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)

Arginine vasopressin, vasopressin antiserum and a specific vasopressin pressor antagonist were injected intracerebroventricularly into adrenalectomized rats before morphine-induced antinociception was tested. In these experiments we have exploited previous findings which showed that the antinociceptive effect of opioids was potentiated after adrenalectomy; rats that were adrenalectomized in the morning under basal resting conditions of the pituitary-adrenal system displayed significantly higher response latencies after morphine administration than rats adrenalectomized in the evening. These effects were measured 7 days after adrenalectomy. The same conditions were used in this study. Both, the vasopressin antiserum and the vasopressin antagonist abolished the morning adrenalectomy-induced hypersensitivity to centrally injected morphine and were not effective when administered to rats that had been adrenalectomized in the evening. The reverse was observed after intraventricular administration of vasopressin. The peptide significantly raised the sensitivity to morphine-induced antinociception of rats that had been adrenalectomized in the evening whereas it did not affect antinociception in animals that had been adrenalectomized in the morning. Vasopressin levels determined by radioimmunoassay in the cerebrospinal fluid were significantly higher in adrenalectomized animals. We propose that vasopressin is a critical neuropeptide factor involved in the adrenalectomy-induced hypersensitivity to morphine antinociception.
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PMID:Vasopressin and adrenalectomy-induced sensitivity to morphine. 321 78

Arginine vasopressin levels in 17 neonates with cardiac disease were compared with control levels in 10 healthy newborn infants. Infants with congestive heart failure who were free of left ventricular outflow tract obstruction had a mean level of 80 +/- 18 pg/ml, which was significantly greater than the mean control level (p less than 0.001). Infants with congestive heart failure and left ventricular outflow tract obstruction had a mean vasopressin level of 3 +/- 0.7 pg/ml, which was lower than the mean control level of 6 +/- 0.7 pg/ml (p less than 0.05). The data suggest that impaired forward flow to high pressure sinoaortic and ventricular baroreceptors is necessary for vasopressin release in congestive heart failure. In left ventricular outflow tract obstruction with heart failure these receptors may be impaired or absent, leading to decreased vasopressin release. Low plasma arginine vasopressin may adversely affect circulatory homeostasis.
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PMID:Variable arginine vasopressin levels in neonatal congestive heart failure. 334 66

The neurohypophysial hormones of the 1-month-old bovine fetus have been identified by their positions in ion-exchange chromatography and their retention times in high-pressure reverse-phase partition chromatography. Arginine vasopressin and oxytocin have been recognized. The molar ratio vasopressin/oxytocin in neurohypophysis is about 6 in the 1-month-old fetus compared with 4 in the 3-month-old fetus, 2.7 in the 7-month-old fetus and 1 in the adult. Vasotocin is virtually absent even in the early fetus (less than 0.1% of arginine vasopressin). The occurrence of a vasotocin gene expressed in the fetus but silent in the adult appears unlikely.
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PMID:Neurohypophysial hormones of the 1-month-old bovine fetus: absence of vasotocin during mammal development. 339 Dec 78

Arginine vasopressin stimulated the accumulation of labeled inositol phosphate in cultured rat aortic myocytes prelabeled with tritiated myo-inositol. This accumulation was prevented by pretreating the myocytes with the phorbol ester PMA. The time-course and concentration-effect curves were similar for inositol phosphate formation in myocytes and contractile effects on isolated aorta. Vasopressin agonists also stimulated inositol phosphate formation, whereas vasopressin-induced response could be inhibited by V1a-specific antagonists. These results suggest that stimulation of inositol phosphate formation in myocytes is due to V1a receptor activation and could be modulated by protein-kinase-C-mediated mechanisms.
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PMID:V1a vasopressin-induced accumulation of inositol trisphosphate in cultured rat aortic myocytes; modulation by protein kinase C. 349 Aug 52

Arginine vasopressin (AVP) not only influences renal water metabolism but also has profound cardiovascular effects. Physiologic levels of the hormone produce a pressor response in the basal state when vasoregulatory reflex mechanisms are interrupted. During hypovolemia, vasopressin affects systemic blood pressure independent of the renin-angiotensin system and efferent sympathetic pathways. Many studies implicate AVP in the pathogenesis of hypertension, but the actual mechanism and relative importance of vasopressin's role remain a matter of intense investigation.
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PMID:Role of arginine vasopressin in regulation of systemic arterial pressure. 351 3

