Module 1: Introduction to Endocrinology, Hypothalamus (Anterior pituitary & Posterior
pituitary)
Homeostatic feedback mechanisms
Many endocrine glands are linked to neural control centers by homeostatic feedback mechanisms.
The two types of feedback mechanisms are:
Negative feedback and positive feedback. Negative feedback decreases the deviation from
an ideal normal value, and is important in maintaining homeostasis. Most endocrine glands
are under the control of negative feedback mechanisms.
Negative feedback
Negative feedback mechanisms act like a thermostat in the home. As the temperature rises
(deviation from the ideal normal value), the thermostat detects the change and triggers the
air-conditioning to turn on and cool the house. Once the temperature reaches its
thermostat setting (ideal normal value), the air conditioning turns off.
An example of negative feedback
The regulation of the blood calcium level. The parathyroid glands secrete parathyroid
hormone, which regulates the blood calcium amount. If calcium decreases, the parathyroid
glands sense the decrease and secrete more parathyroid hormone. The parathyroid hormone
stimulates calcium release from the bones and increases the calcium uptake into the
bloodstream from the collecting tubules in the kidneys. Conversely, if blood calcium increases
too much, the parathyroid glands reduce parathyroid hormone production. Both responses
are examples of negative feedback because in both cases the effects are negative (opposite)
to the stimulus.
Positive feedback
Positive feedback mechanisms control self-perpetuating events that can be out of control and
do not require continuous adjustment. In positive feedback mechanisms, the original stimulus
is promoted rather than negated. Positive feedback increases the deviation from an ideal
normal value. Unlike negative feedback that maintains hormone levels within narrow ranges,
positive feedback is rarely used to maintain homeostatic functions
Example of positive feedback
An example of positive feedback can be found in childbirth. The hormone oxytocin
stimulates and enhances labor contractions. As the baby moves toward the vagina (birth
canal), pressure receptors within the cervix (muscular outlet of uterus) send messages to
the brain to produce oxytocin. Oxytocin travels to the uterus through the bloodstream,
stimulating the muscles in the uterine wall to contract stronger (increase of ideal normal
value). The contractions intensify and increase until the baby is outside the birth canal.
, When the stimulus to the pressure receptors ends, oxytocin production stops and labor
contractions cease.
A simple example of an endocrine feedback loop is the hypothalamic-pituitary-thyroidal axis
The hypothalamus produces the hypophysiotropic hormone, thyrotropin-releasing hormone
(TRH), and releases it into the portal system where it directs the thyrotrophs (or TSH-producing
cells) in the anterior pituitary to secrete thyroid-stimulating hormone (TSH).
TSH circulates to the thyroid and stimulates several steps in the thyroid that are critical in the
production and release of thyroid hormone (thyroxine). Thyroxine is released in the blood and
circulates to the hypothalamus and pituitary to suppress further TRH and TSH production. This
axis can be partially inhibited by adrenal steroids (glucocorticoids) and by cytokines; as a result,
thyroid hormone production may decline during periods of severe physiologic stress.
Thyrotropin releasing hormone (TRH): stimulates the secretion of both TSH and prolactin.
Gonadotropin releasing hormone (GnRH): stimulates both LH and FSH production.
Corticotropin releasing hormone (CRH): Releases ACTH.
Somatostatin (SS): inhibits GH and TSH release from the pituitary.
Vasopressin (ADH: can also stimulate adrenocorticotropin (ACTH) secretion. The main stimulus for ACTH
secretion is Corticotropin-releasing hormone.
Dopamine (prolactin inhibitory factor): Inhibits prolactin release.
Growth Hormone- releasing hormone (GHRH): Releases GH.
Hormones secreted by Posterior pituitary
(1) Oxytocin: Stimulates uterine contractions and lactation.
: Synthesis used to induce labour.
(2) Vasopressin or Antidiuretic Hormone (ADH):
=Changes in serum osmolality or blood pressure turn on secretion and the thirst mechanism.
=ADH then triggers water retention in distal tubules and collecting ducts.
=Vasopressin effect constricts smooth muscle to increase blood volume.
Vasopressin
Vasopressin’s major action is to regulate renal free water excretion and, therefore, has a central
role in water balance. The vasopressin receptors in the kidney (V2) are concentrated in the renal
collecting tubules and the ascending limb of the loop of Henley.
They are coupled to adenylate cyclase and, once activated; they induce insertion of aquaporin-2,
a water channel protein, into the tubular luminal membrane.
Vasopressin is also a potent presser agent and effects blood clotting61 by promoting factor VII
release from hepatocytes and von Willebrand factor release from the endothelium. These
vasopressin receptors (V1a and V1b) are coupled to phospholipase C.
Diabetes insipidus (DI), characterized by copious production of urine (polyuria) and intense
thirst (polydipsia), is a consequence of vasopressin deficiency.
