Blood volume regulation Flashcards
What are the 2 intrinsic mechanisms of blood volume regulation?
Myogenic
Tubuloglomerular feedback
Describe the myogenic mechanism
MAP increases
Vascular smooth muscle cells of the AA stretch
Activates stretch sensitive Ca2+ channels
Contraction of smooth muscle
Vasoconstriction of afferent arteriole
Decreases H.P + GFR
Describe tubuloglomerular feedback
Ascending limb is close to bowmans capsule, cells here are thickened = macula densa cells
Cells of afferent arteriole adapted = granular cells
GFR increases
Macula densa cells detect an increased filtered load of Na+ CL-
Signal sent via adenosine and Ca2+
Causes vasoconstriction of afferent arteriole and vasodilation of efferent arteriole
More blood leaves
H.P decreases and GFR decreases
What comprises the total blood volume?
How do renal mechanisms regulate blood volume?
Effective circulating volume + veneous reservoir
Change the [Na+] plasma via 4 major mechanisms
- Renin-angiotensin-aldosterone system
- ANP
- ADH
- Renal sympathetic nerve
How do renal mechanisms detect the fullness of the circulation?
Sensors = baroreceptors detect degree of stretch/pressure in the vessels
Cardiopulmonary
Arterial
Renal
How does [Na+] plasma control blood volume?
Increased [Na+] ECF
- Increased osmolality and ADH
- Less water excreted
- Increased total blood volume
What happens when blood volume is high?
Increased Blood volume causes vessels to stretch and expand
Increased firing of cardiopulmonary baroreceptors via afferent vagus nerve
Increased ANP
Decreased ADH
Decreased renal sympathetic nerve activity
Decreased RAS activation
Describe activation of the RAAS system?
Low blood volume -> granular cells secrete renin
Renin is an inactive protein converting angiotensinogen to angiotensin
ACE converts ANGI -> ANGII
ANGII promotes releases of aldosterone from adrenal cortex
ANGII + Aldosterone increase Na+ reabsorption in the renal tubule of TAL, DT, CD
Describe the response to a low blood volume
Renal baroreceptors detect decreased pressure in vessels so increases renin secretion
Cardiopulmonary and arterial baroreceptors activate the renal sympathetic nerve
Decreased tubular flow and filtered load of Na+ Cl- delivered to the MD cells
How do we overide tubuloglomerular feedback?
If blood volume is low
Macula densa cells detect a decreased filtered load of Na+ Cl-
MD cells signal to AA to produce renin -> ANGII causes vasoconstriction of efferent arteriole
They would increase filtered load of Na+ Cl- by increasing GFR
BUT when blood volume is low we need to retain more Na+
The renal sympathetic nerve causes vasoconstriction of afferent arteriole > efferent arteriole causes pressure in glomerular capillaries to decrease, GFR decreases and decreased filtered load Na+
What are some actions of aldosterone?
Increases thirst
Increases Na+ appetite
Thirst seeking behaviours
Increased Na+ reabsorption
Causes K+ excretion due to opposing actions with Na+
Aldosterone diffuses through peritubular capillary wall -> intersititium -> basolateral membrane of cells in CD + DT
Binds to cytoplasmic receptors + migrates to nucleus binding to DNA
Increases transcription of proteins involved in Na+ reabsorption
- Increased ATPase, Increases mitochondrial enzymes driving Na+/K+ pump, Increases Na+ transporters on apical membrane
How does tubuloglomerular feedback worsen kidney damage?
Kidney damage causes GFR to decrease
MD cells detect a decreased filtered load of Na+Cl-
Signal via Ca2+ and adenosine to cause vasoconstriction of efferent arteriole and vasodilation of afferent arteriole
MD cells activate renin production + renin-angiotensin-aldosterone system
Hypertension + increased glomerular pressure
Patients treated with ACE inhibitors to prevent ANGI -> ANGII e.g ramipril
How does diabetic nephropathy occur?
More glucose in the urine
More glucose reaches glomerular capillaries + bowmans space
More glucose + NaCl reabsorbed
More water reabsorbed as well
Decreased filtered load of Na+Cl- detected by macular densa cells
Tubuloglomerular feedback: Vasodilation of AA + Vasoconstriction of EA
Increases GFR + glomerular pressure
Increased GP causes matrix deposition and proliferation and hypertrophy of mesnagial cells
Sclerosis occurs which compresses the glomerular capillaries + decreases GFR -> kidney damage
