The effect of osmotic pressure and angiotensin II on arginine vasopressin release from guinea pig hypothalamo-neurohypophyseal complex in organ culture.

@article{Ishikawa1980TheEO,
  title={The effect of osmotic pressure and angiotensin II on arginine vasopressin release from guinea pig hypothalamo-neurohypophyseal complex in organ culture.},
  author={San‐e Ishikawa and T. Saito and S Yoshida},
  journal={Endocrinology},
  year={1980},
  volume={106 5},
  pages={
          1571-8
        }
}
We have developed an organ culture system of the male guinea pig hypothalamo-neurohypophyseal complex (HNC) and investigated the effect of various osmotic agents and angiotensin II on arginine vasopressin (AVP) release in vitro. On the fifth day in culture, ouabain-sensitive ATPase activity was 0.83 ± 0.11 mmol Pi/mg protein·h (mean ± sem), which was 67% of that on the first day in culture. On the fifth day, [6-3H]thymidine incorporated into DNA in the explants of HNC was 1205 ± 185 cpm/μg DNA… 
The effect of prostaglandins on the release of arginine vasopressin from the guinea pig hypothalamo-neurohypophyseal complex in organ culture.
TLDR
It is suggested that PGE2 and PGF2 alpha increase AVP release from the explants of HNC in organ culture, although PGF 2 alpha has a relatively weaker effect than P GE2, and PGs may modulate the regulation of AVPrelease in response to angiotensin II and osmotic stimulation.
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TLDR
Since pressor responsiveness to vasopressin was increased in the rats with DOCA-salt hypertension, vasopressingin may function as a direct pressor agent in the maintenance of high blood pressure in this type of hypertension.
Effect of angiotensin II infusion into rat hepatic portal vessel on arginine vasopression release.
TLDR
The results not only suggest that the osmoreceptors exist in the area located somewhere within the hepatic portal vascular bed, but also that the Osmoreceptor are somewhat different in nature from those of hypothalamic osmoreception.
Pressor responsiveness to vasopressin and angiotensin II in spontaneously hypertensive rats: effects of dietary sodium.
TLDR
The results suggest that AVP may function as a direct pressor agent in the maintenance of high blood pressure in SHR with high sodium intake.
Sodium induces oxytocin release from superfused rat pituitary.
TLDR
The data suggest that oxytocin release from the pituitary is influenced by the level of sodium ion rather than the osmotic pressure.
Biochemical and Immunochemical Studies of Supraoptic and Paraventricular Cultures
TLDR
A tissue culture model was established for the study of hypothalamic peptide synthesis and secretion of Sprague-Dawley rats, and studies were performed to evaluate vasopressin and oxytocin content (medium and tissue levels), immunocytochemical localization, and biosynthetic activity.
Effects of dietary sodium on brain angiotensin II receptors in spontaneously hypertensive rats.
TLDR
The present results suggest that in WKY the decrease of the binding capacity of the A II receptors in the HTSM region in response to a high sodium intake serves to attenuate an osmotical stimulus to AVP secretion.
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TLDR
It is demonstrated that the rat hypothalamo-neurohypophyseal system in organ culture responds appropriately to osmotic challenges within the physiological range, and Verney's concept of an osmoreceptor inasmuch as both NaCl and mannitol were effective Osmotic agents.
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TLDR
It is suggested that action potentials are generated in response to AII stimulation of specific receptors in the HNS and are requisite for VP release in Response to this stimulus.
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TLDR
Organ cultures of the guinea pig hypothalamo-neurohypophysial complex synthesize the octapeptide hormone, vasopressin, a specific product of the neurosecretory cells of the supraoptic nucleus, and inhibitors of both protein and RNA synthesis were found to block vasoppressin biosynthesis.
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TLDR
The data support the hypothesis that angiotensin II, at least in vitro, has a central effect on ADH release which is at the level of the hypothalamus.
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TLDR
It is concluded that AVP secretion is regulated principally by blood osmolality but that the responsiveness of this mechanism may be significantly altered by modest changes in blood volume.
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TLDR
It is concluded that angiotensin II can potentiate the release of ADH in response to an osmotic stimulus and the relationship between the plasma ADH concentration and plasma osmolality appeared to be rectilinear over the range studied.
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TLDR
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TLDR
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TLDR
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