endocrine system pt 2 extra notes

Posterior Pituitary Gland Physiology

Hypothalamic Control of Posterior Pituitary

  • hormones are produced in neurons that are in the hypothalamus

    • hypothalamic nuclei are located in the hypothalamus

      • hormones are transported along axon of hypothalamo-hypophyseal tract

        • hypothalamo-hypophyseal tract: tract of nerve fibers (axons) that transports antidiuretic hormone and oxytocin from the hypothalamus to the posterior pituitary.

  • hormones are released from synaptic knob into capillary bed, entering the blood stream in the posterior pituitary

    • neurons axons extend into posterior pituitary gland, releasing hormones directly into capillary bed

  • although the messenger signal is made in a neuron, it is called hormones (instead of neurotransmitter) because released directly into blood

    • would be called neurotransmitter if it was released directly on synapse

2 Hormones Released by the Posterior Pituitary Lobe:

1. Antidiuretic Hormone (ADH)

  • Target: Kidneys and blood vessels.

  • Effects:

    • stimulation of water retention in kidneys

      • less water is secreted in the urine

      • what gives the hormone its name

    • vasoconstriction of blood vessels.

      • rise in blood pressure due to vasoconstriction

    • Secreted when hydration levels are low (dehydration).

  • Regulation:

    • secretion of ADH is stimulated by hypothalamic osmosensors and angiotensin II

      • osmoreceptors neurons: A sensory neuron in hypothalamus that responds to changes in the osmotic pressure of the surrounding fluid.

    • secretion of ADH is inhibited by Atrial baroreceptors

      • baroreceptors is a type of mechanoreceptor that is a stretch receptor

      • located in left atrium of the heart

      • stimulated when there is a rise in blood volume, causing inhibition

2. Oxytocin

  • Target: Mammary glands and uterus.

  • Effects:

    • Triggers milk ejection during lactation

      • stimulates contraction of mammary gland alveoli and ducts

    • stimulates uterine contractions during childbirth.

  • Regulation: More complex regulation, particularly in reproductive scenarios.


Anterior Pituitary Gland Physiology

Hypothalamic Control of Anterior Pituitary

  • Axons are only in hypothalamus, do not enter anterior pituitary lobe

  • Neurons secrete regulatory hormones into hypophyseal portal system

    • hypophyseal portal system: vascular system with contains two capillary beds, transporting hormones from the hypothalamus to the anterior pituitary

  • regulatory hormones are secreted into first capillary bed at the base of the hypothalamus

    • then delivered to another capillary bed in anterior pituitary gland

  • Regulatory hormones either stimulate or inhibit release of hormones

    • Negative feedback loop can either work at the top in the hypothalamus or at the bottom in the anterior anterior pituitary lobe

Hypothalamic Regulatory Hormones: hormones released in the hypothalamus

  1. Growth Hormone-Releasing Hormone (GHRH)

  2. Growth Hormone-Inhibiting Hormone (GHIH)

  3. Thyroid-Releasing Hormone (TRH)

  4. Corticotropin-Releasing Hormone (ACTH)

  5. Prolactin-Inhibiting Hormone (PIH)

  6. Gonadotropin-Releasing Hormone (GRH)

Anterior Pituitary Hormones: hormones released at anterior pituitary gland

  1. Growth Hormone (GH)

  2. Thyroid-stimulating Hormone (TSH)

  3. Adrenocorticotropic Hormone (ACTH)

  4. Follicle-stimulating Hormone (FSH)

  5. Luteinizing Hormone (LH)

  6. Prolactin (PRL)

1. Growth Hormone (GH): released at anterior pituitary gland
  • Targets: Bone, muscle, adipose tissue, cartilage, and many others

  • Effects:

    • Stimulates growth in bone, cartilage, and muscle

    • increase lipolysis and lipid immobilization

      • break down of lipids (fats) and mobilizes it

  • Hypothalamic Regulatory Hormones:

    • Growth hormone-releasing hormone (GHRH): stimulates release of growth hormone

    • Growth hormone-inhibiting hormone (GHRH): inhibits release of growth hormone

  • Hypothalamic-Pituitary-Somatotropic Axis - Hypothalamic Regulation of Growth Hormone:

    • Negative feedback loop

    • Pituitary gland secretes growth hormone (GH)

      • increase of growth hormone (GH) causes increase in somatomedins from the liver

        • increase of somatomedins levels blocks growth hormone-release hormone AND stimulates growth hormone-inhibiting hormone in the hypothalamus

    • NOT negative product inhibition

2. Adrenocorticotropic Hormone (ACTH): released at the pituitary gland
  • adreno: target of hormone

  • cortico: cortisol

  • tropic: ACTH is a tropic hormone

    • Tropic Hormone: target is another endocrine gland

      • ACTH is released from pituitary gland (endocrine gland) and targets adrenal gland (another endocrine gland)

    • Trophic Hormone: causes growth in target

  • Target: Adrenal cortex.

