Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

In an attempt to test the possibility that sino-aortic baroreceptors may mediate the previously reported stress response in hypothalamic magnocellular neurosecretory cell activity in rats, effects of deafferentation of sino-aortic baroreceptors on plasma levels of vasopressin and oxytocin after fear-related emotional stress were studied in male rats 28-33 days after the surgery. An alpha 1-adrenergic receptor agonist, phenylephrine (1 mg/kg) injected i.p. under anesthesia increased arterial blood pressure in the rats that had received surgical operation of sino-aortic denervation (SAD) and in the rats of sham-operation control (SHAM). Reflex bradycardia after phenylephrine occurred in the SHAM but not in the SAD group. These results indicate that afferent signals originating from sino-aortic baroreceptors were effectively blocked by the SAD surgery. In the similarly prepared SAD group, plasma level of vasopressin was decreased and plasma level of oxytocin was increased significantly to the same extent as in the SHAM group after low-frequency shocks (0.05 Hz, 5 min) or environmental cue signals previously paired with shocks. It is therefore suggested that afferent neural signals originating from sino-aortic baroreceptors are not primarily involved in the suppressive vasopressin or the facilitatory oxytocin response to fear-related emotional stress in rats.
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PMID:Neurohypophysial responses to emotional stress after deafferentation of sino-aortic baroreceptors in rats. 131 20

Administration of interleukin-1 (IL-1) induces increases in plasma ACTH and glucocorticoids. Numerous experiments have implicated the hypothalamic CRH neurosecretory system in these responses, but have failed to provide evidence for involvement of the ACTH secretagogue vasopressin (VP). The rat CRH neurosecretory system contains two types of cells: VP expressing and VP deficient. Hence, the above findings suggested that IL-1 may selectively activate the VP-deficient subtype of CRH neurosecretory cells. In this study we employed postembedding electron microscopic immunocytochemistry to directly assay IL-1-induced depletion of secretory vesicles from identified VP-expressing and VP-deficient CRH neurosecretory axons. IL-1-induced depletion of secretory vesicles from these axons was correlated with increases in plasma ACTH and decreases in plasma PRL. No dose of IL-1 was found that could selectively activate one subtype of CRH neurosecretory axons; at doses of 0.67 microgram/100 g and above for both IL-1 alpha and IL-1 beta, equal depletion of vesicles from the two subtypes was observed. Similar results were previously found after the injection of bacterial lipopolysaccharide, which induces the release of IL-1 from macrophages. The findings unequivocally establish for the first time that IL-1 activates hypothalamic CRH neurosecretory cells in the absence of surgical stress, anesthesia, disruption of the infundibular area, or administration of toxic drugs. In addition, these data clearly demonstrate that IL-1 induces the release of VP from neurosecretory axons in the portal capillary zone of the external zone of the median eminence. Previous studies have shown that the VP-deficient subtype of CRH neurosecretory axons is not strongly activated by several types of stress; therefore, activation of the system by inflammatory mediators involves mechanisms different from those mediating the stress response.
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PMID:Effects of interleukin-1 on the stress-responsive and -nonresponsive subtypes of corticotropin-releasing hormone neurosecretory axons. 131 22

The effect of vasopressin analogues on plasma adenosine 3',5'-cyclic monophosphate (cAMP) concentration was examined in a group of five conscious dogs instrumented for the measurement of arterial pressure and cardiac output (electromagnetic flowmeter). These dogs were infused for 20 min with a selective antidiuretic (V2) agonist, desamino-8-D-arginine vasopressin (DDAVP, 10 ng.kg-1 x min-1). This infusion was repeated on another day in the presence of the combined V1-V2 antagonist d(CH2)5-D-Tyr(Et)-4-valine,8-arginine vasopressin. The dogs also received an infusion of the selective V1 agonist 2-phenylalanine,8-ornithine oxytocin (Phe-OrnOT) at a rate of 10 ng.kg-1 x min-1. The effect of these infusions was compared with those of an isotonic saline infusion. Plasma cAMP measured in the aorta remained unchanged during all infusions but that of the selective V2 agonist DDAVP alone, during which it increased significantly from 22.4 +/- 0.8 to 32.6 +/- 4.6 and 37.0 +/- 4.1 pmol/ml after 10 and 20 min, respectively. In the plasma sampled from the inferior vena cava caudal to the renal veins, cAMP increased during DDAVP infusion from 22.2 +/- 2.5 to 39.2 +/- 3.8 and 36.0 +/- 4.0 pmol/ml after 10 and 20 min, respectively. The infusion of DDAVP was later given to the same dogs under anesthesia after bilateral nephrectomy, which did not modify the effect of DDAVP on arterial plasma cAMP. In another group of four conscious dogs, infusion of DDAVP at the same rate did not induce significant changes in plasma catecholamines.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:cAMP and extrarenal vasopressin V2 receptors in dogs. 133 16

