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ENDOCRINE GLANDS
The different activities of the body are regulated by 2 main
systems:-
1. The nervous system. 2. The endocrine system.
The nervous system: is concerned with regulation of metabolic
activities and secretions of glands. It is a rapid control
system.
The endocrine system: is concerned with regulation of metabolic
functions. It is a slow control system. What is meant by the
endocrine system?
It is a system of ductless glands, which differs from other
types of glands such as the salivary glands in that their
secretions which are called hormones enter the blood stream
directly which carries them to different tissues to produce their
effects. What is a hormone ?
It is a chemical substance secreted into the blood stream by
endocrine glands to act on distant organs called effector organs.
Properties of hormones:
They are secreted in very small amounts. So, their blood and
tissue concentrations are very low. They do not act on the organs
secreting them (endocrine glands) but act on distant organs
(effector organs). Hormones may act on a specific effector organ
e.g. thyrotrophic hormone (TSH) of the anterior pituitary acts
specifically on the thyroid gland, or hormones may act on the body
as a whole e. g. growth hormone (GH) of the anterior pituitary.
Hormones act on the target organ by changing the rate of
biochemical reactions in that organ. This effect persists for a
longer period even after the hormone which produced it becomes
inactivated.
Difference between a hormone and an enzyme:
Hormone Enzyme Some hormones are proteins, some are amino acids
and some are steroids. Hormones act on distant organs and not on
those secreting them. Hormones are continually secreted,
inactivated or excreted.
All enzymes are proteins.
Enzymes act in the same tissues forming them. Enzymes catalyze
biochemical reactions without being destroyed or excreted.
Chemical nature of hormones: Hormones may be derived from:
(1) Amino acids: e.g.
Tryptophan serotonin and melatonin.
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Tyrosine T4 (thyroxine) and T3 (triiodothyronine). (Thyroid
hormones)
Catecholamines (e.g. Adrenaline and Noradrenaline.) (Hormones of
the adrenal medulla) (2) Peptides and proteins: e.g.
All pituitary hormones are either peptides or proteins. The
pancreatic hormones insulin and glucagon (peptides).
(3) Steroids in nature : e.g.
Adrenocortical hormones (cortisol). Sex hormones
(testosterone).
The plasma level of a hormone depends upon 2 factors: 1- The
rate of hormone secretion by the endocrine gland :
rate of secretion plasma hormone level (and vice versa) . N.B.
Some hormones may show daily variation in the rate of secretion
known as the circadian rhythm . 2- The rate of hormone inactivation
and excretion:
rate of inactivation plasma hormone level (and vice versa). N.B.
Inactivation may occur in the effector organ or in the liver, or
may be excreted by the kidney.
Mechanism of Action of Hormones: Hormones change the activity of
the effector organs by changing the
rate of enzymatically catalyzed reactions in them. This may be
the result of:
(1) lncreased rate of enzyme synthesis increased enzyme
concentration. lt is a slow response. e.g. Steroid hormones.
N.B. The rate of a biochemical reaction is to enzyme
concentration. (2) lncreased activity of the enzyme without
increase in its
concentration accelerates a biochemical reaction rapid response.
e.g. peptides and protein hormones .
(3) Both effects. The response in this case is rapid and
prolonged. How does activation of enzymes occur? (Fig.1)
lt occurs through the following series of steps: (1) For non -
steroidal hormones (proteins, peptides and amino acids) : Hormones
are carried by the blood stream to the cells of the effector organ.
Hormones do not pass the cell membrane to the inside of the cells
because of their large molecular size. Therefore, hormones bind to
specific protein receptors on the outer surface of the cell
membrane. This binding activates a protein enzyme on the inner
surface of the cell membrane called adenyl cyclase. Adenyl cyclase
catalyzes the conversion of
ATP cAMP + PPi cAMP inside the cells of the effector organ.
This cAMP diffuses through the cells of the effector organ
acting as
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a second messenger to stimulate the enzyme activity . N.B. The
hormone is the primary messenger.
adenyl cyclase phosphodiesterase
ATP ------------------- ppi + cAMP ------------------------ 5 –
AMP (AC) (PDE)
N.B.
lnhibitors of PDE (e.g. methyl xanthines cGMP, cIMP) cAMP
potentiate hormonal effects.
