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 graded lower body negative pressure (-10 and -40 mm Hg) on vascular resistance and plasma vasopressin, norepinephrine, and renin activity were assessed in seven hypertensive subjects with left ventricular hypertrophy and seven sex-matched and age-matched normotensive subjects. In both groups increasing levels of lower body negative pressure induced a progressive decrease in right atrial pressure and an increase in vascular resistance. In normal subjects plasma vasopressin, norepinephrine, and renin activity were progressively raised, whereas only the higher level of stimulation increased plasma renin activity, norepinephrine, and vasopressin in hypertensive subjects. Propranolol induced a significant increase in plasma vasopressin in normal subjects (from 1.3 +/- 0.1 to 2.0 +/- 0.1 pg/ml; p less than 0.05) but not in hypertensive subjects. In this latter condition -10 mm Hg lower body negative pressure failed to increase plasma vasopressin, norepinephrine, and renin activity in normal subjects. Propranolol abolished the change in plasma renin activity in both groups, reduced the increase in vascular resistance induced by -40 mm Hg lower body negative pressure in normotensive subjects, but did not modify the rise in vasopressin elicited by this stimulus in normal subjects or the humoral and hemodynamic reflex responses evoked in hypertensive subjects. These results suggest that cardiopulmonary receptors are involved in the control of vasopressin release in normal subjects, whereas in hypertensive subjects with left ventricular hypertrophy, this control is altered because of an impaired function of cardiopulmonary receptors.
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PMID:Impaired control of vasopressin release in hypertensive subjects with cardiac hypertrophy. 296 89

The effects of substance K (SK), a newly discovered tachykinin, on the cardiovascular and sympathetic system were evaluated in the pithed rat preparation and in the in situ domestic pig heart. In pithed rats, SK (10 nmol/kg, IV) produced a triphasic mean blood pressure (MAP) response: short depressor, short pressor (+11 +/- 1 mmHg), and prolonged depressor phase (-9 +/- 1 mmHg, n = 9-24, p less than 0.001). Neither effect was significantly affected by pretreatment with propranolol (2 mg/kg) or phentolamine (1 mg/kg). The pressor response was accompanied by increased heart rate (HR): 41 +/- 4 beats/min, while lower doses produced a decrease: -8 +/- 2 beats/min (p less than 0.01). Propranolol abolished the increase in HR. SK inhibited the pressor response evoked by electrical stimulation of the spinal cord (SCS) and by Arg8-vasopressin (AVP). SK increased circulating levels of epinephrine and norepinephrine but did not change release of catecholamines evoked by SCS. Direct intracoronary injections of SK (0.3-100 nmol, intact pig heart) increased coronary blood flow; higher doses decreased MAP and increased HR. These results indicate that: SK can produce pressor and depressor effects in the rat and is a potent coronary dilator in the pig. In the pithed rat SK causes catecholamine release which mediates its cardiac accelerator effect and it antagonizes adrenergic and non-adrenergic pressor stimuli.
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PMID:Substance K: vascular and cardiac effects in rat and pig. 300 74

Carp (Cyprinus carpio) liver maintained normal glycogen content and enzyme complement for several days in organ culture. Epinephrine-stimulated glycogenolysis, phosphorylase activation, and cyclic AMP (cAMP) accumulation in a concentration-dependent manner with EC50s of 100, 100, and 500 nM, respectively. These actions were blocked by the beta-adrenergic antagonist, propranolol, but not by the alpha-adrenergic antagonist phentolamine. Glycogenolysis and tissue cAMP were uninfluenced by 10(-6) M arginine vasotocin, arginine vasopressin, lysine vasotocin, lysine vasopressin, mesotocin, or oxytocin, but were slightly increased by 10(-5) M isotocin and slightly decreased by 10(-6) M angiotensin II. [125I]-iodocyanopindolol (ICP), a beta-adrenergic ligand, bound to isolated carp liver membranes with a KD of 83 pM. Maximum binding of 45 fmol/mg protein was at 600 pM. Propranolol, isoprenaline, epinephrine, phenylephrine, norepinephrine, and phenoxybenzamine displaced ICP with KDs of 100 nM, 2, 20, 20, 60, and 200 microM, respectively. The alpha-adrenergic antagonists, yohimbine and prazosin, showed no specific binding. These data provide evidence that catecholamines act via beta-adrenergic receptors in carp liver and that alpha-adrenergic receptors are not present. Vasoactive peptides play no significant role in regulation of carp liver glycogenolysis.
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PMID:Hormonal regulation of hepatic glycogenolysis in the carp, Cyprinus carpio. 303 3

