Lecture 13: Integration of Salt and Water balance Flashcards Preview

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= AVP = Arginine vasopressin
Function: Increased Water reabsoprtion into ICF/ECF --> concentrated urine + decreased flow
Location: DT + Collecting Tubule (+ collecting duct epithelia) --> Acts at end of circuit as is final bulk water changes
- allows for conservation of water during dehydration


Location of ADH release

ADH = Nonapeptide
Hypothalamus --> osmoreceptor, baroreceptor, cardiopulmonary receptor stimulation) stimulate Supraoptic and Paraventricular neuron --> release of synthesised precursor protein to Posterior Pituitary --> posterior pituitary storage granules situate at nerve terminals


What sort of peptide is ADH



Acute vs Chronic ADH release

Acute: Osmolality change
1. Osmoreceptors in hypothalamus
Chronic: Blood Volume Change
1. Baroreceptors (change pressure)
2. Cardiopulmonary Volume receptors --> STRETCH of atrium and ventricles sensed


Sensitivity of osmoreceptor, baroreceptor and cardiopulmonary receptor to changes

ECF Osmolality change (acute): <1% change (lower threshold (starts earlier), higher sensitivity(quicker/steeper gradient))
ECF Blood Volume change (chronic): >10% change (longer period passes + slower increased release)


Physiological and Non physiological causes of ADH release

1. Increased plasma osmolality
2. Decreased ECF volume
1. Pain, stress
2. Drugs: narcotics, carbazapine, vincristine, chloropropamide, ifosfamise, nicotine, SSRI
3. Carcinomas (esp. small cell)
4. Pulmonary disorders
5. CNS disorders
(6. Alcohol inhibits ADH secretion)


Inhibition of ADH secretion



Is the descending limb of LOH permeable to water?



To what extent can ADH reduce water loss

1L/hour 15mL/hour



Syndrome of Inappropriate ADH release
Increased plasma ADH --> inappropriate water retention ( -ve Free water clearance) --> significantly low osmolality (hypo-osmotic state) --> tasteless urine
1. Brain injury/tumour
2. Some anti cancer drugs
3. Lung cancer and some other cancers
Restricted water consumption --> decreased H2O input --> relatively less able to be retained


Central and Nephrogenic Diabetes insipidus

Low/absent ADH levels --> First sign: High urine volume


Central Diabetes Insipidus

Head Trauma/ brain injury/tumour/infection --> disruption of osmoreceptors --> Central DI --> changing osmolality but unable to produce ADH --> increased urine volume and decreased urine taste
- Rarely hereditary
- Treatment: ADH analogs


Nephrogenic Diabetes Insipidus

ADH release from posterior pituitary --> non-functional V2 receptor in kidney's nephron's CD/DT --> ADH unable to make any changes --> increased volume and diluteness of urine
1. Drugs (Lithium)
2. Hereditary (less common):
- Congenital V2 defect
Inherited AQP-2 defect
No Treatment available


Test to differentiate between Central and Nephrogenic Diabetes Neuropathy

Water Deprivation Test
- give DDADH --> Increase in Central DI not nephrogenic
** grapht


ADH cellular mechanism

ADH binds to V2 receptor on distal tubule --> AQP2 receptor inserts into tubular lumen --> Water enters cell and is reabsorbed


What are causes of significant volume change causing Renin release?

Severe sweating/diarrohea --> haemorrhage/ salt and water loss --> large change in effective circulating volume --> primary stimulus to the granular cells of the juxtaglomarular apparatus --> renin release


What are the primary stimuli for renin release?

1. Afferent arteriolar pressure
2. Sympathetic activity
3. Macula Densa NaCl delivery


What is the most powerful sodium retaining hormone in the body?

Angiotensin II


What are the primary resulting steps after angiotensin II release?

1. Aldosterone release
2. Vasoconstriction of vascular beds
3. Enhances tubuloglomerular feedback


What is the experiment, which tested the relationship b/w Kidney and CVD

significant #case of hypertension is related to kidney function
Experiment: Artificially constricted kidney --> measured blood pressure --> BP is elevated and then remains high
Treatment: Hypertensive medication includes ACE inhibitors (vascular bed) and ARBs Angiotensin II Receptor Blockers


What was the first experiment which hinted at the relationship b/w the kidneys having an effect on blood pressure?

Extracts taken from rabbit kidney --> injected into another animal --> increase in blood pressure
- indicated that there was something in the kidney that has a vasoconstrictor role --> can cause an increase in BP
(renal pressor agent angiotensin II)


What occurs at the cellular level with the RAAS system?

1. Increased renin secretion
2. Increased angiotensin
a. Increased aldosterone
b. Constriction of efferent arteriole
c. binds to AT1 --> reabsorption of AT1