NSC1103 Assignment: Concept Map on ADH and Urine Regulation

This assignment explores the homeostatic mechanisms related to antidiuretic hormone (ADH) and its role in regulating urine formation. The paper begins by explaining how ADH, produced by the hypothalamus and stored in the posterior pituitary gland, influences the kidneys to manage water balance, leading to the production of concentrated or dilute urine based on plasma osmolality. It then delves into diabetes insipidus, a condition characterized by the production of excessive dilute urine due to ADH deficiency, and how this alters the contents of urine. The assignment highlights the interconnectedness of these two aspects, using a concept map to visually represent the physiological processes. The paper details the mechanisms of ADH action, including how it increases the permeability of the kidney's capillary walls to reabsorb water, leading to concentrated urine when ADH levels are high. Conversely, when ADH release is inhibited, the permeability decreases, resulting in dilute urine. The impact of diabetes insipidus is discussed, emphasizing how the lack of ADH leads to decreased water reabsorption, the production of large volumes of dilute urine, and potential complications like dehydration and imbalances in blood sugar levels. Finally, the assignment concludes by explaining the body's compensatory mechanisms to regulate blood sugar and maintain solute balance in the context of diabetes insipidus.

Running head: CONCEPT MAP 1
Concept Map
Student’s Name
Institutional Affiliation

CONCEPT MAP 2
Introduction
Antidiuretic hormone is also referred to as arginine vasopressin. This hormone is
produced by the hypothalamus in the brain and later stored in the posterior pituitary gland. The
hormone is significance in the body system as it helps the kidney manage the amount of water in
the body. On the other hand, diabetes insipidus is a condition characterized by production of
huge amounts of dilute urine. This paper is set to bring forth how the action of ADH regulates
the formation of dilute and concentrated urine. The paper also explores how diabetes insipidus
alters the contents of urine. Most importantly, the application of these two queries is intertwined.
Therefore, a concept map shall be employed for clear illustration of the interconnectivity of the
two quarries.
How ADH Action Regulates the Formation of Concentrated and Dilute Urine
When there is high plasma osmolality, that is when the osmotic pressure is high, the brain
triggers the hypothalamus which in return signals the release of Antidiuretic hormone from the
posterior pituitary gland in the bloodstream (Picker, et, al., 2014). The released ADH acts on the
kidney by increasing the permeability of the capillary walls enhancing reabsorption of water (Pu,
2015). Due to the high rates of water reabsorption from the kidney back into the blood stream,
less water is left for excretion together with plenty solutes such as sodium, potassium, carbon
dioxide and chloride thus production of more concentrated urine.
Production of the excess Antidiuretic hormone causes the walls of the collecting duct to
become more permeable, and a large amount of water is reabsorbed out of the blood plasma
(Picker, et, al., 2014). As a result, the blood sugar will reduce. In other words, the glucose
concentration in the blood will decrease below the normal range. The osmotic pressure of the
blood will, therefore, be lowered (Pu, 2015). As a result, the brain triggers the hypothalamus to

CONCEPT MAP 3
hinder the release of Antidiuretic hormone. The permeability of distal tubules will reduce, hence
minimizing the rate of water reabsorption. As a result, the concentration of the particles in the
urine will be low due to presence of excess water (Oh, & Shin, 2015). Thus a large amount of
dilute urine will be produced.
How Diabetes Insipidus Alters the Contents of Urine
Diabetes insipidus is a certain condition where much fluid is lost from the body through
urination leading to a high risk of dangerous dehydration (Kalra et, al., 2016). The
underproduction of Antidiuretic hormone results in diabetes insipidus condition which interferes
with urinary output. The condition is characterized by decreased production of antidiuretic
hormone from the pituitary gland. The patient’s body is forced to regulate the fluid by balancing
the intake of the liquid and removing extra fluid (Cuesta, et, al., 2015). The low levels of ADH
will act on the kidney to decrease luminal AQP2 which in tur decreases the rate of water
reabsorption. Lower water reabsorption in the kidney will consequently lead to secretion of large
amounts of water in the urine compared to the waste particles. The main sign of either kind of
diabetes is the production of excessive urine (Capatina, Paluzzi, Mitchell, & Karavitaki, 2015).
The low water reabsorption which is accompanies by excess dilute urine production will
ultimately lead to higher concentration of glucose in the blood. Due to the high concentration of
glucose in the blood, the individual undergo stress which includes dehydration that causes dry
mouth, thirst and fatigue. This kind of imbalance is also associated with the damage of the thirst
regulating mechanism in the hypothalamus (Bockenhauer, & Bichet, 2015). Therefore, the mind
has to implement mechanisms that will lead to regulation of the blood sugar level in the body.
However, because the ADH hormone which is supposed to limit the amount of water being
released from the body does not function effectively, other mechanisms have to be employed.

