Pineal Gland Releases Melatonin Biology Essay

D) Thyroid

Released: Thyroxine (T4) and triiodothyronine (T3)

Function: Increases metabolic rate; regulates growth and development

Released: Calcitonin

Function: Lowers blood calcium level

E) Parathyroids

Releases: Parathyroid (PTH)

Function: Raises blood calcium level

F)Thymus

G) Adrenal cortex:

Released: Glucocorticoids (cortisol)

Function: Raise blood glucose level; stimulate breakdown of protein

Released: Mineralocorticoids (aldosterone)

Function: Reabsorb sodium and excrete potassium

Released: Sex hormones

Function: Stimulate reproductive organs and bring about sex characteristics

Adrenal medulla:

Released: Epinephrine and norepinephrine

Function: Emergency situations; raise blood glucose level

H) Pancreas:

Released:Insulin

Function: Lowers blood glucose level and promotes formation of glycogen

Released: Glucagon

Function: Raises blood glucose level

I) Testes:

Released: Androgens (testosterone)

Function: Stimulate male secondary sex characteristics

J) Ovaries:

Released: Estrogens and progesterone

Function: Stimulate female sex characteristics

Table 15.1 Principal Endocrine Glands and Hormones

*See page 309.

Task 2

List all hormones produced by the adrenal cortex and medulla (see figure B)

The adrenal medulla secretes two major hormones: epinephrine

(adrenaline), 80%, and norepinephrine (noradrenaline) 20%. these are both catecholamines. The adrenal cortex secretes three hormone types: mineralocorticoids, glucocorticoids and androgens. All

are similar in structure in that they are steroids

(Criterion 1.2)

Figure B

adrenal-cortexadrenal-medulla

2a. Explain the physiological effects of the catecholamines

2b. Explain the physiological effects of the mineralcorticoids and the glucocorticoids

(Criteria 1.2, 2.1 and 2.2, Max 150 each)

3. Explain how and when adrenaline is secreted by the adrenal glands

(Criteria 2.2 and 3.4 Max 150)

Task 3

1. Explain what happens if blood calcium levels rise above 11mg/100ml

99% of calcium ions (Ca2_) in the body is contained in the bones and teeth. The remaining 1% (around 1.5 gramms) is contained in the blood. The blood calium levels are regulated by hormones and kept within the range of 9mg/100ml to 11mg/100ml. if the blood calcium levels rise above 11mg/100ml in the blood hypercalcemia. Hypocalcemia increases

the permeability of plasma membranes to Na_. As a result,

nerve and muscle tissues undergo spontaneous action potential. generation. Hypercalcemia decreases the permeability of the plasma membrane to Na_, thus preventing normal depolarization

of nerve and muscle cells. High extracellular Ca2_ levels cause the

deposition of calcium carbonate salts in soft tissues, resulting in irritation

and inflammation of those tissues.

Calcitonin which is secreted by the parafollicular

cells of the thyroid gland, reduces extracellular Ca2_ levels.

Elevated Ca2_ levels stimulate calcitonin secretion, whereas

reduced Ca2_ levels inhibit it. Increased calcitonin secretion reduces

blood levels of Ca2_.

Bones also play a role an if blood

calcium levels are too high, osteoclast activity decreases. Less

calcium is released by osteoclasts from bone into the blood than

is taken from the blood by osteoblasts to produce new bone. As a result, a net movement of calcium occurs from the blood to bone,

and blood calcium levels decrease.

PTH

Explain what happens if blood calcium levels drop below 9mg/100ml

Hypocalcemia is a below-normal level of Ca2_ in the extracellular

fluid. Hypocalcemia increases the permeability of plasma membranes to Na_. As a result,

nerve and muscle tissues undergo spontaneous action potential generation.

the secretion of PTH increases resulting in increased numbers of osteoclasts, which causes increased

bone breakdown and increased blood calcium levels

In addition, osteoblasts respond to PTH by releasing

enzymes that result in the breakdown of the layer of unmineralized

organic bone matrix covering bone, thereby making the mineralized

bone matrix available to osteocytes.

The regulation of osteoclast numbers is mediated through osteoblasts

and red bone marrow stromal (stem) cells.When PTH levels

increase, PTH binds to its receptors on osteoblasts/stromal cells.

In response, these cells produce a surface molecule called receptor

for activation of nuclear factor kappa B ligand (RANKL). When

RANKL binds to its receptor on the surface of osteoclast precursor

cells, the cells are stimulated to become osteoclasts.

PTH also regulates blood calcium levels by increasing calcium

uptake in the small intestine Increased PTH

promotes the formation of vitamin D in the kidneys, and vitamin

D increases the absorption of calcium from the small intestine.

PTH also increases the reabsorption of calcium from urine in the

kidneys, which reduces calcium lost in the urine.

Explain the positive feedback mechanism by which oxytocin promotes labour contracts during birth.

