I1i: Describe how body detects and responds to H2O deficit
Define/Quantify
- TBW = 60% body weight = 42L
- TBW = ECF + ICF
- ECF is regulated
- ICF is dependent on ECF regulation, as H2O moves freely across PM
- Regulation of H2O balance is via NEGATIVE FEEDBACK
Regulation
Sensors
Osmoreceptors
BaroR
- High P
- Low P
- Intrathecal
Control
Hypothalamus
Effectors
ADH
Renin
Aldosterone
SNS
Sensors
Osmoreceptors
- ↑osmolality of ECF > 2% (Neutral osmolality = 280 – 295 mOsm/L)
- ↑linear firing from osmoreceptors cause ↑ADH release from SO & PV nuclei of hypothalamus
Low P Baroreceptors
- Walls of atria & great veins
- ≥ 10% volume depletion (4L water, 300mL of plasma)
- Less sensitive (>10%) cf. OsmoR but more potent because can override OsmoR & take volume over tonicity
High P Baroreceptors
- Carotid Sinus & Aortic Arch
- ↓MAP
- ↓BaroR firing → vasomotor & cardiac centres of Medulla
- ↑symp & ↓ output
- Carotid Sinus & Aortic Arch
→ VC, ↑HR, ↑FoC, ↑CO → restore MAP
Intrarenal P Receptors
- BaroR in JG cells
- ↓MAP = ↓afferent arteriole stretch
- ↑RENIN from JG cells
Effectors
Effector
ADH
(3 pronged approach!)
Trigger
↑Osmolarity
Stress/surgery
Nausea
AII
Standing
Mechanism
V1 → VC
V2 → of cortical & medullar C ∆
V2 receptor on BL side
GS
↑cAMP
Promote Aquaporin 2 channel insertion into luminal membrane
V3 → thirst
Result
→ ↓GFR = ↓water filtration
→ ↑water reabsorption
Max urine osmolarity 1400mOsm/L
→ ↑water intake
Effector
Aldosterone
Trigger
AII (Renin)
ACTH
↑K
Sympathetic stimulation
Mechanism
Acts on Mineralocorticoid receptor of PRINCIPLE CELLS
- Upregulates Na/K/ATPase
- Upregulates apical Na+ channel
- ↑Renin peripheral VC
Result
↑Na+ reabsorption
3 Cell Membranes Impermeable to H2O
- Ascending LoH
- Collecting Ducts in absence of ADH
- Bladder Epithelium
- Thirst = the conscious drive to obtain H2O, stimulated by:
- Hypovolaemia (low P BaroR)
- Hypotension (High P BaroR)
- Hyperosmolarity (OsmoR)
- AII
- Physical stimulation i.e. dry mouth