LORMA COLLEGES

COLLEGE OF NURSING

AY 2021-2022
First Semester
BIOCHEMISTRY LECTURE

INDIVIDUAL ACTIVITY #2: WATER BALANCE

Fluid can enter the body as preformed water, ingested food and drink, and, to a
lesser extent, as metabolic water that is produced as a by-product of aerobic
respiration and dehydration synthesis. A constant supply is needed to replenish
the fluids lost through normal physiological activities, such as respiration,
sweating, and urination.

Water generated from the biochemical metabolism of nutrients provides a

significant proportion of the daily water requirements for some arthropods and
desert animals, but it provides only a small fraction of a human’s necessary
intake. In the normal resting state, the input of water through ingested fluids is
approximately 2500 ml/day.

Body water homeostasis is regulated mainly through ingested fluids, which, in turn,
depends on thirst. Thirst is the basic instinct or urge that drives an organism to
ingest water.

Thirst is a sensation created by the hypothalamus, the thirst center of the human
body. Thirst is an important component of blood volume regulation, which is slowly
regulated by homeostasis.

An osmoreceptor is a sensory receptor that detects changes in osmotic pressure

and is primarily found in the hypothalamus of most homeothermic organisms.
Osmoreceptors detect changes in plasma osmolarity (that is, the concentration of
solutes dissolved in the blood).

When the osmolarity of blood changes (it is more or less dilute), water diffusion
into and out of the osmoreceptor cells changes. That is, the cells expand when
the blood plasma is more dilute and contract with a higher concentration.

When the osmoreceptors detect high plasma osmolarity (often a sign of a low
blood volume), they send signals to the hypothalamus, which creates the
biological sensation of thirst. Osmoreceptors also stimulate vasopressin (ADH)
secretion, which starts the events that will reduce plasma osmolarity to normal
levels.

Renin–Angiotensin System-Mediated Thirst

Another way through which thirst is induced is through angiotensin II, one of the
hormones involved in the renin–angiotensin system. The renin–angiotensin
system is a complex homeostatic pathway that deals with blood volume as a
whole, as well as plasma osmolarity and blood pressure.
The macula densa cells in the walls of the ascending loop of Henle of the nephron
is another type of osmoreceptor; however it stimulates the juxtaglomerular
apparatus (JGA) instead of the hypothalamus. When the macula densa is
stimulated by high osmolarity, The JGA releases renin into the bloodstream, which
cleaves angiotensinogen into angiotensin I. Angiotensin I is converted into
angiotensin II by ACE in the lungs. ACE is a hormone that has many functions.

Instruction: Learn the two mechanism of water balance by filling up the blank
spaces.

Antidiuretic hormone (ADH), also called arginine vasopressin is a hormone that helps regulate water
balance in the body by controlling the amount of water the kidneys reabsorb while they are filtering
wastes out of the blood.

ADH is produced by the hypothalamus in the brain and stored in the posterior pituitary gland at the
base of the brain. ADH is normally released by the pituitary in response to sensors that detect an
increase in blood osmolality (number of dissolved particles in the blood) or decrease in blood volume.
Other factors include stress, hypoglycemia, anesthetic agents, heat, nicotine, Antioneoplastic agents,
Narcotics and surgery

The kidneys respond to ADH by conserving water and producing urine that is more concentrated.

The retained water dilutes the blood, lowers its osmolality, and increases blood volume and pressure. If
this is not sufficient to restore the water balance, then thirst is also stimulated so that the affected
person will drink more water.

If there is too little ADH or the kidneys do not respond to ADH, then too much water is lost through
the kidneys, the urine produced is more dilute, and the blood becomes more concentrated. This can
cause excessive thirst, frequent urination, dehydration, and – if you do not drink enough water to
replace what is being lost – high blood sodium.
If there is too much ADH, then water is retained, blood volume increases, and the person may
experience nausea, headaches, disorientation, lethargy, and low blood sodium.
The rennin-angiotensin-aldosterone sytem, RAAS, is a hormonal system that controls blood pressure.
While baroreflex is a short term response to sudden changes in blood pressure, RASS is responsible for
long-term regulation.

In the kidneys, within the walls of afferent arterioles, there are specialized cells producing pronenin
called juxtaglomerular cells. Upon activation by a drop in blood pressure, prorenin is cleaved to form
renin, which is release into the blood.

Renin converts a plasma protein called angiotensinogen, produced by the liver, into angiotensin I, a
peptide of 10 amino acids. Angiotensin I is further converted into angiotensin II, an 8 amino acid
peptide, by the angiotensin converting enzyme (ACE), predominantly present in the lungs and kidneys.

Angiotensin II is a hormone, it binds to Angiotensin II receptors in tissues to exert various effects:

stimulates vasoconstriction in systemic arterioles, promotes sodium reabsorption in proximal
convoluted tubules of the kidneys; it induces the release of aldosterone from the adrenal cortex.
Aldosterone promotes sodium and water retention in the kidneys.

In the central nervous system (CNS), angiotensin II has several effects: it acts in the hypothalamus to
stimulate thirst and encourage water intake; it induces the posterior pituitary to release antidiuretic,
which promotes water retention by the kidneys; it reduces the sensitivity of the baroreceptor
response to increased blood pressure, so that this response would not counteract the effect of RAAS.
All these actions lead to an increase in blood volume and blood pressure.

Angiotensin II is short-lived with a half-life with a half-life of 1 to 2 minutes. It is degraded to Angiotensin

III and IV which has a lesser effects. Over active or inapropriately activated RAAS is a cause of
hypertension. RAAS is a frequent target of anti-hypertensive drugs.

ACE inhibitors and Angiotensin receptor blockers are common treatment for hypertension.