Vascular effects of theophylline and enprofylline, a novel xanthine derivative lacking adenosine receptor antagonism, were studied comparatively in tubular preparations of small human placental arteries mounted in an isometric myograph. Both xanthines produced concentration-dependent (10(-7)-3 X 10(-3) M) relaxation of arteries contracted by PGF2 alpha or PGE2 in both normal Ca2+-medium and in Ca2+-depleted medium. Enprofylline was about three times more potent than theophylline. Also in vasopressin-contracted arteries enprofylline was a more potent vasodilator in both media. In contrast the xanthines were equally potent in relaxation of the tonic as well as the phasic part of a K+-induced contraction, but less potent than in relaxation of PG-induced contractions. Propranolol, phentolamine, atropine, indomethacin or tetrodotoxin did not influence the xanthine relaxations. It is concluded that the theophylline-induced relaxation of small human placental arteries is not due to adenosine receptor antagonism. A common important mechanism of action, in which enprofylline is more potent than theophylline, seems to be interference with intracellular Ca2+-binding/mobilisation processes. Some decrease in cellmembrane Ca2+-permeability produced by the xanthines seems to take part in the mechanism of relaxation.
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PMID:Enprofylline and theophylline on small human placental arteries: studies of in vitro effects and mode of action. 399 86

1. Intramuscular or subcutaneous injections of isoprenaline and dichloroisoprenaline and subcutaneous injection of pronethalol reduced the rates of excretion of water, sodium, potassium and chloride in the urine of conscious, hydrated rats. Inulin excretion usually fell at high, but not at low, dose levels. These changes were attributed to direct stimulant actions on beta-adrenoceptors in the kidney.2. A reduction in perfusion pressure to the kidney may also have contributed to these urinary changes, because isoprenaline produced a transient fall in mean arterial blood pressure when given subcutaneously to anaesthetized rats.3. Intramuscular injection of pronethalol and subcutaneous injection of antidiuretic hormone both reduced the rate of urine flow without modifying other parameters of urinary function (excretion of inulin and electrolytes were not diminished).4. This latter action of pronethalol could not be ascribed to an increased secretion of antidiuretic hormone, for it also occurred in hypophysectomized rats.5. Propranolol increased the renal excretion of sodium and chloride. A small rise in urinary potassium levels also occurred but urine volume and inulin excretion were not modified. Some possible modes of action of propranolol are discussed.
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PMID:The influence of beta-adrenoceptive receptor blocking agents on urinary function in the rat. 438 57

Opiate receptor blockade, or forced imbibition of 2% NaCl to deplete pituitary dynorphin decreases 2-deoxy-D-glucose (2-DG), but not insulin-induced hyperphagia, indicating a possible role for dynorphin in the eating associated with endogenous opiates. Beta-adrenergic receptor blockade decreases vasopressin release induced by 2-DG but not by insulin. Because vasopressin and dynorphin are sometimes co-localized, it was hypothesized that naloxone-sensitive feeding might be selectively inhibited by beta-adrenergic blockade with propranolol. Propranolol in doses as low as 2.5 mg/kg inhibited 4 hr feeding induced by 2-DG (400 mg/kg). Propranolol did not significantly affect feeding induced by ketocyclazocine administration (3.0 mg/kg) or by 24 hr food deprivation. Feeding stimulated by insulin (10 U/kg) was significantly inhibited by propranolol (2.5 mg/kg) only when the propranolol was reinjected during the period 2 hr after insulin injection, when the induced feeding was greatest. In summary, propranolol inhibited opiate-related (2-DG) as well as opiate-independent (insulin) hyperphagias. It also failed to inhibit food intake resulting from the opiate related stimulus of 24 hr food deprivation. Therefore, naloxone sensitive hyperphagias were not specifically inhibited by beta-adrenergic blockade, indicating that vasopressin-associated dynorphin is not involved in opiate related feeding.
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PMID:Differential inhibition by propranolol of feeding induced in rats by various stimuli. 609 26

In an attempt to define more precisely the various mechanisms involved in antidiuretic hormone (ADH) release during positive end-expiratory pressure ventilation (PEEP), experiments were performed on seven groups of dogs. PEEP-10 and PEEP-15 cmH2O caused significant elevations of plasma ADH from basal values of 24.9 +/- 5.2 pg/ml (mean +/- SE) to 64.6 +/- 14.2 and 106.0 +/- 20.6, respectively (P < 0.02, P < 0.005). The ADH levels returned to basal values after cessation of PEEP. This rise in ADH levels was prevented by an infusion of dextran prior to PEEP. The fall in blood pressure and cardiac output that occurred during PEEP was also prevented by the dextran infusion. Changes in ADH levels were unrelated to lung volume, left transmural pressure, and serum osmolality. Bilateral vagotomy and carotid sinus denervation was followed by an attenuated rise in ADH levels in terms of the percent rise above base line, but it did not significantly alter the absolute rise in ADH during PEEP. ADH levels were, however, reduced significantly by decreasing intracranial pressure by the removal of cerebrospinal fluid during PEEP. Propranolol administration prior to PEEP completely blocked plasma renin activity. Although the peak ADH levels were unaffected by propranolol, the rise was delayed. The results obtained indicate that a number of physiological factors may affect plasma ADH levels during PEEP. These include the carotid body and aortic arch baroreceptors as wells as sensors of intracranial pressure.
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PMID:Elevations in plasma ADH levels during PEEP ventilation in the dog: mechanisms involved. 616 Jul 73

