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ADH is synthesized by neurons of the supraoptic and paraventricular nuclei of the hypothalamus and stored in the posterior pituitary gland.
The second phase of the triphasic response is caused by the uncontrolled release of ADH from degenerating posterior pituitary tissue, or from the remaining magnocellular neurons whose axons have been injured (1).
My postdoctoral work focused on developing quantitative methods (radioimmunoassay and high performance liquid chromatography) for measuring physiological changes in the posterior pituitary hormones vasopressin and oxytocin.
In this latter condition, the posterior pituitary is appropriately stimulated by the increased plasma osmolality and duly produces sufficient ADH to which the kidney is unable to respond.
At this time, it was theorized that nicotine stimulates the hypothalamus and results in a release of antidiuretic hormone from the posterior pituitary gland.
The cytologic and architectural features of these tumors are reminiscent of those of the normal posterior pituitary lobe (Figure 3).
Of similar importance, other anterior and posterior pituitary hormone deficiencies should be sought in a child with GH deficiency.

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