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 release of vasopressin and oxytocin is regulated by the electrical activity of magnocellular neurosecretory cells in the supraoptic and paraventricular nuclei, which is under the control of a great variety of neurotransmitters and neuromodulators. The major neural signals to the supraoptic nucleus are from excitatory glutamate inputs and inhibitory GABA inputs. In recent studies, the voltage-clamp mode of the whole-cell patch-clamp technique has been applied to slice preparations from rat hypothalamus to monitor synaptic inputs to supraoptic neurones. Spontaneous excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) are abolished by CNQX and picrotoxin, respectively, but are insensitive to tetrodotoxin, indicating that they represent quantal release of glutamate and GABA, respectively, from nerve terminals of presynaptic neurones. GABA and glutamate show remarkable suppressive effects on both EPSCs and IPSCs via presynaptic GABA(B) and mGlu receptors, respectively. Noradrenaline, which excites supraoptic neurones via postsynaptic alpha1-receptors, also suppresses IPSCs and potentiates EPSCs. On the other hand, prostaglandin E2, which excites supraoptic neurones via postsynaptic prostaglandin E2 (EP) receptors of the EP4 subclass, also suppresses IPSCs via EP3 receptors but has little effect on EPSCs. Thus pre- and postsynaptic mechanisms may act cooperatively to excite supraoptic neurones. Nitric oxide, which inhibits supraoptic neurones, potentiates IPSCs without affecting EPSCs. This provides another example for the preferential modulation of IPSCs of supraoptic neurones. On the other hand, PACAP, which causes a long-lasting increase in the firing frequency via the postsynaptic receptors, has no effect on EPSCs and IPSCs, suggesting that some ligands act only at postsynaptic receptors. Thus multiple patterns for pre- and postsynaptic modulation are present in the supraoptic nucleus, and the electrical activity of supraoptic neurones is regulated via complex mechanisms at both pre- and postsynaptic sites.
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PMID:Pre- and postsynaptic modulation of the electrical activity of rat supraoptic neurones. 1079 17

Oxytocin secretion is important for the normal progress of parturition in the rat. We tested the hypotheses that contractions of the uterus before pup delivery activate oxytocin neurons, and that they do so via a noradrenergic projection. In anesthetized 22-day (term) pregnant rats, i.v. oxytocin pulses enhanced both uterine contractile activity and the firing rate of oxytocin and vasopressin neurons in the supraoptic nucleus, and these were significantly correlated. The same oxytocin treatment also increased the expression of Fos in both the supraoptic nucleus and the nucleus of the tractus solitarius, but not in 21-day pregnant or virgin rats. In five of eight rats on the day of expected parturition, noradrenaline release in the supraoptic nucleus (sampled by microdialysis) exhibited sudden peaks during oxytocin administration, seen in only one of nine rats given vehicle pulses. Noradrenaline release was significantly greater in rats that went into labor or gave birth to a pup than in rats not in labor. In rats infused with the alpha(1)-noradrenergic receptor antagonist, benoxathian, into the supraoptic nucleus before and during iv oxytocin administration, Fos expression in supraoptic neurons was significantly less than that in vehicle controls. Thus, at term pregnancy, uterine contractions activate both oxytocin and vasopressin neurons in the SON, and this activation involves a noradrenergic pathway.
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PMID:Uterine contractile activity stimulates supraoptic neurons in term pregnant rats via a noradrenergic pathway. 1115 34

In the present study, we examined the effects of bath application of vasopressin and noradrenaline on the spontaneous tonic discharge of medial vestibular nucleus (MVN) neurones and investigated if there is an interaction between the two drugs in an in vitro slice preparation of the rat brainstem containing the MVN. The results showed that vasopressin did not affect the spontaneous discharge rate of MVN neurones when applied either as a 60 s pulse or when the drug continuously perfused the slice for a period of 10 min. In contrast, noradrenaline affected the spontaneous discharge rate of the majority of cells tested (53/60, 88%). Noradrenaline excited the majority (46/53, 87%) of MVN neurones through both alpha1 and beta noradrenergic receptor-linked mechanisms. The remaining cells (7/53, 13%) were inhibited by noradrenaline through an alpha2 noradrenergic receptor-linked mechanism. Neither the excitatory nor inhibitory effects of noradrenaline were modified by vasopressin when the two drugs were applied together.
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PMID:Modulation of rat medial vestibular nucleus neurone activity by vasopressin and noradrenaline in vitro. 1116 85