Stretching of the uterine and vaginal tissues towards the end of a pregnancy during labour

initiates nerve impulses to the hypothalamus. The hypothalamus signals the posterior pituitary gland to release the hormone oxytocin. Oxytocin promotes uterine contractions. As the fetus is pushed more against the cervix, more oxytocin is released in a continuous positive feedback cycle Combined with the greater

excitability of the myometrium due to the decline in

progesterone secretion, oxytocin aids labor in its later

stages.

Oxytocin promotes uterine contractions in two ways.

Oxytocin stimulates the release of prostaglandin E2 and prostaglandin F2a in fetal membranes by activation of phospholipase C. The prostaglandins stimulate uterine contractility.

Oxytocin can also directly induce myometrial contractions through phospholipase C, which in turn activates calcium channels and the release of calcium from intracellular stores.

(Criterion 3.3, Max 150 each)

Task 4

1. List all hormones produced by the anterior and posterior pituitary

(Criterion 1.2)

Posterior Pituitary (Neurohypophysis)

Antidiuretic hormone(ADH)

Small peptide

Kidney

Increased water reabsorption (less water is lost in the

form of urine)

Oxytocin

Small peptide

Uterus; mammary glands

Increased uterine contractions; increased milk expulsion

from mammary glands; unclear function in males

Anterior Pituitary (Adenohypophysis)

Growth hormone (GH),

Protein

Most tissues

Increased growth in tissues; increased amino acid uptake

or somatotropin and protein synthesis; increased breakdown of lipids

and release of fatty acids from cells; increased

glycogen synthesis and increased blood glucose

levels; increased somatomedin production

Thyroid-stimulating hormone (TSH)

Glycoprotein

Thyroid gland

Increased thyroid hormone secretion

Adrenocorticotropic hormone (ACTH)

Peptide

Adrenal cortex

Increased glucocorticoid hormone secretion

Lipotropins

Peptides

Fat tissues

Increased fat breakdown

Beta Endorphins

Peptides

Brain, but not all target tissues are known

Analgesia in the brain; inhibition of gonadotropin

releasing hormone secretion

Melanocyte hormone (MSH)

Peptide

Melanocytes in the skin

Increased melanin production in melanocytes to make

the skin darker in color

Luteinizing hormone (LH)

Glycoprotein

Ovaries in females; testes in males Ovulation and progesterone production in ovaries; testosterone synthesis and support for sperm cell production in testes

Follicle-stimulating hormone (FSH)

Glycoprotein

Follicles in ovaries in females; seminiferous tubes in males

Follicle maturation and estrogen secretion in ovaries; sperm cell production in testes

Prolactin

. Protein

Ovaries and mammary glands in females

Milk production in lactating women; increased response

of follicle to LH and FSH; unclear function in males

2a. Explain the physiological effects of the anterior pituitary hormones

2b. Explain the physiological effects of the posterior pituitary hormones

(Criteria 1.2, 2.1 and 2.2, Max 150 each)

3a. Describe how and when ADH is secreted by the posterior pituitary

Antidiuretic hormone (ADH), secreted by

the posterior pituitary gland, passes through the circulatory

system to the kidneys. ADH regulates the amount of water re-

absorbed by the distal tubules and collecting ducts. When

ADH levels increase, the permeability to water of the distal

tubules and collecting ducts increases, and more water is reabsorbed

from the filtrate. Consequently, an increase in ADH

results in the production of a small volume of concentrated

urine. On the other hand, when ADH levels decrease, the distal

tubules and collecting ducts become less permeable to water.

As a result, less water is reabsorbed, and a large volume

of dilute urine is produced

The release of ADH from the posterior pituitary is regulated

by the hypothalamus. Certain cells of the hypothalamus

are sensitive to changes in the solute concentration of the

interstitial fluid within the hypothalamus. An increased solute

concentration of the blood and interstitial fluid results in action

potentials being sent along the axons of the ADHsecreting

neurons of the hypothalamus to the posterior pituitary,

causing ADH to be released from the ends of the axons

(see chapter 10). A reduced solute concentration in the blood

and interstitial fluid within the hypothalamus causes inhibition

of ADH release.

Baroreceptors that monitor blood pressure also influence

ADH secretion. Increased blood pressure causes a decrease

in ADH secretion, and decreased blood pressure increases

ADH secretion

Circulatory shock is defined as inadequate

blood flow throughout the body. As a consequence,

tissues suffer damage resulting from

a lack of oxygen. Severe shock may damage

vital body tissues and lead to death.

In response to reduced

blood pressure, antidiuretic hormone

(ADH) is released from the posterior pituitary

gland, and ADH also enhances the retention of

water by the kidneys. An intense sensation of

thirst leads to increased water intake, which

helps restore the normal blood volume.

