Renal

Renin-Angiotensin-Aldosterone

SNS

Vascular Tone

Water is reabsorbed and urine is concentrated

Where aldosterone has its effects to reabsorb Na and H20 to increase BP, while excreting K

Released from JG cells

Increases Na and water reabsorption, therefore increasing BP

Converts angiotensinogen to angiotensin I

What controls renin release? activation of kidney beta1 receptors, macula densa cells sense too little Na and increase renin secretion, intrarenal baroreceptor senses low BP

Angiotensin I to Angiotensin II

Degrades bradykinin (a vasodilator)

Binds to AT1 receptors in vascular smooth muscle to raise BP

Increases aldosterone secretion to increase BP

Also increases BP by:

Increases SNS activity

Increases Na reabsorption in PCT

Immediate: Direct vasoconstriction and SNS stimulation

Renal effects: Delayed

SNS and renin-angiotensin-aldosterone system stimulate each other and are mutually reinforcing

Sustained high levels can cause cardiac remodeling and hypertrophy

CNS baroreceptor can activate if BP drops

Clonidine and methyldopa are used to reduce BP by targeting vasomotor center to decrease SNS outflow

Alpha or Beta blockers modulate SNS activity

Ca chanels can lead to a wave of depolarization in surrounding cells->targeting them ends spread of depolorization

K channels are normally closed to prevent K from leaving cell and allow depolorization, but if drugs allow it to exit it causes membrane hyperpolorization and relaxation