Antidiuretic Hormone (ADH)/ Vasopressin Cell Communication By: Alejandra Ospina, Megan Campbell

General Information` Controls body water and solute concentration The function of several hormones act on the kidneys and vascular system Also known as Arganine Vasopressin Produced by neurosecretory cells in the hypothalamus  Regulated by osmotic and volume stimuli  Water deprivation increases osmolality of plasma which activates hypothalmic osmoreceptors to stimulate ADH release

Gland Secreted from the posterior pituitary gland The hypothalamus sends signals to the pituitary gland to secrete the hormone. Once hormone is secreted it goes to the kidney to put its purpose into effect.

Base & Structure 9 amino acid structure sequence Peptide based hormone ◦ Hydrophilic – will not go into the cell ◦ Binds with the receptor on the cell’s surface ◦ Six of the amino acids form a ring structure, joined by disulfide bonds.

Pathway & Messenger Vasopressin is released and binds to cell membrane at receptor Binding results in ATP breaking down to cAMP ◦ cAMP is the second messenger ◦ cAMP activates PKA which synthesizes aquaporin ◦ Aquaporins bind in the membrane and let H 2 0 into the cell Does not directly communicate with nucleus Indirectly communicates with cytoplasm and cell membrane.

Pathway continued… The receptor is linked to adenylyl cyclase (AC) enzymes via heterotrimeric G proteins in the membrane; thus, AC is activated as a consequence of VP binding to its V2 receptor resulting in the formation of the second messenger cyclic AMP. Subsequent phosphorylation of protein kinase A is associated with the final step of water reabsorption. Cyclic AMP is rapidly degraded to 5*-AMP by intracellular phosphodiesterase enzymes.

Pathway Diagra m VP- vasopressin AQP- aquaporin PKA- protein kinase A

Cellular Response Once cAMP is rapidly degraded by intracellular enzymes, thus the insertion of water channels into the membrane of the target cell, mediates rapid cross- membrane water transport. There is also an increased movement of aggraphores towards these membranes. The response is an increase of water absorption. Not a transcription factor It does turn an enzyme (protein kinase A) There is no conformational change expect the introduction of more aquaporins into the membrane.

Positive or Negative Feedback? Negative Feedback Decreased water levels in body resulting in more ADH production- increased thirst- will increase the amount of aquaporins being added in increased as well (to reabsorb more water into the kidney) Increased water levels result in a reduced ADH production telling the kidney to reabsorb less water.

Consequences of Disruption When ADH is inhibited, water will not be reabsorbed at the tubules and the body will produce dilute urine. Hyponatremia (not enough sodium (salt) in the body fluids outside the cells.) and hypo-osmolality resulting from inappropriate, continued secretion of the hormone despite normal or increased plasma volume, which results in impaired water excretion. ◦ Symptoms: Confusion, disorientation, delirium, generalized muscle weakness, myoclonus, tremor, asterixis, hyporeflexia, ataxia, dysarthria, Cheyne-Stokes respiration, pathologic reflexes, generalized seizures, coma Incontinence- involuntary urination: Common in elderly people. ◦ Lack of ADH at night leads to bladder overfilling and thus urination.

Consequences of Disruption Continued… Syndrome of inappropriate antidiuretic hormone secretion is also known as SIADH. It is a condition where your body makes too much antidiuretic hormone (ADH). Increased ADH makes water remain inside your body, causing other chemicals in the blood such as salt may decrease. Organs may not function properly

Consequences of Disruption Continued… Hyperosmolality

Works Cited adh.html adh.html hormone-secretion.html hormone-secretion.html