3b. Describe how and when ACTH is secreted by the anterior pituitary

(Criterion 3.1 and 3.4, Max 150 each)

The fetus also plays a role in stimulating parturition. Stress

on the fetus triggers the secretion of a releasing hormone from

the fetal hypothalamus, which, in turn, causes adrenocorticotropic

hormone (ACTH) release from the fetal anterior pituitary.

ACTH stimulates the fetal adrenal gland to secrete cortical

steroids that reduce progesterone secretion, increase estrogen

secretion, and increase prostaglandin production by the placenta.

Prostaglandins strongly stimulate uterine contractions.

1. The fetal hypothalamus secretes a

releasing hormone that stimulates

adrenocorticotropic hormone (ACTH)

secretion from the pituitary. The fetal

pituitary secretes ACTH in greater

amounts near parturition.

2. ACTH causes the fetal adrenal gland to

secrete greater quantities of adrenal

cortical steroids.

3. Adrenal cortical steroids travel in the

umbilical blood to the placenta.

4. In the placenta the adrenal cortical

steroids cause progesterone synthesis to

level off and estrogen and prostaglandin

synthesis to increase, making the uterus

more irritable.

5. The stretching of the uterus produces

action potentials that are transmitted to

the brain through ascending pathways.

6. Action potentials stimulate the secretion of

oxytocin by the posterior pituitary.

7. Oxytocin causes the uterine smooth

muscle to contract.

Regulation of Cortisol Secretion

1. In response to stress or low blood water loss.

glucose, a releasing hormone is

released from the hypothalamus

and passes, by way of the

hypothalamic???pituitary portal

system, to the anterior pituitary,

where it binds to and stimulates

cells that secrete ACTH into the

general circulation.

2. ACTH acts on the adrenal

cortex and stimulates the

secretion of cortisol into the

general circulation.

3. Cortisol, in turn, acts on its

target tissues to increase

protein breakdown and

increase blood glucose.

Explain the functional relationship between the hypothalamus and the pituitary gland (see Figure C)

Hypothalamic Control of the Posterior Pituitary

Both of the posterior pituitary hormones???ADH

and oxytocin, are actually produced in neuron cell bodies of the

supraoptic nuclei and paraventricular nuclei of the hypothalamus.

These nuclei within the hypothalamus are thus endocrine

glands. The hormones they produce are transported along axons

of the hypothalamo-hypophyseal tract to the posterior

pituitary, where they are stored and later released. The posterior

pituitary is thus more a storage organ than a producing gland.

The release of ADH and oxytocin from the posterior pituitary

is controlled by neuroendocrine reflexes. In nursing

mothers, for example, the mechanical stimulus of suckling acts,

via sensory nerve impulses to the hypothalamus, to stimulate the

reflex secretion of oxytocin. The secretion of ADH

is stimulated by osmoreceptor neurons in the hypothalamus in

response to a rise in blood osmotic pressure; its secretion

is inhibited by sensory impulses from stretch receptors

in the left atrium of the heart in response to a rise in blood volume

(chapter 14).

Hypothalamic Control of the Anterior Pituitary

The anterior pituitary is not really the master gland, since secretion

of its hormones is in turn controlled by hormones secreted

by the hypothalamus.

Releasing and Inhibiting Hormones

Since axons do not enter the anterior pituitary, hypothalamic

control of the anterior pituitary is achieved through hormonal

rather than neural regulation. Releasing and inhibiting hormones,

produced by neurons in the hypothalamus, are transported

to axon endings in the basal portion of the hypothalamus.

This region, known as the median eminence contains

blood capillaries that are drained by venules in the stalk of the

pituitary.

The venules that drain the median eminence deliver blood

to a second capillary bed in the anterior pituitary. Since this second

capillary bed is downstream from the capillary bed in the median

eminence and receives venous blood from it, the vascular

link between the median eminence and the anterior pituitary

forms a portal system. The vascular link between the hypothalamus

and the anterior pituitary is thus called the hypothalamohypophyseal

portal system.

Regulatory hormones are secreted into the hypothalamohypophyseal

portal system by neurons of the hypothalamus. These

hormones regulate the secretions of the anterior pituitary (fig. 11.15

and table 11.7). Thyrotropin-releasing hormone (TRH)

stimulates the secretion of TSH, and corticotropin-releasing hormone

(CRH) stimulates the secretion of ACTH from the anterior

pituitary. A single releasing hormone, gonadotropin-releasing

hormone, or GnRH, stimulates the secretion of both gonadotropic

hormones (FSH and LH) from the anterior pituitary.

The secretion of prolactin and of growth hormone from the anterior

pituitary is regulated by hypothalamic inhibitory hormones,

known as prolactin-inhibiting hormone (PIH) and somatostatin,

respectively.

A specific growth hormone-releasing hormone (GHRH)

that stimulates growth hormone secretion has been identified as a

polypeptide consisting of forty-four amino acids. Experiments

suggest that a releasing hormone for prolactin may also exist, but

no such specific releasing hormone has yet been discovered.

Feedback Control

of the Anterior Pituitary