Chapter

18

Fisiologi Sistem
Endokrin
Kelenjar Adrenal

2012 Pearson Education, Inc.

Tujuan Pembelajaran
1. Menjelaskan fisiologi hormon korteks adrenal
2. Menjelaskan fisiologi hormon medula adrenal

Figure 18-14a The Adrenal Gland

Right superior
adrenal arteries

Right and left inferior

phrenic arteries

Celiac trunk
Right adrenal
gland

Left adrenal gland

Right middle
adrenal artery

Left middle
adrenal artery
Left inferior
adrenal arteries

Right inferior
adrenal artery

Left adrenal vein

Right renal artery

Left renal artery

Right renal vein

Left renal vein

Superior mesenteric
artery
Abdominal aorta
Inferior vena cava

A superficial view of the left

kidney and adrenal gland

Figure 18-14c The Adrenal Gland

Adrenal
medulla
Zona
reticularis

Adrenal
cortex

Zona
fasciculata

Zona
glomerulosa
Capsule

Adrenal gland

LM 140

The major regions of an adrenal gland

Cholesterol
Pregnenolone

Progesterone

17-Hydroxyprogesterone

Dihydroepiandrsterone
(Androgens)
Androstenedione
Testes

Corticosterone
(Glucorticoids)
Aldosterone
(Mineralocorticoid)

Cortisol

Testosterone
Ovaries

Estradiol

Figure 18-3 G Proteins and Hormone Activity

Hormone

Protein
receptor
G protein
(inactive)

G protein
activated

Effects on cAMP Levels

Many G proteins, once activated, exert their effects by changing the concentration
of cyclic-AMP, which acts as the second messenger within the cell.

Hormone

Hormone

Protein
receptor

Protein
receptor

G protein
activated
Acts as
second
messenger

Increased
production
of cAMP

adenylate
cyclase

G protein
activated
PDE

Enhanced
breakdown
of cAMP

kinase

Opens ion
channels

Activates
enzymes

If levels of cAMP increase,

enzymes may be activated
or ion channels may be
opened, accelerating the
metabolic activity of the cell.

Examples:
Epinephrine and norepinephrine
( receptors)
Calcitonin
Parathyroid hormone
ADh, ACTH, FSH, LH, TSH
Glucagon

Reduced
enzyme
activity

In some instances, G protein

activation results in decreased
levels of cAMP in the
cytoplasm. This decrease has
an inhibitory effect on the cell.

Examples:
Epinephrine and norepinephrine (2 receptors)

Figure 18-4a Effects of Intracellular Hormone Binding

Diffusion through
membrane lipids

Target cell response

CYTOPLASM
Alteration of cellular
structure or activity

Translation and
protein synthesis
Receptor
Binding of hormone
to cytoplasmic or
nuclear receptors

Transcription and
mRNA production

Receptor
Gene activation
Nuclear
pore
Nuclear
envelope

Binding of
hormonereceptor
complex to DNA

If we are talking about hormones, we always have to think abaout :

1.

The name

2.

The glands/ the cells

3.

The target cells

4.

Function in the target cells

5.

The stimulaters

6.

The inhibitors

7.

Feed back mechanism

Mineralocorticoid
Aldosteron

Source: Zona Glomerulosa (outermost region)

Target Sel:
Tubulus distal
Taste bud

Mineralocorticoid
Efect:
Stimulates conservation of sodium ions and elimination of potassium
ions
Increases sensitivity of salt receptors in taste buds

Stimulator:
Drop in blood Na+, blood volume, or blood pressure via RAA
Rise in blood K+ concentration

Mineralocorticoid
Inhibitor:
Rise in blood Na+, blood volume, or blood pressure
Drop in blood K+ concentration
ANP & BNP

Feed back mechanism

Glucocorticoid
For example, cortisol (hydrocortisone)

Liver converts cortisol to cortisone

Source: Zona Fasciculata
Target sel:?

Glucocorticoid
Efect:

1. Metabolic efect:
overall effect: increase plasma glucose levels,
often at the expense of proteins and fats
a. Carbohydrate

gluconeogenesis

decrease glucose utilization(anti- insulin effect)

b. Protein

proteins are mobilized

lean body mass decreases

Glucocorticoid
Efect:

1. Metabolic efect:
c. Fat

causes lipolysis (enhances catecholamines)

expectations: person will be thin, but if excessive cortisol see unusual fat
distribution (i.e. buffalo hump)

d. Increases Hunger

Glucocorticoid
Efect:

2. Other Effects:
a. Fetal Development

Cortisol aids in maturation of the lungs, especially with the production of

surfactant

b. Adults
i.

