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6 - Concentration and dilution of urine


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What two receptors does ADH bind? What are the effects of binding each?
1.V-1: vasoconstriction
2.V-2: antidiuretic effects
Where is ADH synthesized? Where is it stored and released from?
*synthesized in the supra-optic nucleus of the hypothalamus
*stored and released from nerve endings in the posterior pituitary
What two blood variables influence the release of ADH?
Osmolarity and blood volume.
When blood osmolarity is at its normal level of 295-300mOsm/L, there is no detectable ADH in circulation.
False: even under normal conditions there is a baseline amount of ADH in circulation.
How is blood osmolarity detected for release of ADH? How is blood volume detected?
*osmolarity is detected by special osmosensor cells in the hypothalamus
*blood volume is detected by atrial stretch receptors
What factors result in a greater release of ADH?
1.High osmolarity
2.Low blood volume
What factors result in inhibition of ADH release?
1.Decreases in osmolarity
2.Increases in blood volume
What is the half-life of ADH in circulation?
20-30 minutes.
What happens when ADH binds the V-2 receptor?
Adenylate cyclase is activated and cAMP produced. cAMP activates PKA which phosphorylates serine residues on AQP-2. This causes AQP-2 to be transferred to the apical membrane.
Where is AQP-1 found?
In regions not under the control of ADH (e.g. proximal tubule, vasa recta, dLOH).
Where is AQP-3 found? How is it affected by ADH?
On thhe basolateral membrane of most tubular epithelia. It is not under the regulation of ADH.
Where is AQP-4 found?
On the hypothalamic glial cells, where it possibly plays a role in osmosensation.
What kinds of symptoms are seen in humans who are deficient in AQP-1?
They are normal in the basal state but show an inability to concentrate urine during water restriction. The main effect is seen in the descending loop of Henle.
Does ADH have any short-term or long-term effects in the ascending loop of Henle?
No short-term effects but possible long-term up-regulation of Na+/K+/2Cl- transporters.
What is normal water loss each day, and how is it lost?
Normal loss is 1.5L each day, with 1.0 liters lost through sweat, feces, etc. and 0.5L lost through urine excretion.
Identify the condition seen in dehydration that results in maximal release of ADH.
Hypovolemic hypernaturemia.
What are 4 symptoms of diabetes insipidus?
4.Increased hematocrit
5.Increased plasma osmolarity
6.Low blood pressure
What are two possible causes of central diabetes insipidus?
A genetic mutation resulting in lack of ADH production or damage to ADH-producing cells.
What abberent lab value is seen in the nephrogenic but not the central form of diabetes insipidus?
Patients with nephrogenic diabetes will have high plasma [ADH].
What is the basic defect in nephrogenic diabetes insipidus? What implications does this have for treatment of these patients?
ADH is synthesized, but cells are not responsive. This means that exogenous ADH will be an ineffective treatment.
What are two ways nephrogenic diabetes insipidus can be acquired (i.e. after birth)?
1.Lithium overdose
2.Excessive fluid intake
3.Pregnancy (although this is really pseudonephrogenic DI)
What 2 forms of congenital nephrogenic diabetes insipidus have been found?
1.X-linked dominant mutation of the V-2 receptor.
2.Autosomal recessive mutation of AQP-2
Why is low-dose diuretic an accepted treatment for nephrogenic diabetes insipidus?
It causes a slight contraction of the ECV which activates mechanisms to conserve salt and by extension, water.

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