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40 Cards in this Set

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Vasopressin Antagonist
Conivaptan (Vaprisol®)
Vasopressin Agonists
Desmopressin (Stimate ®)
Vasopressin (ADH-antidiuretic hormone)
2 types
Lysine
vs
Arginine
Vasopressin Receptors
V1a – peripheral smooth muscle. Promotes contraction. Coronary vasospasms.
V1b – Central nervous system. Function unclear.
V2 – Located in cortical collecting ducts. Promote synthesis of water channels.
Desmopressin (Stimate®) TX
central diabetes insipidus
bedwetting
sleep apnea (tablet, NOT NASEL SPRAY)
promote release of VonWillebrand factor for some anemias
diagnostic workups to distinguish central and nephrogenic diabetes insipidus
Desmopressin (Stimate®) general
Synthetic vasopressin replacement (modified vasopressin)
Stimulates V2 receptors to promote urine retention
Administered nasally, intravenously, or as a tablet.
Conivaptan (Vaprisol®) general
vasopressin receptor antagonist
non-peptide
inhibits V1a and V2 subtypes
approved for treating hyponatremia from syndrome of inappropriate antidiuretic hormone (SIADH)
Causes iatrogenic nephrogenic diabetes insipidus.
Adverse Effects: Conivaptan (Vaprisol®)
Blocks vasopressin receptors in the cortical collecting ducts.
Interferes with insertion of aquaporin channels, that normally promote water reabsorption from the cortical collecting duct.
Blockade results in WATER loss.
Promotes formation of copius amounts of dilute urine (like the astronauts, deep sea divers).
Vasopressin Disorders
Central Diabetes Insipidus
Nephrogenic Diabetes Insipidus
Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH)
Central Diabetes Insipidus
causes/Tx/condition
Condition: reduced pituitary vasopressin production/release
Causes: head trauma, drugs, alcohol, genetic
Treatments:
Desmopressin (Stimate®)
Chlorpropamide (Insulase®)- a sulphonylurea used to treat diabetes mellitus
Thiazide diuretics – in diabetes insipidus, sodium excretion seems to trigger water retention. Mechanism unknown.
Carbamazepine (tricyclic antidepressant)
Nephrogenic Diabetes Insipidus
causes/Tx/condition
Condition: reduced renal responsiveness to vasopressin
Causes: metabolic, drugs (ie lithium), genetic
Treatments:
Adequate water intake (replacement)
thiazide diuretics – in nephrogenic diabetes insipidus, sodium excretion seems to trigger water retention. Mechanism unknown.
Amiloride (Midamor®) (potassium sparing) – Off Label: blocks lithium reabsorption from the cortical collecting tubule to control lithium-induced diabetes insipidus
Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH)
condition/cause/TX
Hormone (SIADH)

Condition: Impaired excretion of water, hyponatremia and hypo-osmolality due to inappropriate elevations in vasopressin.
Causes: unclear
Treatments:
Managed restrictions on water intake
Conivaptan (Vaprisol®) to blockV1a and V2 receptors. Available only for parenteral preperation.
Lithium – consider if unresponsive to other therapies. DANGER of renal damage after long-term therapy.
Demeclocycline (Declomycin®) – Off Label - tetracycline antibiotic that also inhibits V2 receptors.
Tolvaptan (Samsca) NOT FDA approved, orally administered vasopressin antagonist.
Arginine Vasopressin
from
Humans, horses, squirrels
Lysine Vasopressin
from
Hippopotamuses, pigs, Syrian hamsters…
Vasopressin (ADH-antidiuretic hormone
source
posterior pituatary
Stimulus of ADH
-increased plasma osmolarity
-hypothalamic input
-“volume receptors” (suppress)
Effect of ADH
-vasoconstriction via V1 receptors
-circulates to kidney cortical collecting duct
-stimulates renal synthesis of aquaporin (V2 receptors)
-permits renal H2O reabsorption
-restores plasma osmolarity
Vasopressin stimulates “V? receptors” in the cortical collecting tubules.
V2
V2 receptors drive synthesis of _____ that increase water permeability in the duct.
aquaporins in CCD
What? Creates the path for water passage through the collecting tubule.
aquaporins in CCD
V1a
peripheral smooth muscle. Promotes contraction. Coronary vasospasms.
What receptor?
peripheral smooth muscle. Promotes contraction. Coronary vasospasms.
V1a
V1b
Central nervous system. Function unclear.
What receptor?
Central nervous system. Function unclear.
V1b
V2
Located in cortical collecting ducts. Promote synthesis of water channels.
What receptor?
Located in cortical collecting ducts. Promote synthesis of water channels.
V2
What Osmolraity?
Low ADH
LOW
What Osmolraity?
HIgh ADH
high
Vasopressin Agonist
Desmopressin (Stimate®)
Vasopressin Antagonist
Conivaptan (Vaprisol®)
What drug?
Stimulates V2 receptors to promote urine retention
Desmopressin (Stimate®)
What drug?
Administered nasally, intravenously, or as a tablet.
Desmopressin (Stimate®)
non-peptide******
Conivaptan (Vaprisol®)
inhibits V1a and V2 subtypes
Conivaptan (Vaprisol®)
Causes iatrogenic nephrogenic diabetes insipidus.
Conivaptan (Vaprisol®)
Promotes formation of copius amounts of dilute urine (like the astronauts, deep sea divers).******
Conivaptan (Vaprisol®)
Conivaptan (Vaprisol®)
Adverse effect:*****
Hyporvolemia and increased blood osmolarity.
sodium excretion seems to trigger water retention. Mechanism unknown.*****
Thiazide diuretics – in diabetes insipidus,and Nephrogenic Diabetes Insipidus
reduced renal responsiveness to vasopressin
Nephrogenic Diabetes Insipidus

Causes: metabolic, drugs (ie lithium), genetic
Treatments:
Adequate water intake (replacement)
thiazide diuretics – in nephrogenic diabetes insipidus, sodium excretion seems to trigger water retention. Mechanism unknown.
Amiloride (Midamor®) (potassium sparing) – Off Label: blocks lithium reabsorption from the cortical collecting tubule to control lithium-induced diabetes insipidus
: reduced pituitary vasopressin production/release
Central Diabetes Insipidus

Causes: head trauma, drugs, alcohol, genetic
Treatments:
Desmopressin (Stimate®)
Chlorpropamide (Insulase®)- a sulphonylurea used to treat diabetes mellitus
Thiazide diuretics – in diabetes insipidus, sodium excretion seems to trigger water retention. Mechanism unknown.
Carbamazepine (tricyclic antidepressant)