Substances which potentiate the effect of PDE (e.g. ammonium
ions
) cAMP and antagonize the hormonal effects.
Other second messengers include cGMP and prostaglandins (PGs).
(2) For steroidal and thyroid hormones :
Hormones are carried by the blood stream to the cells of the
effector organ.
Being lipid soluble, they enter the cell and bind to specific
receptors inside the cytoplasm forming a complex.
The hormone-receptor complex moves towards the nucleus and
enters through the nuclear membrane.
ln the nucleus, it accelerates RNA formation from DNA
(transcription).
Newly formed RNA (mRNA) leaves the nucleus to the cytoplasmic
ribosomes where the process of protein synthesis is stimulated
according to the genetic code carried by mRNA (translation). Thus,
the enzyme protein is increased.
N.B. Thyroid hormones bind directly to nuclear receptors.
(A) (B)
Mechanism of hormonal action of (A) protein hormones and (B)
steroid hormones
Methods of Studying Endocrine Functions: 1) By measuring the
concentration of a specific hormone in the plasma
using a highly sensitive method as radio immunoassay (RIA).
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2) By observing the effects of injury or removal of part or all
of the gland on body functions.
3) By observing the effects of injection of glandular
extracts.
THE PITUTARY GLAND (HYPOPHYSIS)
Anatomically: - lt is a small gland present at the base of the
brain, occupying the sella
turcica. - lt is 0.5 to 1 gm in weight; being slightly heavier
in females. - lt is connected to the hypothalamus by the pituitary
stalk (infundibulum)
Physiologically : The pituitary gland is formed of 2 parts,
which differ both embryologically and functionally and are
considered as 2 separate glands:
(1) The Anterior Pituitary (Adenohypophysis ): - lt develops
from the roof of the buccal (Rathk's pouch ) and is of
epithelioid nature. - lt is formed of 3 parts:
1. Pars distalis. 2. Pars tuberalis. 3. Pars intermedia
(intermediate part, or sometimes called
intermediate lobe.)
(2) The posterior pituitary (Neurohypophysis ): - lt develops
from the floor of the 3rd ventricle. - lt is divided into :
1. The pituitary stalk (infundibulum); connecting the pituitary
to the hypothalamus.
2. The nervous part (pars nervosa . N.B. There is no
intermediate lobe in the human pituitary gland.
HORMONES OF THE PITUITARY GLAND (1) Anterior Lobe Or Anterior
Pituitary Hormones :
1- Growth Hormone (GH, Somatotropin, STH). 2- Thyroid
Stimulating Hormone (TSH, Thyrotropin). 3- Adrenocorticotrophic
Hormone (ACTH, Corticotropin). 4- Follicle Stimulating Hormone
(FSH). 5- Luteinizing Hormone or lnterstitial Cell Stimulating
Hormone (LH,
ICSH) N.B. FSH and LH are referred to as gonadotrophic hormones
(GnH).
6- Prolactin (PL), Lactogenic Hormone, Mammotropin,
Luteoptrophic Hormone (LTH).
(2) lntermediate Lobe hormones :
- Melanocyte stimulating Hormone (MSH) . N.B. This hormone does
not appear to have function in man .
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(3) The Posterior Lobe Hormones : 1- Antidiuretic Hormone (ADH,
or Vasopressin, AVP). 2- Oxytocin.
THE ANTERIOR PITUITARY GLAND
(ADENOHYPOPHYSIS)
Histologically: With the use of acid - base stains the anterior
pituitary cells are
classified into 3 types: 1- Acidophil cells: Their cytoplasm is
granular and the granules stain with acid dyes.
They from 35% of the total cells. They secrete protein hormones
: growth hormone (GH) and prolactin
(PL) . 2- Basophil cells : Their cytoplasmic granules stain with
basic dyes. They form 15 % of
the cells. They secrete :
- Polypeptide hormones (ACTH and MSH). - Glycoprotein hormones
(FSH, LH and TSH). 3- Chromophobe cells : Their cytoplasm is
non-granular. They form 50% of the cells. Their exact function is
not fully determined .
