BIO 3302 Lecture Notes - Lecture 18: Macula Densa, Renal Function, Afferent Arterioles
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Thursday November 17, 2016
Lecture 18 –Control of Salt and Water Balance
Control of GFR:
• The purpose of these mechanisms is to keep urine formation constant as you get minor
fluctuations in blood pressure
• Blood pressure in the glomerulus drives filtration; this reflects overall systemic blood pressure;
• We dot at these ariatios i lood pressure to affet urie produtio
• There are two mechanisms: one that regulates BP within the glomerulus, and one that monitors
filtrate flow
• Autoregulatory Mechanisms (intrinsic control mechanism)---keeps filtration constant
1. Myogenic Mechanism
o Purpose is to keep constant glomerular BP
o The afferent blood vessel is short, wide arteriole
o So, any change in BP will tend to transmit to BP in the glomerulus
o The afferent arteriole responds to changes in BP (sees as a stretch in arteriole
width), and it responds to increases in BP by constricting
o This response keeps glomerular BP constant (making filtration also constant)
2. Paracrine Mechanism
o Called this because there are cells surrounding the afferent arteriole (called
jutagloerular ells
o These cells produce vasoactive compounds that can act on the afferent arteriole
(have local affect)
o They are released in response to signalling from sensory cells in the distal tubule
o The distal tubules runs in between the afferent and efferent arterioles; there
are sensory cells in the distal tubule called the Macula densa which monitor
filtrate flow
o If filtrate flow decreases, Macula densa sends signals to the Juxtaglomerular
cells to produce compounds which cause vasodilation; this then increases BP in
the glomerulus, which then increases filtration to bring filtrate flow to where it
should be
o If filtrate flow increases, the Macula densa sends signal to the Juxtaglomerular
cells to produce a vasoconstrictor, which will reduce glomerular filtration and
bring it to where it should be
o So, goal is to produce constant flow of filtrate
• Extrinsic Control Mechanism ---alters glomerular BP
▪ They are activated because of a need to conserve water
▪ Loss of blood can cause these mechanisms to reduce filtration
▪ They act on the afferent arteriole to cause it to constrict, which reduces BP and
filtration in the glomerulus
▪ Neural Mechanisms (Sympathetic Nervous System) acts on the afferent arteriole
▪ Hormonal Mechanism also act on afferent arteriole:
o Angiotensin II – which is also a vasoconstrictor
o ADH (antidiuretic hormone) – AVP (Arginine Vasopressin) or AVT cause
constriction
o They act as a water conservation mechanism
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Thursday November 17, 2016
Control of Na+ Reabsorption:
-Renin angiotensin system
• Renin is an enzyme that is released from the Juxtaglomerular cells, which acts to cleave a
plasma protein called Angiotensinogen (always present in the plasma)
• This produces Angiotensin I, which is still an inactive form of the hormone
• It needs to get cleaved again to produce the active form, which is Angiotensin II
• The second cleavage is catalyzed by the Angiotensin Converting Enzyme, which is known as ACE
• Angiotensin II is a vasoconstrictor – so it can act on afferent arteriole to reduce filtration
• Secondly, it acts on the adrenal cortex to cause the production of Aldosterone
• Aldosterone acts on the distal tubule to increase sodium reabsorption
• We have two main effects from this system:
1. Increase in BP because of Angiotensin II acting as a vasoconstrictor
2. Increase in sodium reabsorption, which increases plasma volume (slow affect process)
• These two things counteract low BP
• The stimuli for renal secretion signal low BP; thus triggering the secretion of renin
• The other thing that triggers renin is decrease in Sodium Concentration in the filtrate (detected
by Macula densa)
-Aldosterone
• Is a steroid hormone, that is synthesized by the adrenal cortex
• Steroid hormones tend to regulate gene transcription; they bind to receptors that are ligand
active transcription factors,
• So, Aldosterone increases transcription of proteins involved in Na+ reabsorption at the distal
tubule
• This includes an increase in the number of Sodium Channels and Sodium Pumps
• Comparative considerations: fish lack aldosterone
o Aldosterone is found only in tetrapods
o In fish, the control of Na+ reabsorption, is under the control of cortisol (rather than
aldosterone)
Control of Water Reabsorption:
-ADH secretion controls water reasorptio…
• From the distal tubule and/or the collecting duct depedig o hether oure talkig aout
fish, mammals, etc.
• Collecting Duct permeability in mammals (AVP)
• Distal Tubule permeability in Fresh Water fish, amphibians (AVT)
• Diuresis refers to increasing water flow; so Anti-diuretic hormone reduces urine flow by
favouring water reabsorption
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Document Summary
Lecture 18 control of salt and water balance. If filtrate flow decreases, macula densa sends signals to the juxtaglomerular cells to produce compounds which cause vasodilation; this then increases bp in the glomerulus, which then increases filtration to bring filtrate flow to where it should be. Secondly, it acts on the adrenal cortex to cause the production of aldosterone: we have two main effects from this system: Increase in bp because of angiotensin ii acting as a vasoconstrictor. Is a steroid hormone, that is synthesized by the adrenal cortex. Steroid hormones tend to regulate gene transcription; they bind to receptors that are ligand active transcription factors, So, aldosterone increases transcription of proteins involved in na+ reabsorption at the distal tubule: this includes an increase in the number of sodium channels and sodium pumps, comparative considerations: fish lack aldosterone, aldosterone is found only in tetrapods. In fish, the control of na+ reabsorption, is under the control of cortisol (rather than aldosterone)