CONCEPT MAP 4
Therefore, the mind will promote the release of the solutes from the body through mechanisms
like sweating. Excess release solutes through sweating will lower the concentration of blood
beyond the normal range. As a result, the mind shall be signaled again to limit the release of
ADH. The low ADH will also act on the kidney thus decreasing luminal AQP2 (Pu, 2015).
Decreased luminal AQP2 will ultimately reduce water reabsorption thus promoting the release of
dilute urine (Pu, 2015). This cycle will proceed constantly until a mechanism of promoting ADH
release is established. Therefore, diabetes insipidus alters the contents of the urine by promoting
higher amounts of water in the urine and decreasing the amount of solutes like sodium,
potassium and chlorine.

CONCEPT MAP 5
Concept Map
Normal State
Low water reabsorption
Dilute
Urine
Increases blood sugar levelHigh plasma osmolality
Causes
posterior
pituitary
release of ADH
Acts on the Kidney
to increase
AQP2
Water
Reabsorption
Increasing
Other metabolic
actions like
sweating to
reduce blood
sugar level.
Excess water reabsorption
Concentrated
Urine
Lowers the concentration of blood sugar
Low blood sugar
concentration
Triggers the
hypothalamus
to limit ADH
release
Low APQ2
Decreasing
Water Reabsorption

CONCEPT MAP 6
References.
Bockenhauer, D., & Bichet, D. G. (2015). Pathophysiology, diagnosis and management of
nephrogenic diabetes insipidus. Nature Reviews Nephrology, 11(10), 576.
Capatina, C., Paluzzi, A., Mitchell, R., & Karavitaki, N. (2015). Diabetes insipidus after
traumatic brain injury. Journal of clinical medicine, 4(7), 1448-1462.
Cuesta, M., Gupta, S., Salehmohamed, R., Dineen, R., Hannon, M. J., Tormey, W., &
Thompson, C. J. (2015). Heterogenous patterns of recovery of thirst in adult patients with
adipsic diabetes insipidus. QJM: An International Journal of Medicine, 109(5), 303-308.
De Picker, L., Van Den Eede, F., Dumont, G., Moorkens, G., & Sabbe, B. G. (2014).
Antidepressants and the risk of hyponatremia: a class-by-class review of
literature. Psychosomatics, 55(6), 536-547.
Kalra, S., Zargar, A. H., Jain, S. M., Sethi, B., Chowdhury, S., Singh, A. K., ... & Malve, H.
(2016). Diabetes insipidus: The other diabetes. Indian journal of endocrinology and
metabolism, 20(1), 9.
Oh, J. Y., & Shin, J. I. (2015). Syndrome of inappropriate antidiuretic hormone secretion and
cerebral/renal salt wasting syndrome: similarities and differences. Frontiers in
pediatrics, 2, 146.
Pu, S., Long, Y., Yang, N., He, Y., Shan, F., Fan, Y., ... & Cong, G. (2015). Syndrome of
inappropriate antidiuretic hormone secretion in patients with aquaporin-4
antibody. Journal of neurology, 262(1), 101-107.
Low ADH
which
decreases
AQP2