N.B. Recent classification using immunocytochemistry and
electron microscopy: 5 types of secretory cells were distinguished:
1. Somatotropes, which secrete growth hormone. 2. Lactotropes (also
called mammotropes), which secrete prolactin. 3. Thyrotropes, which
secrete TSH. 4. Gonadotropes, which secrete both LH and FSH. 5.
Corticotropes, which secrete both ACTH and B-LPH.
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Functions Of The Adenohypophysis: 1) lt stimulates growth of the
body and skeleton. 2) lt stimulates growth and functions of target
glands (thyroid, adrenal
cortex , testes and ovaries). Adenohypophyseal hormones are
called therefore trophic hormones.
3) lt stimulates reproduction and sexual activities. 4) lt
stimulates general and specific metabolism. Regulation Of
Adenohypophyseal Function
The hormonal secretion by the anterior pituitary is regulated
through 3 mechanisms : 1) The hypothalamic control. 2) Feed back
control by the hormones of the effector organs (target glands).
This is the long loop feed back . 3) Feed back control by the
pituitary hormones themselves. This is the short loop feed back .
1- The Hypothalamic Control : The hypothalamus is a large nervous
center that receives many afferent nerve fibers carrying
information about the changes that occur outside or inside the
body. According to information, the hypothalamus secretes
hypothalamic factors (neurohormones) that reach the anterior
pituitary (through the hypothalamic - hypophyseal portal
circulation) to regulate its
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secretion. Since the hypothalamus is the " mayestro " of the
other endocrine glands, the function of these glands is regulated
to face the original change and maintain homeostasis.
The hypothalamic- hypophyseal portal circulation:
The venous blood collected from the capillaries of the
hypothalamus from venous channels that pass to the anterior
pituitary where they pour their blood into a second set of
capillaries and sinuses in-between the anterior pituitary cells.
Significance:
i. The anterior pituitary receives its main blood supply from
the venous blood collected from the hypothalamus.
ii. The hypothalamic neurohormones reach the anterior pituitary
through this portal circulation to regulate its secretion.
The hypothalamic neurohormones (Releasing and lnhibitory
Hormones): They are formed by special hypothalamic neurones that
end in the
median eminence or tuber cinereum. They are secreted at their
nerve terminal into the tissue fluid by
exocytosis. They are immediately carried by the capillaries of
the portal
circulation to the anterior pituitary. Function: They control
the secretion of the anterior pituitary
hormones. For each type of anterior pituitary hormone there is a
corresponding
releasing hormone. Some anterior pituitary hormones have in
addition a corresponding
inhibitory hormone i.e. (both releasing and an inhibitory
hormone exist). Most anterior pituitary hormones are controlled
predominantly by
releasing hormones, except in case of prolactin where the
inhibitory hormone predominates.
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2- Feed back control by the endocrine target organs (Long Loop
Feed Back)
Feed back control means the effect of the target hormones on the
secretion of both the hypoth. Neurohormones and pituitary trophic
hormones i.e. either at a hypothalamic or pituitary levels.
lf this effect is inhibitory, the feed back is - ve.
lf this effect is stimulatory , the feed back is + ve. -
Example:
Stress stimulates the hypothalamus Release of CRF Ant. Pit.
ACTH carried by blood to adrenal cortex Cortisol inhibit
hypothalamic CRF
3- Feed back control by the pit . hormones themselves (Short
Loop Feed Back )
portal circulation
Stimulus Hypothalamus Release of neurohormone ------------- Ant.
Pit. To hypothalamus by blood or back diffusion
Ant.Pit. hormones
------------------------------------------------------------
inhibit the release of the corresponding releasing hormone.
Importance of the feed back control :
1. Maintain the normal level of the target gland hormone in
blood. 2. Prevent over stimulation of the target gland by the
corresponding
trophic hormone. 3. Adjust the rate of secretion of the target
gland hormones according
to the body need.