Anti-inflammatory

during tissue damage, phospholipase A2 activity increases releasing

arachadonic acid to aid in synthesis of prostaglandins & leukotrienes

glucocorticoids enhance production of macrocortin which inhibits

phospholipase A2 and thus the inflammatory response

Glucocorticoid
Efect:
2. Other Effects:
b. Adults
ii.

Immune Response

glucocorticoids suppress the immune system by decreasing the number of

T lymphocytes

used frequently after organ transports

iii. Vasoconstriction

Glucocorticoids necessary for vasocontriction effects of the catecholamines

iv. Stimulates Erythropoietin

v.

Increases Bone Reabsorbtion

vi. Decreases REM Sleep

Glucocorticoid
Stimulator:
1. CRH
2. ACTH

3. Hypoglicemia
4. Stress
* Stress and hypoglycemia can also trigger the release of CRH

Glucocorticoid
Inhibitor:-

Feed back mechanism

Androgen
DHEA

Source: Zona Reticularis

Target sel: ?
Efect:
sexual characteristics
Anabolic

Androgen
Stimulator
ACTH

Inhibitor
Feed back mechanism

18-6 Adrenal Glands

The Adrenal Medulla
Contains two types of secretory cells
One produces epinephrine (adrenaline)
75% to 80% of medullary secretions
The other produces norepinephrine (noradrenaline)
20% to 25% of medullary secretions

18-6 Adrenal Glands

Epinephrine and Norepinephrine
Activation of the adrenal medullae has the following
effects:
In skeletal muscles, epinephrine and norepinephrine
trigger mobilization of glycogen reserves

And accelerate the breakdown of glucose to provide ATP

This combination increases both muscular strength and
endurance

In adipose tissue, stored fats are broken down into fatty

acids
Which are released into the bloodstream for other
tissues to use for ATP production

18-6 Adrenal Glands

Epinephrine and Norepinephrine
Activation of the adrenal medullae has the following
effects:
In the liver, glycogen molecules are broken down
The resulting glucose molecules are released into the
bloodstream
Primarily for use by neural tissue, which cannot shift to
fatty acid metabolism
In the heart, the stimulation of beta 1 receptors triggers an
increase in the rate and force of cardiac muscle
contraction

Table 18-5 The Adrenal Hormones

Table 18-9 Clinical Implications of Endocrine Malfunctions

The Hormonal Responses to Stress

General Adaptation Syndrome (GAS)
Also called stress response
How body responds to stress-causing factors

Is divided into three phases

1. Alarm phase
2. Resistance phase

3. Exhaustion phase

Figure 18-20 The General Adaptation Syndrome

Alarm Phase (Fight or Flight)

Immediate Short-Term
Responses to Crises

Brain
General
sympathetic
activation

Adrenal medulla
Sympathetic
stimulation

Epinephrine,
norepinephrine

Increased mental alertness

Increased energy use by
all cells
Mobilization of glycogen and
lipid reserves
Changes in circulation
Reduction in digestive activity
and urine production
Increased sweat gland
secretion
Increased heart rate and
respiratory rate

Figure 18-20 The General Adaptation Syndrome

Resistance Phase
Growth hormone
Pancreas
Glucagon
Sympathetic
stimulation
ACTH

Adrenal cortex

Glucocorticoids
Kidney
Mineralocorticoids
(with ADH)

Renin-angiotensin
system

Long-Term Metabolic
Adjustments
Mobilization of remaining
energy reserves: Lipids are
released by adipose tissue;
amino acids are released by
skeletal muscle
Conservation of glucose:
Peripheral tissues (except
neural) break down lipids to
obtain energy
Elevation of blood glucose
concentrations: Liver
synthesizes glucose from
other carbohydrates, amino
acids, and lipids
Conservation of salts and
water, loss of K+ and H+

Figure 18-20 The General Adaptation Syndrome

Exhaustion Phase
Collapse of Vital Systems
Exhaustion of lipid reserves
Cumulative structural or
functional damage to vital
organs
Inability to produce
glucocorticoids
Failure of electrolyte balance