Download Biochemistry Objectives 44

Biochemistry Objectives 44
1.
Vasopressin:
a.
Gene coding and neurophysin II carrier: vasopressin is produced as
preprovasopressin and subsequently cleaved into provasopressin
(composed of vasopressin, neurophysin II, and a glycoprotein).
b.
Neurogenic and nephrogenic diabetes insipidus: both caused by a
decreased response to ADH:
a. Neurogenic (nonhereditary) diabetes insipidus: results from a
problem in the neuronal pathway of vasopressin release. Can be
caused by a problem in the supraoptic nucleus (defective
preprovasopressin gene), blocked transit to the axon terminal, or
blocked exocytosis.
b. Nephrogenic (hereditary) diabetes insipidus: results from a problem
in the nephron receptor response to vasopressin. Can be caused by a
problem in V2 receptor sensitivity to ADH, aquaporin-2 channel
production, or any point in the pathways converging to aquaporin
integration into the apical membrane.
c.
Secretion control at the following levels:
a. Physiological: secretion can be induced by three major mechanisms:
increased plasma osmolarity sensed by osmoreceptors in the
supraoptic nucleus, decreased volume sensed by volume receptors in
the atrium, and decreased pressure sensed by baroreceptors in the
carotid sinus/aortic arch.
b. Biochemical: a neural impulse is given in response to physiological
changes via acetylcholine. Acetylcholine increases intracellular Ca2+,
and causes vesicles to release vasopressin and neurophysin II.
d.
Aquaporin-2 water channel regulation: vasopressin initiates Gs protein
cascade  cAMP  PKA which phosphorylates aquaporin-2 channels.
Phosphorylated aquaporin-2 channels integrate into the apical membrane
to increase reabsorption of water in the distal nephron.
2.
Hypothalamic releasing and inhibiting factors:
a.
TRH: acts on thyrotrophs to release TSH (Gq, IP3/DAG/Ca2+)
b.
GnRH: acts on gonadotrophs to release FSH and LH (Gq, IP3/DAG/Ca2+)
c.
CRH: acts on corticotrophs to release ACTH (Gs, increased cAMP)
d.
GHRH: acts on somatotrophs to release GH (Gs, increased cAMP)
e.
GHIH: acts on somatotrophs to inhibit GH release (Gi, decreased cAMP)
3.
GnRH binding  LH, FSH release: GnRH binds to a Gq protein linked
receptor, causing an increase in PLC, Ca2+, and CaM-kinase. CaM-kinase
phosphorylates enzymes, and in conjunction with Ca2+, induces FSH, and LH
vesicles to fuse with the gonadotrope membrane.
4.
Neuromodulator peptides induce desired behavior:
a.
CCK-PZ: satiety (no more food needs to be eaten when CCK-PZ is
secreted to digest food)
b.
GLP-1: suppresses appetite (causes insulin release, no more food needs to
be eaten when glucose is already being stored)
c.
GnRH: mating behavior (increases LH and FSH, increased procreative
capability)
d.
Oxytocin: maternal behavior (causes labor and milk ejection)
e.
Vasopressin: memory and learning (causes water reabsorption, and
memory of place where water was so dehydration is avoided)