Hypothalamohypophyseal connection and control of pituitary
gland
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GROWTH HORMONE ( GH, SOMATOTROPHIC HORMONE) - It is secreted by
the acidophil cells of the ant. pit. (somatotropes). - lt is
protein in nature (190 amino acids ) and shows species specificity.
- lts rate of secretion is higher in younger than in older peoples
and
shows daily variations. - The basal blood level is 3 ng / m1
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Factors Affecting The Secretion Of Growth Hormone :
(A) Factors That Stimulate GH Secretion : 1. Hypoglycaemia. 2.
Fasting and severe malnutrition. 3. Exercise. 4. Amino acid
infusion specially arginine. 5. Neural stimuli e.g. emotional
stress and onset of deep sleep.
6. Hormones as oestrogens, androgens, adrenaline ( adrenergic
effect.) (B) Factors That Inhibit GH Secretion:
lncreased blood glucose level.
Corticosteroids.
Regulation of GH Secretion:
The hypothalamus controls GH secretion by means of 2 hormones:
1- Growth H releasing hormone GRH which stimulates the acidophil
cells
of the ant. Pit. to secrete GH. 2- Growth H inhibitory hormone
(GIH, Somatostatin) which inhibits GH
secretion. N.B. Somatostatin is also secreted by the delta cells
of the pancreas and the duodenal mucosa. lt has an inhibitory role
on the pancreatic hormones and gastric secretion. Functions of
Growth Hormone: 1- Effect On Growth - GH Promotes growth of all
tissues of the body that are capable of
growing through increase both size and No. of cells by mitosis.
- GH stimulates growth of cartilage and bone indirectly.
Mechanism:
GH stimulates the formation of small proteins called somatomedin
from the liver, muscles and kidney. Somatomedin, in turn acts
directly on cartilage and bone to promote their growth via the
deposition of chondroitin sulphate and collagen. N.B. - There is no
growth in length of bone after adulthood due to closure of
the epiphysis, and GH then causes only increase in thickness of
long bones.
- Some physiologists believe that somatomedin is the growth H
mediating factor which mediates most of the important functions of
GH .
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2- Metabolic Effects of GH :
A- On Protein Metabolism:
GH stimulates protein synthesis by:
lncreasing Am. Ac. uptake by the cells.
lncreasing formation of RNA in the nucleus (transcription).
Stimulation of the ribosomes.
Decreasing catabolism of proteins and Am. Ac. to provide
energy.
B- On Fat Metabolism:
GH produces lipolysis i.e. Triglycerides free fatty acids F.
Acids in blood.
GH enhances -oxidation of Fatty acids energy. Thus spares
proteins and carbohydrates.
N.B. Excess GH Ketogenesis. C- On Carbohydrate Metabolism : GH
causes:
glucose utilization by the cells.
Mechanism: Enhanced F.A. oxidation accumulation of acetyl Co.
A
inhibits glycolysis.
lncreased glycogen deposition inside the cells due to
accumulation of glucose inside the cells.
lncrease in blood glucose level (diabetogenic effect).
Mechanism: utilization of glucose by cells accumulation of
glucose inside the cells accumulation of glucose in the cells
transport
of glucose across the cell membrane glucose accumulates in the
blood. 3-Lactogenic Effect:
GH resembles prolactin in structure and thus it has some
lactogenic effects.
DISORDERS OF GROWTH HORMONE SECRETION : 1) Increased Secretion
of GH :
In these conditions there is loss of the mechanisms that
regulate and control the secretion of GH. The acidophil cells
continue to secrete GH in excess amounts. Cause: hyperplasia or
acidophil cell adenoma. Effects: Depends on the age of
occurrence;
I. lf it occurs before puberty i.e. (before closure of
epiphysis) Gigantism.
II. lf it occurs after puberty i.e.(after closure of epiphysis)
Acromegaly .
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I. GIGANTISM:
lt occurs due to excess secretion of GH before puberty.
GH stimulates excess growth of all tissues of the body.
Effect on long bones :
1. There is a delay in the union of epiphysis increase in bone
length so, the giant patient may reach 3 meters in height.
2. The growth in length of long bones is proportionate i.e.
The span = The height
The span is the distance between the distal ends of the
laterally extended arms .
