 +/- 5.9 mmHg and cardiac output increased from 115.4 +/- 8.7 to 163.0 +/- 14.4 ml min-1 kg-1. Total peripheral resistance decreased from 41.6 +/- 3.7 to 27.8 +/- 3.6 units and heart rate increased from 79.2 +/- 5.9 to 123.2 +/- 5.9 beats/min. Blood flow increased significantly in the myocardium, fat and skeletal muscle vascular bed. 3. In another group of six dogs subjected to a similar protocol 24 h after bilateral nephrectomy, mean arterial pressure fell from 102.2 +/- 5.3 to 82.7 +/- 3.4 mmHg and cardiac output increased from 125.6 +/- 3.0 to 171.2 +/- 4.0 ml min-1 kg-1. Total peripheral resistance decreased from 39.3 +/- 3.4 to 23.4 +/- 1.3 units and heart rate increased from 84 +/- 4.9 to 113.3 +/- 4.3 beats/min. The increase in cardiac output and the fall in total peripheral resistance did not differ significantly between intact and anephric dogs. Regional blood flow responses differed in some respects in the two groups studied, but there was no evidence that the vasodilatory action of VDAVP depended on the presence of the kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of a specific antidiuretic agonist on cardiac output and its distribution in intact and anephric dogs. 334 38

The goal of this study was to examine humoral mechanisms that regulate blood flow to the choroid plexus. We determined the effects of arginine vasopressin on blood flow (microspheres) to the choroid plexus in anesthetized and awake rabbits. In anesthetized rabbits, blood flow to the choroid plexus was 342 +/- 31 (mean +/- SEM) ml/min/100 g under control conditions. Intravenous infusion of vasopressin at 4 and 40 mU/kg increased plasma vasopressin levels from 11 +/- 1 to 55 +/- 15 and 441 +/- 120 pg/ml, respectively, and blood flow to the choroid plexus decreased by 48 +/- 6% and 70 +/- 4%. Cerebral blood flow was not affected by infusion of vasopressin. Similar responses to infusion of vasopressin were observed in awake rabbits. The V1 antagonist [d(CH2)5Tyr(Me)AVP] (10 micrograms/kg i.v.) had no effect on resting blood flow, but abolished the effect of vasopressin on blood flow to the choroid plexus. Vasoconstrictor responses of the choroid plexus to intravenous infusion of phenylephrine were not attenuated by the V1 antagonist. Thus, circulating vasopressin, at plasma levels that are observed under physiological and pathophysiological conditions, has marked effects on blood flow to the choroid plexus. These effects appear to be mediated through a V1 receptor. We speculate that vasopressin may play an important role in regulation of blood flow to the choroid plexus and perhaps in the regulation of cerebrospinal fluid production.
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PMID:Humoral regulation of blood flow to choroid plexus: role of arginine vasopressin. 339 58


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