Acute hypertensive responses during nitrous oxide-opioid-relaxant anesthesia are a common clinical problem. In adult men undergoing radical prostatectomy procedures and anesthetized with a standardized technique, we evaluated the effectiveness of alfentanil, isoflurane, and trimethaphan in treating acute hemodynamic and stress hormone responses to surgical stimulation. Stress hormone concentrations were measured 1 min before skin incision, after the onset of an acute hypertensive response, and after returning the mean arterial pressure to within 10% of the preincision values with one of the three treatment modalities. Pretreatment plasma alfentanil concentrations (151 +/- 47 to 156 +/- 47 ng.ml-1) and end-tidal nitrous oxide concentrations (66 +/- 2 to 68 +/- 2%) were similar in all three groups. Acute hypertensive events were associated with significantly increased concentrations of catecholamines and vasopressin (antidiuretic hormone [ADH]). Whereas intravenous alfentanil returned all hormone concentrations to preincision values, norepinephrine and glucose concentrations were significantly increased after adjunctive isoflurane administration. Although trimethaphan decreased the norepinephrine concentration, the epinephrine, beta-endorphin, cortisol, ADH, and glucose concentrations were significantly increased compared to preincision values. However, the persistent elevation in the posttreatment ADH concentration in the trimethaphan group was the only significant difference between the three groups. Mean (+/- standard deviation) times to awakening (2.8 +/- 3.3 to 3.8 +/- 4.2 min), extubation (8.1 +/- 4.8 to 10.3 +/- 8.5 min), and orientation (19.6 +/- 20.4 to 24.6 +/- 19.1 min) were similar in all three groups. Naloxone was required more frequently in patients in the alfentanil (35%) and isoflurane (24%) groups than in the trimethaphan group (4%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of stress response during balanced anesthesia. Comparative effects of isoflurane, alfentanil, and trimethaphan. 134 82

During radical prostatectomy procedures under total intravenous anesthesia, acute hemodynamic responses to retropubic dissection (30% +/- 8% to 36% +/- 12% [mean +/- SD] increases in mean arterial pressure) were treated with supplemental doses of either an opioid analgesic (alfentanil) or a sedative-hypnotic (propofol) to return the mean arterial pressure to within 10% of the preincision value. Although both drugs were effective, control with propofol required 10.1 +/- 2.5 min compared with 6.3 +/- 2.6 min in the alfentanil group (mean +/- SD; P < 0.01). Plasma stress hormone concentrations increased significantly in response to this surgical stimulus: epinephrine increased from 246% +/- 169% to 283% +/- 330%; norepinephrine increased from 44% +/- 33% to 83% +/- 104%; and antidiuretic hormone increased from 1300% +/- 1591% to 1700% +/- 1328%. Both alfentanil and propofol were equally effective in returning the catecholamine concentrations to their preincision levels. However, antidiuretic hormone levels remained above preincision values in both groups. Despite earlier awakening (3.4 +/- 2.9 vs 9.1 +/- 6.8 min; P < 0.05) in the alfentanil treatment group, there was no difference in time to spontaneous ventilation or tracheal extubation between the groups. In addition, 36% of the alfentanil-treated patients required antihypertensive therapy in the postanesthesia care unit compared with only 9% in the propofol group (P < 0.05). Postanesthesia care unit and hospital discharge times were similar in both treatment groups. We conclude that supplemental doses of alfentanil or propofol were equally effective in controlling acute hemodynamic and hormonal responses to surgical stimuli during total intravenous anesthesia.
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PMID:Total intravenous anesthesia: effects of opioid versus hypnotic supplementation on autonomic responses and recovery. 135 2

Hindquarter (terminal aortic) blood flow (HQF) and arterial pressure (AP) were observed in rats with an electromagnetic flow probe implanted around the terminal aorta and an arterial indwelling cannula. Hindquarter peripheral resistance (HQR) was calculated by dividing mean AP by HQF. Under pentobarbital anesthesia, HQR was decreased significantly (p less than 0.001) by ganglionic blockade with hexamethonium bromide (C6). Since C6 does not change HQR significantly without anesthesia, we interpret that pentobarbital anesthesia generated a sympathetic vasoconstrictor tone in hindquarter resistance vessels. This was further substantiated by the observation that the increase in HQR on infusion of vasopressin was obscure under pentobarbital anesthesia: Presumably, the increase was offset by reflex inhibition of the hindquarter tone induced by anesthesia. The generation of hindquarter vasoconstrictor tone by pentobarbital was for the most part ascribable to the baroreceptor reflex to compensate for the depressor effect of this anesthetic, because it was greatly diminished after severance of the buffer nerves.
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PMID:Sympathetic vasoconstrictor tone induced by pentobarbital anesthesia in hindquarters of rats. 135 76