Effect on skeletal muscles : lncreased strength due to
overgrowth at first, followed by marked weakness due to excess
stretch by the growing long bones.
Effect on soft tissues: Overgrowth of the viscera
(splanchonmegaly).
Effect on the gonads: The gonads remain infantile. How? The
acidophil adenoma presses on the other pit. cells causing their
atrophy. Atrophy of basophils Gonadotrophic Hs Failure of
development of the gonads remains infantile.
Hyperglycemia glucosuria. (Diabetes) N.B. This type of diabetes
is insulin resistant, because its cause is excess GH and not
insulin deficiency.
metabolic rate. II. ACROMEGALY:
It occurs due to excess production of GH after puberty. GH
stimulates growth of all tissues of the body except growth in
length of long bones. Effect the skeleton:
1) lncreased thickness of all bones: The skull:
i) The mandible is thickened and protruded (prognathism), with
widely separated teeth.
ii) The nose is enlarged. iii) The supraorbital ridges and
frontal
bosses are prominent. The vertebral column:
Thickening and enlargement of the vertebrae kyphosis. The hands
and feet :
They become larger, broad with thick fingers and palms . - - - -
- - - - - - - - - - - - - -- - Effect on soft tissues :
1. splanchnomegaly. 2. SK . muscle overgrowth. 3. Overgrowth of
the skin, especially of the scalp and face
it becomes wrinkled
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(Bulldog scalp). Effect on the gonads :
ln the early condition, there is hyperfunction of the sex
organs. Later, these functions are depressed.
Hyperglycemia and increased metabolic rate. 2) Reduced Secretion
of GH : (A) HYPOPITUITARY DWARFISM:
lt is due to arrested skeletal growth as a result of deficiency
of GH or lack of the normal tissue response to GH, occurring before
puberty. Causes : 1) Destructive lesions of the pituitary gland. 2)
The secretion of inactive GH. The children have normal or even
increased blood GH level but it is ineffective. These children
can respond to exogenous human GH.
3) Lack of target organ response to endogenous GH. 4) Laron
dwarfism : GH release is normal, but there is a hereditary
deficiency of somatomedin. Features: The height is not more than
1 to 1.2 meters. The retardation of growth is symmetrical
(proportionate) i.e.
The span = The height
Growth of all soft tissues is arrested. Mental development
occurs normally, but the patient is emotionally unstable.
The gonads often show hypofunction infantilism (failure of
sexual development).
(B) PITUITARY INFANTLLISM :
Pituitary infantilism refers to the condition of dwarfism
combined with hypoganadism. The cause is deficiency of both GH and
gonadotrophic Hs occurring since birth.
P A N H Y P O P I T U I T A R I S M: It is called also Simmond
's Disease or pituitary Cachexia.
- Cause: Atrophy of the ant. lobe of the pituitary deficiency of
the trophic
hormones severe depression of the activity of the thyroid,
adrenal cortex and gonads. This is due to one of the following:
1. Chromophobe adenoma pressure atrophy on other cells.
2. Craniopharyngioma.
3. Shehan's syndrome: postpartum haemorrhage
thrombosis of the pit. blood vessels pituitary necrosis. - The
manifestations are due to decreased secretion of the pituitary
trophic hormones:-
Decreased growth H causes: A. Loss in body weight (pituitary
cachexia). B. Asthenia and easy fatigability.
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C. Premature senility in the form of: - The patient looks older
than his actual age. - Premature graying of hairs. - Decay and
falling of teeth. - Dry wrinkled skin. - Easy fatigability.
Decreased activity of the thyroid:
Decreased tolerance to cold due to B.M.R. Decreased activity of
the gonads
Atrophy of the accessory sex organs and decline in sexual
activity:
- ln females: Amenorrhoea, genital atrophy, atrophy of the
breasts and loss of axillary and pubic hair.
- ln males: Failure of spermatogenesis, loss of sexual desire
and impotence .
Decreased activity of the adrenal cortex:
Hypoglycaemia and excretion of 17- ketosteroids in urine.
