Notes on Fluid and Electrolyte Balance Lecture

Overview

Stimulates thirst center in the hypothalamus
- Increases blood volume and pressure
Causes vasoconstriction
- Immediate effect to increase blood pressure
Stimulates hypothalamus
- Triggers release of ADH from the posterior pituitary
Adrenal Cortex
- Releases aldosterone, leading to sodium retention
- Water follows salt, aiding in fluid balance
Mechanism
- Low blood pressure detected by juxtaglomerular apparatus
- JG cells release renin
- Liver releases angiotensinogen
- Renin converts angiotensinogen to Angiotensin I
- ACE converts Angiotensin I to Angiotensin II
Effects of Angiotensin II
- Increases peripheral resistance and blood pressure
- Decreases GFR, reducing urine output
- Stimulates ADH and aldosterone release

Released by posterior pituitary
- In response to signals from the hypothalamus
Stimuli for release
- Low blood pressure
- High blood osmolarity
Effects of ADH
- Increases blood volume and pressure
- Decreases osmolarity
- Increases water reabsorption in kidneys via aquaporins
- Causes vasoconstriction
ADH Deficiency
- Results in excessive urine production
- Treatment with nasal vasopressin spray or alternative methods

Steroid hormone
- Released from adrenal cortex
Stimuli for release
- Angiotensin II
- Decreased plasma sodium, increased potassium levels
Mechanism
- Increases sodium-potassium pumps and sodium channels
- Causes sodium and water reabsorption, potassium excretion
- Maintains blood osmolarity

Released from heart atria
- Due to stretching from high blood volume
Functions
- Vasodilates systemic blood vessels
- Increases GFR and urine output
- Inhibits sodium and water reabsorption
- Decreases blood volume and pressure
Opposes
- Renin, ADH, and aldosterone actions