It is likely that central cholinergic pathways to the paraventricular and supraoptic nuclei participate in the control of vasopressin release. We have shown previously that this is due, in part, to activation of muscarinic, but not nicotinic, receptors in the paraventricular nucleus. There is, however, reason to believe that this cholinergic effect in the supraoptic nucleus may be the result of activation of nicotinic receptors. To test this possibility, we have studied in conscious unrestrained rats the effect of microinjection of muscarinic and nicotinic agonists into the supraoptic nucleus on vasopressin release, mean arterial blood pressure, and heart rate. Under ether anesthesia, a stainless steel guide cannula was placed in the supraoptic nucleus 5-7 days before the experiment, and femoral, arterial, and venous catheters were implanted 1 day before the experiment. Microinjection of nicotine into the supraoptic nucleus at doses of 1 and 10 micrograms resulted in transient increases in the plasma vasopressin concentration that were 7-fold and 11-fold greater, respectively, than control values at 3 min. There were also small transient increases in mean arterial blood pressure, but heart rate was unchanged. The microinjection of 2 and 20 ng of oxotremorine, a muscarinic agonist, into the supraoptic nucleus had no effect on the plasma vasopressin concentration, mean arterial blood pressure, or heart rate. These doses of oxotremorine were previously shown to have potent stimulatory effects on vasopressin release when microinjected into the paraventricular nucleus. These findings suggest that the central cholinergic stimulation of vasopressin release is due, in part, to activation of muscarinic receptors in the paraventricular nucleus and nicotinic receptors in the supraoptic nucleus.
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PMID:Effect on vasopressin release of microinjection of cholinergic agonists into the rat supraoptic nucleus. 140 34

Controlled mechanical ventilation (CMV) with positive end-expiratory airway pressure decreases urine output and renal sodium excretion. This study investigates--independent of surgical stress, general anesthesia, and sedation--the influences of antidiuretic hormone, atrial natriuretic peptide, plasma renin activity, and aldosterone on decreased urine output and renal sodium excretion during CMV with positive end-expiratory airway pressure. Hemodynamic, renal, and hormonal parameters were measured over a 4-h period in six trained, nonanesthetized, chronically tracheotomized dogs under two conditions: 1) control: hours 1-4, spontaneous breathing at continuous positive airway pressure of 4 cmH2O; and 2) CMV 20: hour 1, continuous positive airway pressure of 4 cmH2O; hours 2 and 3, CMV with a mean airway pressure of 20 cmH2O; and hour 4, continuous positive airway pressure of 4 cmH2O. Throughout the experiments, 0.5 ml.kg body weight-1.min-1 balanced electrolyte solution was administered intravenously. During the 2nd and 3rd h of CMV 20, urine volume decreased by 43% and sodium excretion decreased by 44% when compared with control values (P less than 0.05). The glomerular filtration rate decreased from 4.4 +/- 0.1 to 3.9 +/- 0.1 ml.kg-1.min-1 (P less than 0.05) during the 2nd h and from 4.4 +/- 0.1 to 4.1 +/- 0.1 ml.kg-1.min-1 (P less than 0.05) during the 3rd h of CMV 20. Fractional sodium excretion decreased from 4.7 +/- 0.3% to 2.9 +/- 0.2% (P less than 0.05) during the 2nd h and from 7.5 +/- 0.3% to 4.6 +/- 0.2% (P less than 0.05) during the 3rd h of CMV 20, compared with values during the control period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Positive end-expiratory pressure reduces renal excretion without hormonal activation after volume expansion in dogs. 141 67

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a disorder in which a sustained release of antidiuretic hormone occurs because of certain diseases, pharmacological agents, or trauma. Fluid volume expands with a resultant hyponatremia which, depending on the degree, may be asymptomatic or result in death. This case report describes a 38-year-old male in whom SIADH was strongly suspected secondary to Tegretol therapy to control a seizure disorder. Medical consultation is imperative for these patients before administering a fluid challenge during general anesthesia.
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PMID:Suspected inappropriate secretion of antidiuretic hormone in a male with mental retardation. 144 Jan 23

Pathophysiologic mechanisms of bradycardia during epidural anaesthesia (L3-L4 with 1% lidocaine, 38 ml) were evaluated by studying changes in selected cardiovascular and hormonal parameters. Six of eight subjects (analgesia to T8-T10) remained circulatory stable with no significant changes in heart rate (HR), mean arterial pressure (MAP) and thoracic impedance (TI). In one of two subjects MAP decreased after 25 min from 85 to 50 mmHg (11.3 to 6.7 kPa), HR from 80 to 45 beats.min-1 while thoracic impedance increased from 25.5 to 26.5 ohm. End-systolic diameter (ESD) and end-diastolic diameter (EDD) of the left ventricle determined with echocardiography were reduced from 3.8 to 3.2 cm (17%) and 5.6 to 5.0 cm (11%), respectively. In the other subject MAP decreased after 25 min from 75 to 50 mmHg (10.0 to 6.7 kPa) and HR from 82 to 60 beats.min-1 while thoracic impedance increased from 28.8 to 29.6 ohm. ESD was reduced from 3.8 to 3.3 cm (13%), and EDD from 5.6 to 5.0 cm (11%). Both subjects recovered after infusion of saline and being placed in the head-down position. There were no consistent changes in plasma catecholamines, whereas pancreatic polypeptide increased from 5 and 3 to 152 and 69 pmol.l-1, vasopressin from 3 and 2 to 152 and 46 pmol.l-1, and aldosterone from 282 and 229 to 383 and 485 pmol.l-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduced left ventricular diameters at onset of bradycardia during epidural anaesthesia. 146 23


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