Arginine vasopressin is hypothesized to act as a neurotransmitter or neuromodulator in the ventral septal area of the rat brain. To examine this role of vasopressin further, it was applied by microiontophoresis or micropressure from multiple-barrelled micropipettes onto spontaneously active or glutamate-activated neurons. Applied in this manner, vasopressin reduced glutamate-evoked excitation in 32 of the 47 cells studied. Further, micropressure application of the vasopressin antagonist d(CH2)5Tyr(Me)AVP reversed the vasopressin effects. In contrast, administration of vasopressin had no effect on excitations evoked by acetylcholine iontophoresis or on the spontaneous activity of the majority of the ventral septal neurons studied. These observations suggest that vasopressin may be acting on a V1-like receptor on specific neurons in the ventral septal area as a modulator of glutamate actions. Evoked responses were also obtained in the same population of ventral septal cells following stimulation of a variety of limbic areas. Inhibitory input onto most of the vasopressin responsive neurons studied was obtained following electrical stimulation of the paraventricular nucleus and bed nucleus of the stria terminalis, two cell groupings that are potential sources of vasopressin to the ventral septal area. Thus, the similarity in action of exogenously applied vasopressin and the evoked responses following paraventricular nucleus and bed nucleus stimulation suggests that vasopressin may be a neurotransmitter in this pathway.
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PMID:Modulation by arginine vasopressin of glutamate excitation in the ventral septal area of the rat brain. 356 16

Arginine vasopressin is reported to have an excitatory effect on hippocampal neurons in the slice preparation. However, vasopressin also has a classic vasopressor action on mammalian blood vessels. We used the rat hippocampal slice to examine the effects of this peptide on central neural and vascular targets. The hippocampus is densely vascularized and pyramidal cells are enmeshed in a network of microvessels. Vasopressin increased the excitability of impaled neurons without substantially altering membrane potential or resistance. The peptide also caused pronounced vasoconstriction in penetrating microvessels when applied at micromolar concentrations. The concerted action of vasopressin on neurons and blood vessels and the physical proximity of these cell types suggest mechanisms whereby these responses may be associated.
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PMID:Action of vasopressin on neurons and microvessels in the rat hippocampal slice. 359 83

1. Renal function and the effect of neurohypophysial hormone replacement was investigated in anaesthetized, acutely hypophysectomized, male rats. 2. Although urine production was only slightly lower over the 8 h post-operative study period in hypophysectomized rats, sodium excretion was greatly depressed reaching only 3.5 +/- 1.4 mumol/min compared with a peak of 13.2 +/- 1.0 mumol/min in intact animals. 3. In association with a decline in mean arterial blood pressure, glomerular filtration rate in hypophysectomized rats fell to 2.1 +/- 0.2 ml/min 8 h after operation by comparison with a mean rate in intact rats of 3.2 +/- 0.2 ml/min. 4. Plasma corticosterone levels were much lower in hypophysectomized (4 +/- 2 ng/ml) than in intact (36 +/- 4 ng/ml) rats, plasma aldosterone was reduced to a lesser extent (0.41 +/- 0.08 compared with 0.76 +/- 0.04 ng/ml). While oxytocin was not detectable in hypophysectomized rat plasma, trace levels of vasopressin (0.16 +/- 0.04 mu u./ml) were found. In intact unanaesthetized rats basal plasma levels of oxytocin were 0.32 +/- 0.13 mu u./ml and vasopressin were 0.85 +/- 0.19 mu u./ml. 5. Administration of oxytocin at 150 mu u./min, which produced plasma hormone levels (24.0 +/- 2.5 mu u./ml) greatly in excess of basal concentrations, increased renal sodium excretion but did not alter urine flow. Oxytocin administration at the lower rate of 15 mu u./min producing plasma hormone levels of 2.60 +/- 0.1 mu u./ml, did not alter renal sodium excretion. 6. Arginine vasopressin administered at 12 mu u./min induced plasma hormone levels of 1.54 +/- 0.09 mu u./ml and produced a large antidiuresis and small increase in the rate of sodium excretion. 7. The natriuretic response to vasopressin was potentiated by concurrent administration of oxytocin at 15 mu u./min. The peak sodium excretion of 5.8 +/- 1.0 mumol/min, however, remained well below that seen in intact rats. 8. It is concluded that, as restoration of posterior pituitary hormones at or above the physiological range only partially restored sodium excretion, the absence of anterior pituitary factors may also contribute directly or indirectly to the renal sodium retention of the hypophysectomized rat.
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PMID:The influence of neurohypophysial hormones on renal function in the acutely hypophysectomized rat. 362 41