The development of adrenergic sensitivity in nociceptors has been suggested as a mechanism of neuropathic pain. We sought to determine if nociceptors in the skin of normal subjects exhibit adrenergic sensitivity. We investigated the effects of intradermal administration of norepinephrine, phenylephrine, and brimonidine on heat pain sensitivity. Norepinephrine and phenylephrine (in concentrations ranging from 0.1 to 10 microM by factors of 10), brimonidine (at 0.01-1 microM), and saline were injected (30 microl volume) in a random, double-blind manner to different sites on the volar surface of the forearm in ten subjects. Before and after the injections, heat testing was performed with a non-contact laser thermal stimulator. Heat pain threshold was measured by means of a 'Marstock' technique in which subjects pressed a reaction time key when they perceived that a slowly increasing heat stimulus (1 degrees C/s ramp from a 36 degrees C base) was painful. In addition, the subjects used magnitude estimation techniques to rate the intensity of pain to a suprathreshold heat stimulus (47 degrees C, 2 s). Mechanical testing was done using 200-microm diameter probes attached to calibrated weights that provided forces over the range of 16-512 mN. The intradermal injections of norepinephrine, phenylephrine and brimonidine produced little evoked pain. However, a dose-dependant decrease in heat pain threshold, but not mechanical pain threshold, was observed. At the highest drug dose injected, all three adrenergic compounds produced a significant decrease in heat pain threshold compared to the saline injection. A significant increase in response to the suprathreshold heat stimulus was also found. One possible explanation for this apparent heat hyperalgesia is that the decrease in perfusion due to the localized vasoconstriction may alter the heat response. However, in control studies we found that the non-adrenergic vasoconstrictors, angiotensin II and vasopressin did not produce heat hyperalgesia at doses that produced comparable decreases in blood flow. In addition, occlusion of blood flow with a blood pressure cuff did not lead to heat hyperalgesia. Thus, the heat hyperalgesia observed with the adrenergic agonists is not due to a decrease in perfusion associated with the injection. These results indicate that alpha(1)- and alpha(2)-adrenoceptor-mediated mechanisms may play a role in sensitization of nociceptors to heat stimuli in normal skin.
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PMID:Heat, but not mechanical hyperalgesia, following adrenergic injections in normal human skin. 1116 66

A 39-year-old female with alcoholic cirrhosis was admitted with signs of an alcoholic hepatitis. Within one week a hepatorenal syndrome (HRS) (Creatinin 5.83 mg/100 ml, Harnstoff 235 mg/100 ml) evolved in the absence of additional causes. She had a diminished water (urine volume 31 ml/h) and sodium excretion (10 mmol/l). Urine flow was increased to 131 ml/h by plasma expansion with i.v. infusion of volume and albumin and with infusion of dopamine (3 micrograms/kg/min) and, as there was no diuretic pretreatment and thus, no HRS secondary to diuretic treatment, furosemide (500 mg/24 h). However, impairment of renal function remained unchanged with this therapy. Therefore, norepinephrine (NE) therapy was initiated. A dosage of 0.1-0.12 microgram/kg/min was necessary to achieve the desired increase in the mean arterial pressure of 10-20 mm Hg. During the NE infusion the urine volume increased further to 231 ml/h, the sodium excretion raised to 44 mmol/l, and serum levels of creatinine and urea decreased to 1.91 mg/100 ml and 141 mg/100 ml, respectively. With recovering liver function the NE infusions could be discontinued after 5 days without recurrence of a HRS until discharge after 3 weeks. Beside the vasopressin analogon ornipressin, the combination of norepinephrine and dopamine seems to be useful for the therapy of HRS. Norepinephrine has the advantage of an easy accessibility in ICUs and seems to exert less side effects.
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PMID:[Successful therapy of hepatorenal syndrome with norepinephrine]. 1119 84