    • (adrenal medulla is stimulated by Sympathetic Nervous System from hypothalamus)

  • Effects: Stimulates the secretion of glucocorticoids (e.g., cortisol)

    • glucocorticoids: hormones whose effects include glucose metabolism

      • also stress hormones

    1. increases gluconeogenesis

      • gluconeogenesis: production of glucose from a non-carbohydrate

    2. increases lipolysis

    3. increase protein degeneration

      • protein degeneration: protein digestion

    4. depresses immune/inflammatory response

      • all stress hormones have same functions on immune system

  • Hypothalamic Regulatory Hormones:

    • Corticotropin-Releasing Hormone (CRH)

      • tropic hormone

      • targets pituitary gland to stimulate release of Adrenocorticotropic Hormone (ACTH), causing release of cortisol

        • stress stimulates higher brain centers →\rightarrow higher brain centers stimulate hypothalamus to release CRH →\rightarrow CRH stimulates anterior pituitary gland to release ACTH →\rightarrow ACTH targets adrenal cortex →\rightarrow adrenal cortex increases cortisol levels

  • Hypothalamic-Pituitary-Adrenal Axis:

    • anterior pituitary often has negative feedback inhibitions at two levels:

      1. hypothalamus

        • increase of cortisol inhibits hypothalamus’ secretion of Corticotropin Releasing Hormone (CRH)

          • hypothalamus has cortisol receptors that detect elevated cortisol levels

            • hypothalamus acts as sensor and integrating center

          • leads to a decrease in CRH production

            • adrenal cortex acts as effector, decreasing amount of cortisol being secreted

      2. Pituitary

        • increase in cortisol inhibits anterior pituitary’s responsiveness of Corticotropin Releasing Hormone (CRH)

          • anterior pituitary has cortisol receptors detect elevated cortisol levels, decreasing responsiveness to CRH, leading to a reduction in Adrenocorticotropic Hormone (ACTH) secretion and thus lower cortisol production from the adrenal glands.

            • anterior pituitary acts as sensor, integrating center and effector

  • Adrenal Insufficiency Disease: disease involving hypo-secretion (not enough secretion) of glucocorticoids

    • Two Types:

      • Primary Adrenal Insufficiency

        • disease of adrenal cortex

          • adrenal cortex is stimulated by ACTH but is unable to produce cortisol

        • most common type: Addison’s disease

          • autoimmune disease of the adrenal cortex

          • other causes include congenital, drug-related, infections

          • common symptoms: hair loss, blurred vision, abdominal pain, decreased appetite, darkening of skin, shaking or tremors, depression

      • Secondary Adrenal Insufficiency

        • disease at the anterior pituitary where it does not produce enough ACTH, leading to inadequate stimulation of the adrenal cortex and resulting in decreased cortisol production.

    • Testing to diagnose primary or secondary adrenal insufficiency: injection of ACTH

      • if nothing happens after injection, diagnosis is primary adrenal insufficiency

        • problem is in the adrenal cortex because adrenal cortex does not increase levels of cortisol

      • if injection causes an production of cortisol, diagnosis is secondary adrenal insufficiency

        • problem is in the anterior pituitary because it fails to produce adequate amounts of adrenocorticotropic hormone (ACTH), which stimulates the adrenal cortex to release cortisol.