P R O L A C T I N lt is secreted by the acidophil cells of the
adenohypophysis. lt is protein in nature. Functions:
Prolactin stimulates mainly the synthesis of milk and its
constituents including fat, casein and lactose by the mammary gland
which becomes ready for subsequent secretion. The mammary gland
must be prepared (primed) for the action of prolactin by the
ovarian hormones (oestrogen and progesterone). Regulation of
Prolactin Secretion:
Normally, prolactin secretion is continually inhibited by the
hypothalamic neurohrmone (prolactin inhibitory hormone; PIH). PIH
proved to be dopamine. Prolactin, when released exerts a short loop
feedback on the
hypothalamus to PIF and consequently inhibits its own secretion.
Factors Which lncrease Prolactin Secretion:
1. Stress and exercise. 2. After the onset of deep sleep and
persists during sleep. 3. Oestrogens.
4. lncreases during pregnancy to a maximum at delivery lt
decreases immediately after delivery for 8 days lt increase
again by the suckling reflex.
5. All drugs which inhibit dopamine (PIH) increase prolactin
e.g. chlorpromazine.
Factors Which Decrease Prolactin Secretion All drugs which
stimulate dopamine synthesis or stimulate the
dopaminergic receptors e.g. L- Dopa, apomorphine and
Bromocriptine.
MELANOCYTE STIMUKATING HORMONE - lt is formed by the basophil
cells of the intermediate lobe in animals but
not in man. - lt has no physiological role in man.
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- ln animals, it stimulates dispersion of melanin pigment
granules in the
melanocytes of the skin darkening of the skin (essential for the
process of camouflage). lt may also stimulate melanin
production.
- ln man MSH resembles part of ACTH molecule and therefore
conditions in which ACTH secretion is increased are accompanied by
pigmentation of the skin.
THE POSTERIOR PITUITARY (NEUROHYPOPHYSIS)
The posterior pituitary is connected to the hypothalamus by
the
pituitary stalk which contains the hypothalamo-hypophyseal
tract. The tract is formed of the axons (nerve fibers) of the
supraoptic and paraventricular nuclei of the hypothalamus. These
fibers terminate in the posterior pituitary. Remember : A nucleus
is a collection of nerve cells (cell bodies) in the C.N.S., having
the same function.
The posterior pituitary secretes 2 peptide hormones : 1) Anti-
diuretic hormone (ADH or vasopressin). 2) Oxytocin. Both ADH and
oxytocin are formed by the neurones of the supraoptic
and paraventricular nuclei of the hypothalamus. N.B. The
supraoptic forms mainly ADH, while the paraventricular forms mainly
oxytocin.
The two hormones are then transported along the
hypothalamo-hypophyseal tract to reach their nerve terminals in the
posterior pituitary where they are stored in combination with a
carrier protein; Neurophysin. The two hormones are released from
their storage granules in the nerve terminals of the posterior
pituitary according to nerve impulses descending from the
hypothalamus along the hypothalamo-hypophyseal tract.
After producing their effects, ADH and oxytocin are rapidly
inactivated through:
1) Metabolism in the liver via the 2 enzymes; vasopressinase and
oxytocinase respectively.
2) Excretion by the kidney.
(1) ANTI- DIURETIC HORMONE (ADH OR VASOPRESSIN). FUNCTIONS OF
ADH:
(1) On The Kidney: ADH increases water reabsorption from the
cells of the distal
convoluted and collecting tubules of the kidney urine volume.
How?
ADH (vasopressin) released Kidney ADH fix to receptors on
the kidney activate adenyl cyclase cAMP in these cells
activate protein kinase enzyme inside the cells phosphorylation
of
proteins of cell wall widening of cell membrane pores
reabsorption of water.
(2) On The Smooth Muscles of Blood Vessels: Physiological doses
that are normally secreted and produce
antidureasis have no effect on smooth muscles of B.V.
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Excess doses generalized vasoconstriction (hence its name
vasopressin) Blood pressure & myocardiac ischaemia due to
coronary vasoconstriction.
(3) On other Smooth muscles:
ADH stimulates all smooth muscles colics.
ADH stimulates the smooth muscles of the uterus stimulate
uterine contractions.