The effect of the beta-adrenoceptor agonist isoprenaline on the plasma concentrations of beta-endorphin (beta-E) and beta-lipotropin (beta-LPH) was investigated in conscious rats. Isoprenaline (i.m.) elevated plasma beta-endorphin-like immunoreactivity (beta-EI) as measured by radioimmunoassay of unextracted plasma, with peak values 24 min after drug administration. This effect was dose-dependent. The lowest effective dose of isoprenaline was 15 micrograms kg-1; 240 micrograms kg-1 exerted a maximum effect, raising plasma beta-EI about ten-fold above control values. Plasma vasopressin concentrations also increased in response to isoprenaline following a time-course identical to that of plasma beta-EI. (+/-)-Propranolol (1 mg kg-1) but not phentolamine (10 mg kg-1) rendered isoprenaline (240 micrograms kg-1) injections almost ineffective. Because of the cross-reactivity of beta-LPH in the radioimmunoassay used, plasma was extracted by means of a cation exchange resin and subjected to gel chromatography on a Sephadex G-50 column, avoiding artefactual degradation of the peptides. In isoprenaline-treated rats about 50% of the beta-EI behaved similar to human beta-LPH, whereas 45% co-migrated with human beta-E; immunoreactivity corresponding to beta-LPH or beta-E comprised about 70% or 30%, respectively, in the plasma extract of vehicle-treated rats. Dexamethasone pretreatment reduced the isoprenaline-induced increase in plasma beta-EI by 87%, but left the simultaneous elevation of plasma vasopressin concentrations unchanged. These data demonstrate that isoprenaline stimulates beta-LPH and beta-E release in vivo. The possibility of an interrelationship between vasopressin and beta-E release is discussed.
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PMID:The effect of isoprenaline on plasma concentrations of immunoreactive beta-endorphin and beta-lipotropin in the conscious rat. 627 32

Intravenous (10 micrograms/kg) or intracisternal (1 microgram/kg) clonidine inhibited the diuretic response to negative pressure breathing (NPB) and left atrial distension (LAD) in chloralose anesthetized dogs. The drug reduced the induced tachycardia, but not the increase in respiratory rate caused by NPB, and did not change the blood pressure. Propranolol (1 mg/kg i.v.) did not change the NPB-induced diuresis. Intravenous yohimbine (1 mg/kg i.v.) opposed the effects of intravenous or intracisternal clonidine, whereas prazosin (0.05 mg/kg i.v.) had no effect. These results show that the adrenergic receptor implicated in the volumetric control of vasopressin secretion could be of the alpha 2 subtype. This alpha 2 adrenoceptor could be centrally located. Clonidine might therefore be proposed to combat the dehydration observed after long-term weightlessness.
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PMID:Evidence for the involvement of central alpha 2 mechanisms in intrathoracic volume expansion--induced diuresis: a study with clonidine and propranolol. 628 49

1. Intravenous (10 micrograms/kg) or intracisternal (1 microgram/kg) clonidine inhibited the diuretic response elicited by negative pressure breathing (NPB) or left atrial distension (LAD) in chloralose anaesthetized dogs. The drug reduced the induced tachycardia, but not the increase in respiratory rate elicited by NPB. Blood pressure was unchanged. 2. Propranolol (1 mg/kg IV) did not change NPB-induced diuresis. 3. Intravenous yohimbine (1 mg/kg IV) restored these two diuresis inhibited by intravenous or intracisternal clonidine, whereas prazosin (0.05 mg/kg IV) was without effect. 4. These results show that the adrenergic receptor implicated in the volumetric control of vasopressin secretion could be of the alpha 2 subtype. This alpha 2 adrenoceptor could be localized at a central level. 5. The possible clinical consequences (hydrosaline retention and antihypertensive drugs; use of clonidine in aerospace medicine) of these data are discussed.
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PMID:Clonidine inhibits diuresis caused by negative pressure breathing and left atrial distension: role of central adrenergic alpha 2 receptors. 628 86


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