Comparative in vitro Studies on Corticotropin Releasing Activity of Vasopressin and Hypothalamic Median Eminence Extract

Lutz-Bucher, B.; Koch, Bernard; Mialhe, C

doi:10.1159/000122666

Cited by 39 publications

(17 citation statements)

References 4 publications

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“…Finally, pituitary desensitization to AVP may occur (similar to what has been shown for CRF in in vivo animal studies) independently of any steroid feedback (45). The anterior pituitary contains specific receptors for AVP which are distinct from those for hypothalamic CRF (46,47), and prior injections of AVP might cause down-regulation of the AVP specific receptor on pituitary cells (47). To determine which, if any, of the explanations is correct will require further study.…”

Section: Discussionmentioning

confidence: 83%

Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH.

Salata¹,

Jarrett²,

Verbalis³

et al. 1988

J. Clin. Invest.

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The diurnal response of ACTH release to intravenously administered arginine vasopressin was tested in normal volunteers given consecutively moderate doses of vasopressin every 15 min (0.1, 03, 1.0, and 3.0 IU) at 2200 h and again at 0700 h (PM/AM). This protocol was repeated 4 wk later with the times reversed (AM/PM). A dose-related increase in ACIH secretion was observed in all subjects. When the AM response of the AM/PM protocol was compared with the PM response of the PM/AM protocol, the release of ACTH was greater in the morning (P < 0.05) as evaluated by the following criteria: peak value of ACTH (129.9±30.4 pg/ml in the AM vs. 57.1±20.2 in the PM), area under the curve (689 in the AM vs.259 in the PM); and, sensitivity of the ACTH dose-response curve (first significant increase in ACTH with 1 IU of vasopressin in the AM but not significant even after 3 IU in the PM). In addition, when the AM vasopressin testing followed a previous evening stimulation (PM/AM protocol), there was a blunted ACTH response compared with the AM/PM protocol.Corticotropin-releasing factor (CRF) is probably the major ACTH secretagogue, but since vasopressin acts synergistically with CRF to produce an augmented release of ACTH, we suggest that the ACTH response to administered vasopressin depends upon the ambient endogenous level of CRF. We interpret our data and published data that CRF produces a lesser release of ACTH in the AM as follows: in the morning endogenous CRF is high and administered CRF produces little further release of ACTH, but administered vasopressin acting synergistically with high endogenous CRF causes a greater release of ACTH; conversely, in the evening endogenous CRF is low and administered CRF causes a greater release of ACHI, but vasopressin (a weak secretagogue by itself) gives a low ACTH response. We conclude that vasopressin stimulation of ACTH secretion can be used as an in vivo bioassay of endogenous CRF, and that there is a diurnal rhythm of CRF in hypophyseal portal blood.

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Section: Discussionmentioning

confidence: 83%

Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH.

Salata¹,

Jarrett²,

Verbalis³

et al. 1988

J. Clin. Invest.

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“…The conten: of AVP in effluent media was measured by means of a specific radioimmunoassay, at 3 different dilutions as previ ously described [9], Results depicted in the figures are related to a representative experiment, which was repealed at least 3 limes. A composite graph is shown, that summarizes data from 3-7 experi ments per group and gives the peak secretion of AVP as the percen tage of basal release of the peptide.…”

Section: Methodsmentioning

confidence: 99%

Modulation by Leu-Enkephalin of Peptide Release from Perifused Neurointermediate Pituitary

Zein¹,

Lutz-Bucher²,

Koch³

1984

Neuroendocrinology

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This study examines the effect of leu-enkephalin on K⁺, veratridine and isoproterenol stimulation of vasopressin (AVP) release from perifused neurointermediate pituitaries of rats. As opposed to catecholamine-evoked release of peptide, the secretory response to high K⁺ and veratridine involves Ca²⁺ influx, as the effect of both factors was blocked by Ca-chelation and the channel blocker D 600. Leu-enkephalin was found to antagonize AVP secretion induced by K⁺ and veratridine depolarization, by acting through a naloxone-sensitive receptor system. In contrast, the opiate failed to significantly affect isoproterenol-stimulated release of AVP, which we show to be correlated to cAMP accumulation in pure neurohypophyseal tissue. These results support the view that opiates modulate AVP secretion triggered by depolarization of nerve terminals by regulating Ca²⁺ fluxes.

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“…Re-examination of CRF concentration us ing AVP-AS showed that it was still highest in ME, but was significantly higher in PVN than in SON, SCN and ARC. These results suggest that the PVN is an important nucleus for producing corticotropin-releasing hormone.The relationship between vasopressin and corticotropin releasing factor (CRF) is being discussed again in the litera ture, although many investigators have suggested that vaso pressin differs from authentic CRF [2,20,27, 30]. Vasopres sin-and neurophysin-containing fibers were found in large numbers in the external layer of the median eminence (ME) and many fibers terminated on the primary portal plexus [7, 35].…”

mentioning

confidence: 99%

Distribution and Characterization of Corticotropin-Releasing Factor and Arginine Vasopressin in Rat Hypothalamic Nuclei

et al. 1982

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Corticotropin-releasing factor (CRF) was bioassayed and arginine vasopressin (AVP) radioimmunoassayed from punched-out hypothalamic nuclei. The highest concentration of CRF was found in the median eminence (ME), followed by the paraventricular nucleus (PVN), supraoptic nucleus (SON), suprachiasmatic nucleus (SCN), arcuate nucleus (ARC), dorsomedial nucleus (DMN) and ventromedial nucleus (VMN). The AVP concentration was in the order of ME, SON, PVN, SCN, ARC, VMN and DMN. Sephadex G-25 gel filtration of the ME extracts showed one peak for AVP and two peaks for CRF. One CRF peak appeared on the void volume (big CRF) and the other (small CRF) was coeluted with AVP. Gel filtration of the PVN and SON extracts showed one peak for AVP but three or four peaks for CRF. The addition of anti-AVP serum (AVP-AS) to pituitary cell cultures reduced the CRF activities of AVP and ME extracts by approximately 80 and 40%, respectively. When the small CRF fraction of ME extracts was treated with AVP-AS on affinity chromatography, the unbound fraction (AVP-free) still showed significant CRF activity. Re-examination of CRF concentration using AVP-AS showed that it was still highest in ME, but was significantly higher in PVN than in SON, SCN and ARC. These results suggest that the PVN is an important nucleus for producing corticotropin-releasing hormone.

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Comparative in vitro Studies on Corticotropin Releasing Activity of Vasopressin and Hypothalamic Median Eminence Extract

Cited by 39 publications

References 4 publications

Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH.

Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH.

Modulation by Leu-Enkephalin of Peptide Release from Perifused Neurointermediate Pituitary

Distribution and Characterization of Corticotropin-Releasing Factor and Arginine Vasopressin in Rat Hypothalamic Nuclei

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