POSTERIOR PITUITARY

Hypothalamic Control of Posterior Pituitary

• Hypothalamic neuron cell bodies produce:

ADH: supraoptic nuclei.Oxytocin: para ventricular nuclei.• Transported along

hypothalamo-hypophyseal tract.

• Stored in posterior pituitary.

• Release controlled by neuroendocrine reflexes.

• The osmoreceptor neurons in the hypothalamus are extremely sensitive and are able to maintain ECF osmolarity within a very narrow range.

• There is a reseting of the osmostat downward in pregnancy, the men-strual cycle, and with volume depletion. In the latter case osmoregula-tion is secondary to volume regulation; a return of circulating volume will occur even as osmolarity decreases.

• Volume receptors are less sensitive than osmoreceptors and a change of 10–15% in volume is required to produce a measureable change in ADH.

• Cortisol and thyroid hormone restrain the release of ADH.

At the kidney (collecting duct)

Nephron lumen

Interstitial Space

V2

ADHcAMP

Vesicles containing

AQP2

’s AQP2 production

ACTIONS OF ADH

1.ACTION ON KIDNEY Maintenance of ECF volume & Osmolarity Acts on DCT and CD of kidney Reabsorbs water Maintenance of volume more important that

maintenance of osmolarity2.VASOCONSTRICTOR EFFECT

3.ACTION ON ANTERIOR PITUITARY-cause increased ACTH secretion from the corticotroph

Effect of Alcohol and Weightlessness on ADH Secretion

• Ingesting ethyl alcohol or being in a weightless environment suppresses ADH se-cretion. In weightlessness, there is a net shift of blood from the limbs to the abdo-men and chest.

• This results in greater stretch of the volume receptors in the large veins and atria, thus suppressing ADH secretion

PATHOPHYSIOLOGIC CHANGES IN ADH SECRETION

Central diabetes insipidus

• Sufficient ADH is not available to affect the renal collecting ducts.

• Causes include familial, tumors (craniopharyngioma), autoimmune, trauma

• Pituitary trauma – transient diabetes insipidus • Sectioning of pituitary stalk – triphasic

response: diabetes insipidus, followed by SIADH, followed by a return of diabetes insipidus

Nephrogenic diabetes insipidus

• Due to inability of the kidneys to respond to ADH

• Causes include familial, acquired, drugs (lithium)

Syndrome of Inappropriate ADH Secretion (SIADH)

• Excessive secretion of ADH causes an inappropriate increased reabsorption of water in the renal collecting duct.

• CausesEctopic production of ADH (small cell carcinoma of the lung)Drug induced Lesions in the pathway of the baroreceptor system • Pathophysiology Increased water retention, hyponatremia, but clinically euvolumicVolume expansion increases ANP, decreases renin creating a natriuresis, which contributes to the hyponatremia Inappropriate concentration of urine, can be greater than plasma osmo-larity A small, constant secretion of ADH by a tumor may have a minimal effect on the ability to form dilute urine but has a major effect on the ability to excrete a large water load.• Treatment Fluid restriction but not salt restriction

Oxytocin

• 9 AA peptide • Stored in Herring bodies • Nerve stimulation release • Half life ~ 4 minutes

Hypothalamus

Posterior Pituitary

Oxytocin

Nursing Pressure against cervix

At the target cell

Smooth muscle cell

Oxytocin

IP3 & DAG Ca2+

Contraction

Actions of oxytocinIn females: Milk ejection Contraction of uterus during labor In females: during coitus causes uterine contraction and transport

of sperms

In Males: Increases at time of ejaculation May cause increase contraction of smooth muscle of vas deferens

- propelling sperm through urethra

milk-ejection reflex

IN THE CLINIC-- hypophysectomy (pituitary removal)

• Because posterior pituitary hormones are synthesized in the hypothalamus rather than the pituitary, hypophysectomy (pituitary removal) does not necessarily permanently disrupt synthesis and secretion of these hormones.

• Immediately after hypophysectomy, secretion of the hormones decreases.

• However, over a period of weeks, the severed proximal end of the tract will show histological modification and pituicytes will form around the neuron terminals. Secretory vacuoles are seen, and secretion of hormone resumes from this proximal end. Secretion of hormone can even potentially return to normal levels.

• In contrast, a lesion higher up on the pituitary stalk can lead to loss of neuronal cell bodies in the PVN and SON.