11. Renal structure and function 2 Flashcards
Give a brief overview of how blood volume within the body is controlled if e.g. there is a loss of volume
How is this mechanism regulated?
If there is a loss of volume, sympathetic nervous system compensates via immediate vasoconstriction
There may be a slight increase in heart rate and peripheral vascular resistance
The blood pressure will remain steady
Blood volume control system then detects the loss of fluid and reduces the urine flow and increases thirst to compensate for the volume loss
This is a slower acting mechanism than pressure control mechanism
Blood volume is regulated by neuronal volume sensors and hormonal volume sensors
Describe the role of neuronal volume sensors in the control blood volume
These are sensory nerve fibres found in the tissues of the right atrium (and in the left atrium to a lesser extent) and are at the ends of the great veins
These act as stretch receptors and are called BARORECEPTORS in the same way as stretch receptors in the carotid sinus
When the venous return increases, they become stretched and expand and if the returning volume is too little, they shrink - hence, they signal the volume of blood returning to the heart per minute - SO stretch of the receptors can inhibit sympathetic output and decrease the blood pressure
These baroreceptors connect to the Vagus nerve and hence, the information is carried up to the Vagus nerve to the brainstem
The brain integrates this signal to obtain information on the total blood volume
Describe the role of hormonal volume sensors in the control of blood volume
These are hormonal volume cells - specialised muscle cells in the tissue of the right atrium and inferior vena cava
They also act as stretch receptors
In response to stretch, the cells release ATRIAL NATRIURETIC PEPTIDE (ANP) which decreases the Na+ reabsorption in the distal tubule of the kidney (opposite action of aldosterone) - SO this results in a reduced reabsorption of water and a lowered blood volume which decreases the blood pressure
The heart muscle can also release BRAIN-DERIVED NATRIUERETIC PEPTIDE (BNP) - these levels are normally very low in a healthy person - BNP is normally only released when the ventricles are overstretched in e.g. heart failure - SO this is a sign of damaged/overstretched ventricles - key clinical marker of heart failure
Describe the hypothalamus and the two hormones released in this area - describe the structures required for their release
Essentially a series of tiny nuclei packed closely together
Lies on the third ventricle of the brain
Just above the pituitary gland
Two nuclei; the SUPRAOPTIC and the PARAVENTRICULAR nuclei contain axons that project down the pituitary stalk to the posterior pituitary
These axons end as secretory terminals within the posterior pituitary and these nuclei secrete ANDTIDIURETIC HORMONE (ADH) into the capillaries
The ADH is made in the cell body and a small amount is secreted into the venous blood all the time (this is known as BASAL RELEASE)
Another hormone OXYTOCIN is also released from these nuclei to the capillaries of the posterior pituitary gland
Describe the role of osmoreceptors in the brain
In the paraventricular and supraotic nuclei, there are ‘osmoreceptors’ that measure the osmotic pressure of the blood passing through them
Describe the mechanism that occurs if there is hypo-osmalarity and how this can impact ADH release
If the osmoreceptors detect hypo-osmalarity then:
1) sympathetic innervation stimulates direct renin release which then increases the release of aldosterone - the increased renin increases the Na+ reabsorption from the urine and compensates for the low plasma Na+
2) there is an inhibition of ADH release from the pituitary which allows more water to be lost in the urine and the Na+ concentration of the plasma to increase
How else can ADH release be affected?
Sympathetic arousal - when the sympathetic NS is aroused for fight or flight then the signal is sent to the hypothalamus to increase the ADH release (production of urine is reduced)
These signals come from the volume receptors in the atria
Describe the effects of an inhibition of ADH secretion
This allows an increased volume of urine to be excreted
SO both water and Na+ will be excreted
This will reduced blood volume
Describe the effects of increased secretion of ADH
This means that there is a decreased volume of urine to be excreted
SO water loss is reduced
Behavioural thirst is increased
ANP secretion is reduced
Renin secretion increases - aldosterone release increases
Sodium retention increases
Briefly describe how the kidney is able to make concentrated urine
Concentrated urine is formed by having concentrated fluid in the extracellular space in the renal medulla
Normally, the osmolality of the ECF in the renal medulla is much higher than the plasma of the rest of the kidney
The concentration gradient is built up by a countercurrent multiplier system and is maintained by a countercurrent exchange mechanism
The loops of Henle of the juxtamedullary neurones are surrounded by a network of capillaries called VASA RECTA
Give the overall mechanism of the formation of concentrated urine through the nephron
Fluid comes out of the glomerulus at the same osmolality as the plasma
As the fluid descends down the descending loop of Henle, the tubule becomes more and more concentrated because it is in equilibrium with the high concentration of solutes in the ECF in the renal medulla - hence there are aquaporins which allow water to leave the tubule to maintain this concentration
SO as fluid reaches the bottom of this loop, it is very concentrated
The fluid then reaches up to the thick part of the ascending loop and there are no more aquaporins but there are ATP consuming membrane pumps - these pump Na+ and Cl- out of the fluid in the ascending loop via active transport (this is how the medulla becomes very concentrated) - allows the high concentrated of ECF in the renal medulla to be maintained - Oxygen is supplied by the capillaries of the vasa recta
Fluid then passes through the distal tubule where there is a ‘fine-tuning’ via active transport of the materials
The dilute fluid then enters the collecting duct and passes down into the ureter and bladder - the collecting duct has more aquaporins that are opened by ADH which allows more water to leave the collecting duct depending on how much regulation is required
Most of the water is reabsorbed down it’s concentration gradient into the concentrated ECF SO the urine becomes more and more concentrated
SO THE MORE CONCENTRATED YOU MAKE THE ECF, THE MORE CONCENTRATED YOU CAN MAKE THE URINE
What happens in the urine concentration mechanism in the absence of ADH?
In the absence of ADH, the urine just remains at the dilute level and you excrete dilute urine
Describe the role of urea in the formation of concentrated urine
Urea contributes to the osmotic gradient in the medullary pyramids
It is actively pumped into the interstitial fluid from the collecting ducts by urea transport proteins in the collecting ducts
This increases the solute concentration in the renal medulla
Some urea also appears in the urine
What is the countercurrent multiplier system?
This is the process of pumping out salt into the ECF around the loop of Henle
What is the countercurrent exchange system?
This is provided by the vasa recta to preserve the concentration gradient despite a blood flow through the vasa recta capillaries