Hormones secreted by anterior pituitary
pituitary)
Homeostatic feedback mechanisms
Many endocrine glands are linked to neural control centers by homeostatic feedback mechanisms.
The two types of feedback mechanisms are:
Negative feedback and positive feedback. Negative feedback decreases the deviation from
an ideal normal value, and is important in maintaining homeostasis. Most endocrine glands
are under the control of negative feedback mechanisms.
Negative feedback
Negative feedback mechanisms act like a thermostat in the home. As the temperature rises
(deviation from the ideal normal value), the thermostat detects the change and triggers the
air-conditioning to turn on and cool the house. Once the temperature reaches its
thermostat setting (ideal normal value), the air conditioning turns off.
An example of negative feedback
The regulation of the blood calcium level. The parathyroid glands secrete parathyroid
hormone, which regulates the blood calcium amount. If calcium decreases, the parathyroid
glands sense the decrease and secrete more parathyroid hormone. The parathyroid hormone
stimulates calcium release from the bones and increases the calcium uptake into the
bloodstream from the collecting tubules in the kidneys. Conversely, if blood calcium increases
too much, the parathyroid glands reduce parathyroid hormone production. Both responses
are examples of negative feedback because in both cases the effects are negative (opposite)
to the stimulus.
Positive feedback
Positive feedback mechanisms control self-perpetuating events that can be out of control and
do not require continuous adjustment. In positive feedback mechanisms, the original stimulus
is promoted rather than negated. Positive feedback increases the deviation from an ideal
normal value. Unlike negative feedback that maintains hormone levels within narrow ranges,
positive feedback is rarely used to maintain homeostatic functions
Example of positive feedback
An example of positive feedback can be found in childbirth. The hormone oxytocin
stimulates and enhances labor contractions. As the baby moves toward the vagina (birth
canal), pressure receptors within the cervix (muscular outlet of uterus) send messages to
the brain to produce oxytocin. Oxytocin travels to the uterus through the bloodstream,
stimulating the muscles in the uterine wall to contract stronger (increase of ideal normal
value). The contractions intensify and increase until the baby is outside the birth canal.
, When the stimulus to the pressure receptors ends, oxytocin production stops and labor
contractions cease.
A simple example of an endocrine feedback loop is the hypothalamic-pituitary-thyroidal axis
The hypothalamus produces the hypophysiotropic hormone, thyrotropin-releasing hormone
(TRH), and releases it into the portal system where it directs the thyrotrophs (or TSH-producing
cells) in the anterior pituitary to secrete thyroid-stimulating hormone (TSH).
TSH circulates to the thyroid and stimulates several steps in the thyroid that are critical in the
production and release of thyroid hormone (thyroxine). Thyroxine is released in the blood and
circulates to the hypothalamus and pituitary to suppress further TRH and TSH production. This
axis can be partially inhibited by adrenal steroids (glucocorticoids) and by cytokines; as a result,
thyroid hormone production may decline during periods of severe physiologic stress.
Thyrotropin releasing hormone (TRH): stimulates the secretion of both TSH and prolactin.
Gonadotropin releasing hormone (GnRH): stimulates both LH and FSH production.
Corticotropin releasing hormone (CRH): Releases ACTH.
Somatostatin (SS): inhibits GH and TSH release from the pituitary.
Vasopressin (ADH: can also stimulate adrenocorticotropin (ACTH) secretion. The main stimulus for ACTH
secretion is Corticotropin-releasing hormone.
Dopamine (prolactin inhibitory factor): Inhibits prolactin release.
Growth Hormone- releasing hormone (GHRH): Releases GH.
Hormones secreted by Posterior pituitary
(1) Oxytocin: Stimulates uterine contractions and lactation.
: Synthesis used to induce labour.
(2) Vasopressin or Antidiuretic Hormone (ADH):
=Changes in serum osmolality or blood pressure turn on secretion and the thirst mechanism.
=ADH then triggers water retention in distal tubules and collecting ducts.
=Vasopressin effect constricts smooth muscle to increase blood volume.
Vasopressin
Vasopressin’s major action is to regulate renal free water excretion and, therefore, has a central
role in water balance. The vasopressin receptors in the kidney (V2) are concentrated in the renal
collecting tubules and the ascending limb of the loop of Henley.
They are coupled to adenylate cyclase and, once activated; they induce insertion of aquaporin-2,
a water channel protein, into the tubular luminal membrane.
Vasopressin is also a potent presser agent and effects blood clotting61 by promoting factor VII
release from hepatocytes and von Willebrand factor release from the endothelium. These
vasopressin receptors (V1a and V1b) are coupled to phospholipase C.
Diabetes insipidus (DI), characterized by copious production of urine (polyuria) and intense
thirst (polydipsia), is a consequence of vasopressin deficiency.
Hormones secreted by anterior pituitary
