Factors that Modulate RBF and GFR Flashcards
Factors That Modulate RBF and GFR
- Renin-angiotensin-aldosterone axis
- Sympathetic Division of the Autonomic Nervous System
- Arginine Vasopressin (antidiuretic hormone)
- Atrial Natriuretic Hormone
- Epinephrine
- Dopamine
- Endothelins
- Prostaglandins
- Leukotrienes
- Nitric Oxide
Renin-angiotensin-aldosterone axis
Angiotensin II reduces blood flow and GFR
Sympathetic Division of the Autonomic Nervous System
Sympathetic stimulation increases afferent and efferent arteriolar resistances, causing reduction in RBF and GFR.
Sympathetic stimulation also triggers renin release, raising levels of angiotensin II
Sympathetic tone signals tubule cells to increase their reabsorption of Na+
Arginine Vasopressin (antidiuretic hormone)
An increase in the osmotic pressure of the extracellular fluid causes AVP release from the posterior pituitary.
AVP increases water absorption in the collecting duct and increase vascular resistance
Atrial Natriuretic Hormone
Atrial myocytes release atrial natriuretic peptide in response to increased atrial pressure.
This peptide vasodilates afferent and efferent arterioles to increase cortical and medullary blood flow
lowers the sensitivity of the TGF loop. The net effect is an increase in RPF and GFR.
Epinephrine
Released by the chromaffin cells of the adrenal medulla, has similar effect on kidneys as norepinephrine does
Dopamine
The renal effect of dopamine is to vasodilate, which is opposite to the effects of epinephrine and norepinephrine.
Endothelins
The endothelins has a very short half-life, and act locally to constrict smooth muscles of renal vessels.
Prostaglandins
Provide a buffer against excessive vasoconstriction, especially during increased sympathetic outflow to the kidney or activation of the renin-angiotensin system
Leukotrienes
Cause local, strong vasoconstriction to reduce RBF and GFR
Nitric Oxide
Produces strong vasodilation