The purpose of this study was to assess the endocrine status, thoracic impedance, blood concentration, and hemodynamic dose-responses using different angles of passive head-up tilt (HUT) ranging from 12 degrees to 70 degrees in the same subjects. Measurements were performed during 20 min supine position (pre-HUT), 30 min upright (HUT12, HUT30, HUT53, or HUT70), and 20 min supine (post-HUT); subjects 70 min in the supine position only (HUT0) served as resting controls. Norepinephrine increased above resting control values by 19, 44, 80, and 102%; epinephrine by 30, 41, 64, and 68%; aldosterone by 29, 62, 139, and 165%; plasma renin activity n. s., 41, 91, and 89%; vasopressin n.s., 27, 47, and 59%; thoracic bioimpedance n. s., 8, 13, and 16%; heart rate n. s., 5, 26, and 45%, and mean arterial pressure n. s., 5, 7, and 10%; at min 27 of HUT12, HUT30, HUT53, and HUT70, respectively. Pulse pressure decreased with HUT53 and HUT70 by 4 and 10%. Hematocrit increased by 0.2, 1.7, 6.3, and 7.2%, respectively. Blood density increased by 2.3 and 3.0 g/l, plasma density by 1.7 and 1.8 g/l with HUT53 and HUT70. After finishing HUT, heart rate fell to values which stayed below pre-HUT, and also below resting control levels for > or = 5 min ("post-orthostatic bradycardia") even after the lowest orthostatic load (HUT12). Thoracic impedance and arterial pressure remained increased after terminating HUT30, HUT53, and HUT70. In conclusion, passive orthostatic loading of different extent produces specific dose-responses of different magnitude in the endocrine system, blood composition, thoracic impedance, and hemodynamic variables. The heart rate is depressed even after HUT12, while arterial blood pressure and thoracic impedance exceed pre-stimulus levels after greater head-up tilt, indicating altered cardiovascular response after passive orthostasis.
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PMID:Cardiovascular and hormonal changes with different angles of head-up tilt in men. 1130 Feb 29

The aim of our study was to quantitate, in the same test subjects, hormonal, thoracic bioimpedance, blood composition, and hemodynamic dose-responses during different angles of passive orthostatic loading (head-up tilt, HUT) ranging from 12 degrees to 70 degrees. Measurements were performed with 20 min supine (pre-HUT), 30 min upright (HUT-12 degrees, HUT-30 degrees, HUT-53 degrees, or HUT-70 degrees), and 20 min supine (post-HUT); or supine only (HUT-0 degree, rest control). Norepinephrine increased above rest control by 19, 44, 80 and 102%; epinephrine 30, 41, 64, and 68%; aldosterone 29, 62, 139, and 165%; plasma renin activity n. s., 41, 91, and 89%; vasopressin n. s., 27, 47, and 59%; thoracic bioimpedance n. s., 8, 13, and 16%; heart rate n. s., 5, 26, and 45%, and mean arterial pressure n. s., 5, 7, and 10%; respectively, at min 27 of HUT-12 degrees, -30 degrees, -53 degrees, and -70 degrees. Pulse pressure narrowed with HUT-53 degrees and -70 degrees by 4 and 10%. Hematocrit increased 0.2, 1.7, 6.3, and 7.2%, respectively. Blood density increased by 2.3 and 3.0 g/l, plasma density by 1.7 and 1.8 g/l with HUT-53 degrees and -70 degrees. After finishing HUT, heart rate fell to values which stayed below pre-HUT, and also below rest control levels for > or = 5 min ("post-orthostatic bradycardia") even after the lowest orthostatic load (HUT-12 degrees). Thoracic bioimpedance and arterial blood pressure stayed increased after finishing HUT-30 degrees, -53 degrees, and -70 degrees. In summary, passive orthostasis of different degree produces specific dose-responses of different magnitude within endocrine, blood concentration, thoracic bioimpedance, and hemodynamic variables. Heart rate is depressed even after HUT-12 degrees, while arterial blood pressure and thoracic bioimpedance exceed pre-stimulus levels after HUT of higher degree, indicating altered cardiovascular state after passive orthostasis.
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PMID:[Cardiovascular and humoral adaptation with passive orthostasis in men]. 1137 90

