Determinants of Renal Blood Flow Flashcards
Oxygen consumption of the kidneys
-kidneys have 7x more blood flow compared to the brain
-kidneys use twice as much oxygen as the brain (per mass of tissue)
>most of the oxygen is needed for active reabsorption of sodium
GFR reduction and kidneys oxygen levels
-less Na reabsorption is needed and less oxygen is required
Renal blood flow
-depends on the pressure gradient across renal vasculature
>smaller arteries and arterioles increase the resistance to blood flow
Renal pressure gradient
(Renal artery pressure-renal vein pressure)/Total renal vascular resistance
Renal artery pressure
-general vascular pressure
-~100 mmHg
Renal vein pressure
3-4 mm Hg
What determines renal vascular resistance?
1.interlobular arterioles (causes 16% reduction)
2. Afferent arterioles (causes 26% reduction)
3. Efferent arterioles (causes 43% reduction)
Fluctuations of arterial pressure
-affect renal blood flow, but the renal auto-regulation mechanism maintain a constant renal blood flow when arterial pressure changes between 80-170 mmHg
Factors that can affect renal vascular resistance
1.sympathetic nervous system
2.hormones and autacoids
Glomerular hydrostatic pressure
-important factor controlling GFR
Sympathetic nervous system affecting renal blood flow
-innervation of all renal vessels
-less critical for normal physiological changes
-severe conditions such as hemorrhage and brain ischemia cause activation of sympathetic NS, leading to vasoconstriction, increased renal total vascular resistance and reduced renal blood flow
- important for restoring blood volume and prevents loss of water and electrolytes
Hormones impact on renal blood flow
-main hormones are NE and EPI
-less critical for normal physiological changes
-cause constriction of afferent and efferent arterioles, reduction of renal blood flow and GFR
-their concentrations correlate with activation of sympathetic NS, so their function in regulating renal blood is important under severe conditions such as hemorrhage
Endothelin
-released by damaged renal endothelial cells (and other tissues)
-acts as vasoconstrictor reducing blood flow and blood loss when tissue damage occurs
*under pathological conditions such as toxemia, acute renal failure and chronic uremia reduces GFR
Angiotensin II
-can work locally or as a circulating hormone
-Release occurs when there is volume depletion or reduced arterial pressure resulting in decreased GFR to maintain water and electrolytes. Fewer waste products are removed
-Ang II constricts efferent arterioles, resulting in increase in the hydrostatic pressure of glomerular capillaries which increases GFR and causes more waste products to be removed even under the low arterial pressure conditions
-Constriction of efferent arterioles also reduces the pressure in the peritubular capillaries which facilitates the reabsorption process so less water and Na are lost
-prevents the reduction of GFR
Peritubular capillaries
-tiny blood vessels of the kidneys
Endothelial-derived nitric oxide
-released by endothelial cells
-vasodilator
-increases GFR (reducing resistance), allowing for increases excretion of sodium and water
-damage to endothelial cells and reduced NO production can lead to hypertension
Prostaglandins (PGE2, PGI2, bradykinin)
-vasodilators
>reduce the vasoconstriction effect of Ang II on the afferent arterioles, so that the vasoconstriction effects of Ang II work only on efferent arterioles
-increase GFR, but not critical under normal physiological conditions
What is the purpose of autoregulation of renal blood flow?
-to maintain GFR and excretion of water and solutes in spite of changes in arterial pressure
Mechanisms involved in autoregulation of Renal blood flow
1.Autoregulation for maintaining GFR= tubuloglomerular feedback and myogenic autoregulation
2.Glomerulotubular balance mechanism for increasing tubular reabsorption
Tubuloglomerular feedback
-for regulation of GFR
-feedback mechanism is based on Na-Cl and the juxtaglomerular complex structure and includes two responses
1.Afferent arteriolar feedback
2.Efferent arteriolar feedback
Process of tubuloglomerular feedback
-Macula densa- specialized cells in distal tubules
-distal tubule and macula densa runs right near bowman’s capsule and juxtaglomerular cells
-GFR is low when blood flow is low in loop of Henle and therefore there is more Na and Cl reabsorbed in ascending tubules because flow is slowed down and there is more time for absorption. Since more Na and Cl is reabsorbed, there is less Na and Cl that reach the distal tubule and macula densa respond by sending signals by unknown mechanisms
Where do the macula densa send signals?
- Reduce resistance in afferent arterioles, leading to increased hydrostatic pressure and increased GFR
- Increase renin release from the juxtaglomerular cells that increases formation of Ang I and then Ang II, leading to constriction of efferent arterioles and increased glomerular hydrostatic pressure and GFR
Myogenic Autoregulation of renal blood flow and GFR
-individual blood vessels can resist stretching when there is increased arterial pressure
Myogenic Mechanism
Stretch of the vascular wall leads to transfer of extracellular Ca++ into smooth muscle cells, causing contraction of these cells which further reduces the stretch of the vascular wall and prevents increased renal blood flow and GFR
**important to prevent renal damage in cases of sudden increases in blood pressure