Regulation of homeostasis by the kidney: fluid balance Flashcards
ADH
The most important hormone that regulates water balance
A nonapeptide with Mw just over 1000
Vasopressin or 8-arginine vasopressin
Plasma half life 10-15 mins
Acts of V2 receptors on basal membrane of principal cells in collecting duct
Leads to insertion of AQP2 into apical surface
Actions of ADH
Interacts with V2 receptors on basolateral surface of principal cells in collecting duct of tubule
Increased permeability of collecting duct to H2O by AQP2 on apical surface
Volume regulation by ADH
Released in response to changes in plasma osmolality and effective circulating volume
Changes detected by osmoreceptors and baroreceptors
Result of ADH action
More water reabsorbed from collecting ducts in kidney back into circulation
Increased osmolality also stimulates a second group of osmoreceptors in the hypothalamus which triggers thirst
Promotes water intake which enters circulation
Role of plasma osmolality and effective circulating volume
Sensors: osmoreceptors
ADH pathway
- effector: kidneys
- affects: renal excretion of water
Thirst pathway
- effector: brain
- affects: water intake
Effective circulating volume
Sensors: baroreceptors
Efferent pathways: ADH, RAAS, ANP, sympathetic NS
Effector
- short term: heart, blood vessels
- long term: kidney
Affects
- short term: blood pressure
- long term: Na+ excretion
Central vascular sensors
Low pressure blood volume receptors (very important)
- large systemic veins
- cardiac atria
- pulmonary vasculature
High pressure arterial stretch receptors (less important)
- carotid sinus
- aortic arch
- renal afferent arteriole
Control of effective circulating volume
Feedback control of ECV mediated by baroreceptor stimulation
Changes in ECV trigger 4 parallel effector pathways which act on the kidney
- RAAS
- SNS
- ADH release
- ANP release
Renin angiotensin aldosterone system
Principal factor controlling plasma AngII levels is renin release from JGA
Decreased ECV stimulates renin release via
- decreased renal perfusion pressure detected in afferent arteriole
- decreased Na+ concentration in DT detected by macula densa
- decreased systemic BP triggers effects of SNS supplying JGA
RAAS pathway
Renin makes Angiotensinogen to Ang I
ACE makes Ang I to Ang II
Ang II causes increased secretion of aldosterone
This increases Na+ reabsorption by DT
This inhibits Juxtaglomerular cells secreting renin
Important actions of AngII
All designed to increase ECV
- Enhances tubular Na+ transport in the kidney (promotes Na+ and water reabsorption)
- Stimulation of aldosterone release from adrenal cortex (more Na+ and water is reabsorbed from DT/ collecting duct)
- Acts on hypothalamus to stimulate thirst and ADH release into circulation (water intake adds to ECV; ADH increases water reabsorption from collecting duct)
More important actions of AngII
Vasoconstriction of renal and other systemic vessels so systemic BP increases
Long term causes renal cell hypertrophy so more protein synthesis of Na+ transporters and channels
Important actions of aldosterone
Stimulates Na+ reabsorption in DT and collecting duct
Exerts indirect negative feedback on RAAS by increasing ECV and lowering plasma K+ concentrations
Conserves Na+ and water and prevents large variation in plasma K+ levels
Volume regulation pathways 1- the RAAS
Decreased ECV >
Detected by renal baroreceptors and renal Na+ sensors >
Activation of RAAS >
Aldosterone and Ang II >
Reduced Na+ excretion by kidney and increased renal Na+ reabsorption >
Increased ECV
Volume regulation pathways 2- the ANS
Decreased ECV >
Detected by peripheral baroreceptors >
Signals to hypothalamus in brain >
Activation of the ANS >
Direct effects on renal haemodynamics and activation of RAAS >
Reduced Na+ excretion by kidneys and increased renal Na+ reabsorption >
Increased ECV