1. Renal function and the effect of oxytocin and vasopressin replacement have been examined in anaesthetized male neurohypophysectomized rats. 2. Rates of urine flow were higher but sodium excretion markedly lower in neurohypophysectomized rats than in intact animals receiving hypotonic saline infusion (33.8 +/- 2.3 vs. 27.0 +/- 0.7 ml and 472 +/- 84 vs. 1946 +/- 124 mumol respectively for the third to sixth hour of study). 3. In intact animals, mean arterial blood pressure stabilized at 106 mmHg. Haematocrit (46%) remained stable but glomerular filtration rates declined slightly over the 8 h of study to 2.5 +/- 0.2 ml/h. These values in neurohypophysectomized rats did not differ significantly from those in intact rats. 4. Although plasma corticosterone levels (54 +/- 13 ng/ml) did not differ significantly from those in intact rats, neurohypophysectomy was associated with greatly reduced aldosterone concentration (0.12 +/- 0.03 vs. 0.76 +/- 0.04 ng/ml). Trace levels of vasopressin (0.17 +/- 0.03 microunit/ml) were found in neurohypophysectomized rat plasma. 5. Oxytocin administration at 15 microunits/min, which produced plasma hormone levels of 1.62 +/- 0.19 microunit/ml, had no detectable effect on sodium excretion but increased urine flow. Arginine vasopressin administration (12 microunits/min) inducing plasma levels of 1.24 +/- 0.08 microunit/ml, reduced urine flow by 80% and produced a small increase in sodium excretion. 6. Concurrent administration of oxytocin (15 microunits/min) potentiated the natriuretic response to vasopressin (12 microunits/min). Total sodium excretion during the 3 h combined hormone infusion (1256 +/- 149 mumol) greatly exceeded that in animals receiving vasopressin alone (549 +/- 132 mumol) and approached that observed in intact animals (1946 +/- 124 mumol). Combined hormone administration at the lower rate of 5 microunits/min oxytocin and 4 microunits/min vasopressin produced a similar large increment in sodium excretion. 7. It is concluded that replacement of both neurohypophysial hormones, at plasma levels within the physiological range, largely reverses the renal sodium retention of neurohypophysectomized rats, oxytocin considerably potentiating the natriuretic action of vasopressin. This synergism between the two neurohypophysial peptides to promote salt excretion may be an important component of the non-steroidal management of sodium.
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PMID:A synergistic effect of oxytocin and vasopressin on sodium excretion in the neurohypophysectomized rat. 362 42

Arginine vasopressin, a potent vasoconstrictor, does not raise arterial pressure in normal humans even at pathophysiological plasma levels. To examine whether the pressor effect of vasopressin in humans is buffered by baroreceptor reflex inhibition of sympathetic nerve activity, we recorded postganglionic muscle sympathetic nerve activity directly from the peroneal nerve in 12 normal men before, during, and after a 20-minute intravenous infusion of vasopressin, 4 ng/kg/min, that increased mean plasma concentrations from 6.2 +/- 0.6 to 320 +/- 68 (SE) pg/ml. During the first 5 minutes (n = 8), mean arterial pressure increased from 91 +/- 3 to 97 +/- 4 mm Hg (p less than 0.05) and integrated sympathetic nerve activity decreased from 271 +/- 45 to 156 +/- 33 units (p less than 0.05). At 15 minutes (n = 12), arterial pressure did not differ from control values whereas forearm vascular resistance fell (p less than 0.05) and central venous pressure and heart rate increased (p less than 0.05). Sympathetic nerve activity remained below control levels throughout the infusion (202 +/- 31 vs 254 +/- 40 units before infusion; p less than 0.05). An effect of vasopressin on ganglionic transmission was excluded, since the sympathoexcitatory response to apnea was not attenuated during vasopressin. Thus, pathophysiologic levels of vasopressin in humans cause inhibition of muscle sympathetic nerve activity that is not due to a ganglionic blocking action. The sympathoinhibition may be caused in part by the modest increases in mean arterial and central venous pressures and attendant stimulation of arterial and cardiac baroreceptors. The reflex decrease in sympathetic nerve activity would be expected to buffer the direct vasoconstrictor effects of vasopressin.
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PMID:Inhibition of muscle sympathetic nerve activity in humans by arginine vasopressin. 365 69


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