CONTROL OF ADH SECRETION :
ADH secretion depends upon the following factors: (1) Osmotic
Pressure Of The Plasma The hypothalamus controls the O.P. of the
plasma through the
osmoreceptors. These osmoreceptors are specialized neurones
affected by changes in O.P. of plasma in the capillaries
surrounding them.
Example: O.P. of plasma dehydration of neurones of
osmoreceptors
sends impulses to stimulate the supra-optic nucleus of the
hypothalamus send impulses along the hypothalamo-hypophyseal tract
to nerve terminals in the
posterior pituitary ADH release retention of water by the
kidney
O.P. of plasma to normal. O.P. of plasma has the opposite
effect. (2) Changes in Volume of ECF and Blood: These changes act
through stretch receptors (Volume receptors) to
regulate ADH secretion. Sites of volume receptors:
ln the wall of the atria and big veins. ln the wall of the
carotid sinus and aortic arch.
Mechanism of regulation :
1. Minor in blood volume not sufficient to cause in blood
pressure (B.P.) stimulates only the atrial volume receptors.
2. Marked in blood volume ( HAEMORRHAGE) sufficient to cause
in
B.P. will stimulate both atrial and arterial receptors.
3. The receptors when stimulated afferent impulses to the
ADH
release water reabsorption by the kidney the blood volume.
4. in plasma volume has the opposite effect. N.B. Haemorrhage is
one of the most powerful stimuli of ADH release. The same mechanism
for ADH release also releases
ALDOSTERONE from the adrenal cortex and both hormones act
together to the plasma volume. (3) Nervous Factors :
Stressful stimuli ADH
Exposure to cold ADH (4) Some Drugs :
Morphine, Nicotine and acetylcholine ADH.
Ethyl alcohol ADH (Alcoholics excrete more urine). ABNORMALITIES
OF ADH RELEASE:
A) DIABETES INSIPIDUS: - It is due to a lesion in the
hypothalamus destroying the regions of the
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supraoptic and paraventricular nuclei ADH secretion. N.B. A
lesion destroying the pit. stalk and the H-H tract cause only
temporary diabetes insipidus because the hormone continues to be
synthesized and released by the proximal healthy ends of the cut
neurones. Manifestations: 1. Due to deceased ADH, urine volume is
markedly increased
(polyuria). lt may reach 20 liters / day in severe cases. 2. The
specific gravity of urine is very low and fixed ate 1002 -
1004.
3. Loss of large volume of urine excessive thirst and intake of
water (polydypsia).
4. Loss of water soluble vitamins in urine. 5. Marked increase
in basal metabolic rate.
B) NEPHROGENIC DIABERES INSIPIDUS
A condition in which ADH is secreted at the normal rate but the
response of the cell wall of the kidney tubular cells is impaired
due to receptor
defect the same manifestations. N.B.Diabetes insipidus responds
to exogenous ADH administration but nephrogenic diabetes insipidus
does not.
(2) 0 X Y T O C I N Functions of Oxytocin :
1) Milk ejection:
- lt is the most important function oxytocin. - Oxytocin
stimulates the myoepithelial cells around the mammary
acini to contract and squeeze the alveoli and fine ducts, thus
ejecting milk.
2) lt stimulates contraction of the uterine smooth muscles.
Significance:
lt helps the process of normal labor. lt helps involution of the
uterus after delivery. lt helps the ascent of spermatozoa in the
female genital
tract. 3) Oxytocin has a slight pressor and antidiuretic
effects. Control of Oxytocin Secretion:
Oxytocin is secreted in response to Neuroendocrine reflex.
Afferent impulses reach the hypothalamus from different sites and
stimulate the paraventricular nucleus to release oxytocin. Source
of stimuli :
1) afferent impulses from the nipple during sucking initiate the
suckling reflex. 2) afferent impulses during coitus, from the
female genital tract.
Significance: Oxytocin released stimulates uterine contractions
that help the
transport of seminal fluid in the female genital tract. 3)
afferent impulses from the female genital tract during
delivery.
Significance : Oxytocin stimulates uterine contractions and
facilitates delivery.