  • Cushing's Syndrome: hyper-secretion (excessive secretion) of glucocorticoids causing increased lipolysis and redistribution of fat

    • Two types:

      • Primary Cushing Syndrome: typically from tumor in adrenal cortex

        • excessive cell division of adrenal cortex cells, causing more cells to secrete cortisol

      • Secondary Cushing Syndrome: typically from tumor in pituitary gland

        • excessive cell division of pituitary gland cells, causing more cells to secrete ACTH, increasing cortisol levels


3. Thyroid-Stimulating Hormone (TSH): released at anterior pituitary gland
  • Target: Thyroid gland.

    • tropic hormone AND Trophic hormone

      • tropic: released by anterior pituitary gland

      • trophic: increase size of thyroid

  • Effects: Stimulates the secretion of thyroid hormones, Triiodothyronine (T3) and Thyroxine (T4)

    • increases basal metabolic rate and body temperature

    • increases catabolism of carbohydrates and proteins

  • Hypothalamic Regulatory Hormones:

    • Thyrotropin Releasing Hormone (TRH)

      • hypothalamus secretes Thyrotropin Releasing Hormone (TRH) →\rightarrow TRH triggers anterior pituitary gland to produce thyroid-stimulating hormone (TSH) →\rightarrow TSH causes thyroid to secrete Triiodothyronine (T3) and Thyroxine (T4) AND increases growth of thyroid

  • Hypothalamic-Pituitary- Thyroid Axis:

    • Negative Feedback Inhibition at two levels:

      • hypothalamus

        • increase of T3 and T4 inhibits hypothalamus’ secretion of Thyrotropin Releasing Hormone (TRH)

          • hypothalamus has receptors that detect elevated T3 and T4 levels

            • hypothalamus acts as sensor and integrating center

          • leads to a decrease in TRH production

            • thyroid acts as effector, decreasing amount of T3 and T4 being secreted

      • Pituitary

        • increase in T3 and T4 inhibits anterior pituitary’s responsiveness of Thyrotropin Releasing Hormone (TRH)

          • anterior pituitary has T3 and T4 receptors detect elevated T3 and T4 levels, decreasing responsiveness to TRH, leading to a reduction in TSH secretion and thus lower T3 and T4 production from the thyroid glands

            • anterior pituitary acts as sensor, integrating center and effector

  • Synthesis of thyroid hormone requires iodide (iodine)

    • iodide must be in diet

      • if there is not enough iodide in diet, there is no production of Triiodothyronine (T3) and Thyroxine (T4)

    • Goiter Disease: insufficient dietary iodide leads to hypertrophy of thyroid gland

      • excessive growth of thyroid gland

      • if not enough iodide, leads to low levels of T3 and T4

        • results in lack of negative feedback inhibition causing anterior pituitary gland to secrete excessive TSH

          • excessive TSH causes abnormal growth of thyroid

  • Graves’ Disease: an autoimmune disease, caused by auto-antibodies binding to TSH receptors, which stimulates overproduction of thyroid hormones



Hypothalamic Regulation of Adrenal Medulla

Sympathetic Nervous System Control of Adrenal Medulla
  • adrenal medulla is stimulated by hypothalamus through sympathetic innervation

  • Effects: stimulate secretion of epinephrine and norepinephrine, which target other organs:

    • increase heart rate

    • dilate bronchioles

    • vasoconstriction in skin

    • vasodilation in muscle

“Fight or Flight” Response


Hormonal Regulation of Blood Calcium Levels

Calcitonin and Parathyroid Hormone (PTH)
  • Calcitonin: produced by thyroid glands, inhibits dissolution of Ca2+ from bone and stimulates Ca2+ excretion

    • if blood calcium is too high, thyroid gland produces calcitonin

      • Lowers blood calcium by causing calcium deposition in bone (inhibiting osteoclast activity) and increasing renal excretion of calcium

        • leads to blood calcium levels decreasing

  • Parathyroid Hormone. (PTH): Produced by parathyroid glands, promotes dissolution of Ca2+ from bone and inhibits Ca2+ excretion

    • if blood calcium is low, parathyroid gland produces parathyroid hormone

      • raises blood calcium by releasing stored calcium from bone (stimulating osteoclasts and inhibiting osteoblast activity) and enhancing reabsorption of calcium in kidneys (decrease calcium excretion in kidneys)

        • increases blood calcium levels

  • Calcitonin and Parathyroid Hormone work in antagonist effects


Therapeutic Use of Cortisol Mimics

  • Cortisol Mimics: Synthetic molecules that act like cortisol, binding to cortisol receptors, causing same physiological response as cortisol

    • most often used for immunosuppressive effects

      • depresses immune’s systems response and reduces inflammation

  • Common Medications:

    • Prednisone

    • Prednisolone

    • Dexamethasone

  • Caution: Long-term use can lead to adrenal suppression

    • careful dosing and tapering are necessary to prevent withdrawal symptoms.