The mammalian pineal gland is known to receive a noradrenergic sympathetic efferent signal from the suprachiasmatic nucleus (SCN) via the superior cervical ganglion. Arg-vasopressin (AVP) containing neurons in the SCN is one of the output paths of circadian information to the other brain areas. AVP release from the SCN is suppressed by melatonin. In turn, we determined the direct effect of AVP on melatonin release using pineal gland explant culture. AVP (1 microM) suppressed melatonin release. Noradrenaline stimulated melatonin release was attenuated by AVP. In turn, the expression of the melatonin synthesis enzyme arylalkylamine N-acetyltransferase mRNA in the rat SCN was reported. We measured melatonin content in the SCN in rats kept under the light-dark cycle and constant dim light. Melatonin in the SCN was higher during the dark period than that in the light. A similar tendency was also observed in the SCN of animals kept under a constant dim light. It was suggested that the reciprocal regulation of melatonin release and AVP release occurs in the SCN and pineal gland.
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PMID:Circadian rhythm of melatonin release in pineal gland culture: arg-vasopressin inhibits melatonin release. 1168 43

Vasopressin is released not only from axon terminals in the neurohypophysis but also from soma/dendrite regions in the supraoptic nucleus. In order to investigate presynaptic roles of dendritically released vasopressin, we examined effects of local application of vasopressin upon noradrenaline release within the supraoptic nucleus by a microdialysis method. Noradrenaline release within the supraoptic nucleus was facilitated by local perfusion with high K+ or an NMDA receptor antagonist. Vasopressin augmented noradrenaline increase after high K+ but reduced it after an NMDA receptor antagonist, AP-5. The results suggest that dendritically released vasopressin modulates noradrenaline release within the supraoptic nucleus in a bimodal fashion.
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PMID:Vasopressin differentially modulates noradrenaline release in the rat supraoptic nucleus. 1173 1

The possibility that drugs administered to Skylab 3 (SL-3) and 4 (SL-4) crewmen for space motion sickness may have interfered with their biomedical evaluation in space was investigated. Healthy volunteers received combinations of Scopolamine/Dexedrine for four days in regimens similar to those used in these missions. Urine samples, heart rate, body temperature, mood and performance were analyzed for drug-related changes. Twenty-four hour urine samples were analyzed by the same procedures as those used to analyze the flight samples. Hormone concentrations determined included cortisol, epinephrine, norepinephrine, aldosterone and antidiuretic hormone (ADH). In addition, volume, specific gravity, osmolarity, sodium (Na), potassium (K), calcium (Ca), magnesium (Mg), chloride (Cl), inorganic phosphate, uric acid and creatinine were measured. Performance was not affected by the Scopolamine/Dexedrine. The drug combination increased daily mean heart rate (HR) significantly in all the subjects and daily mean rectal temperature (RT) in some of the subjects. A 2-4 hr phase shift in the HR circadian rhythm was also observed which indicates that internal circadian synchrony was disturbed by the drugs. Psychological and subjective evaluation indicated that the subjects could usually identify which days they were given the drugs by an increase in tension and anxiety, decreased patience, restlessness, decreased appetite, difficulty in sleeping and feelings of increased heart rate and body temperature. Urinary electrolytes were not changed significantly by the drug, but marked and significant changes occurred in urine volume and hormone excretion patterns. Scopolamine/Dexedrine caused consistent elevations in urinary cortisol and epinephrine and a transient elevation in ADH. Norepinephrine excretion was decreased, but there was no significant change in aldosterone excretion or in 24 hr urine volume. A comparison of these findings with the first four days of inflight data from the SL-3 and SL-4 missions leads to the conclusion that the dramatic increases in aldosterone excretion during the first three days of spaceflight probably can be directly attributed to weightlessness, whereas the antimotion sickness medication could have substantially contributed to the early increased excretion of epinephrine and cortisol during these missions.
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PMID:Space motion sickness medications: interference with biomedical parameters. 1182 24


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