Control of Filtration

Juxtaglomeruluar Apparatus

The kidney can make adjustments with or without consideration for the rest of your body.  Renal autoregulationThe kidney’s ability to maintain a stable glomerular filtration rate (GFR) despite changes in bloo is when the kidney tightly controlsVariables that remain constant to ensure a fair test. its filtrationThe process by which fluid moves out of capillaries into surrounding tissues due to hydrostatic pre rate despite changes in blood pressureThe force exerted by gases in the respiratory system, affecting airflow and gas exchange..  So, if you eat a salty meal, the kidney makes a small adjustment. This adjustment is very minute compared to how much the osmolarityA measure of solute concentration in fluid; affects fluid movement between compartments. of your whole blood changes. 

We have to make the anatomyThe study of the structure of the human body. of the renal corpuscleThe structure in the nephron that consists of the glomerulus and Bowman’s capsule, where filtratio even more complicated before talking about how your nephrons regulate the rate of filtration. First, we must understand that additional complex details exist. There is a group of cellsThe basic structural and functional units of life. within the glomerulusA network of capillaries in the nephron where blood filtration occurs.. Another group is closely located to it. Together, they are called the juxtaglomerulus apparatus. This is a feedback mechanism of sensory inputs. It consists mostly of smooth muscle outputs. These help the kidney control its filtration rate despite changes in your blood pressure.

Within the glomerulus are mesangial cellsSpecialized cells in the glomerulus that provide structural support and help regulate blood flow. between the podocytesSpecialized cells in the glomerulus that form filtration slits, preventing large molecules from ente, kinda like filling in space.  There are also mesangial cells our here between the afferent and efferent arteriolesSmall arteries that regulate blood flow into capillaries through vasoconstriction and vasodilation.  Sometimes we call these two populations different names such as the intraglomerular mesangial cells or the extraglomerular mesangial cells.  These cells are smooth muscle cells.

Remember how we said that a nephronThe functional unit of the kidney that filters blood and produces urine. is not really all stretched out?  The loop bent back around so that the DCT could come close to the renal corpuscle.  This is the DCT.  In the calls of the DCT are some cells called the macula dense.  These cells are essential chemoreceptors that monitor the amount of sodium(Na⁺): Major ECF cation; important for fluid balance, nerve function. in your filtrateThe fluid that is filtered from the blood into the nephron and will eventually become urine.. 

Granular or juxtaglomerular cellsCells that secrete renin in response to changes in blood pressure. are smooth muscle cells that surround the afferent arterioleThe small artery that carries blood into the glomerulus of the nephron. and a little bit surrounds the efferent.

Renal Autoregulation

When the kidney makes adjustment without regard for the rest of your body, this is called renal autoregulation.  There are two ways the kidney can employ to stabilize GFR despite changes in the systemic circuitThe part of the circulatory system that carries oxygenated blood from the heart to the body and retu.  So, if you are blooding out, the kidney uses these mechanisms to maintain GFR. 

The myogenic mechanism concerns the afferent arteriole and the volume of blood it is allowing into the glomerulus.  When blood pressure goes high, the afferent arteriole stretches.  But, it stretches so much that it snaps back like a rubber band.  As a response to high blood pressure, the afferent arterioles all constrict and reduce the glomerular hydrostatic pressureThe force exerted by a fluid, such as the pressure of blood pushing against the walls of capillaries.  Remember that this was the only pressure encouraging filtration.  Reducing this will reduce the rate of filtration.

Here’s one way in which the tubuloglomerular mechanismA feedback mechanism in which the macula densa regulates glomerular filtration rate based on sodium works.  The macula densaA group of specialized cells in the distal convoluted tubule that detect sodium concentration and he chemoreceptorSensory receptors that detect chemical stimuli, such as odors or blood pH. cells in the wall of the DCT sense a high amount of sodium in the filtrate.  They interpret this to mean that filtration is happening to fast and we are losing too much sodium.  The macular densa can communicate with the mesangial cells making them constrict.  This constriction makes the filtration membrane smaller and reduces filtration. 

GFR Nervous & Hormonal  Regulation

Your kidney can take input from the rest of your body.  It doesn’t HAVE to, but it will.  Your kindey is innervated with sympathetic and parasympathetic fibers.  Most of the time the parasympathetic fibers are in control, helping you maintain a good GFR.  But, these parasympathetic fibers can be overrun by the activation of the sympathetic fibers.  These sympathetic fibers decrease GFR.  You are responding to a threat, you don’t need to make filtration.  But, it’s not just nervous input that the kidney is subjected to.  There are also hormonal inputs that control the kidney.

Renin-Angiotensin-Aldosterone Mechanism

When the granular cellsSpecialized cells in the juxtaglomerular apparatus that secrete renin in response to low blood press on the afferent arteriole sense low systemic blood pressure, they release reninAn enzyme secreted by the juxtaglomerular cells that helps regulate blood pressure by triggering the.  Renin is converted to angiotensin IAn inactive precursor formed from angiotensinogen by renin; it is later converted into angiotensin I by an enzyme from the liverA large organ that produces bile, detoxifies blood, and stores nutrients..  Then, in the lungs, angiotensin I is converted to angiotensin IIA powerful vasoconstrictor that increases blood pressure and stimulates aldosterone release.. This change is facilitated by another enzyme called the angiotensin-converting enzyme, or ACE.  Now, Angiotensin II circulates through your body, targeting different organs.  First and foremost, angiotensin II is a powerful vasoconstrictor of all your blood vessels.  So, right from the start angiotensin raises blood pressure.  But, it doesn’t stop there.  It encourages the release of ADH from the posterior pituitary gland(PPG): Stores and releases oxytocin and ADH produced by the hypothalamus.. It also prompts the release of aldosteroneA hormone that increases sodium and water reabsorption in the kidneys, helping regulate blood pressu from the zona glomerulus in the adrenal cortexOuter portion of the adrenal glands producing corticosteroids..  These circulate in blood and go back to the kidney and affect the DCT and CD mainly.  ADH inserts aquaporins in the DCT and CD, allowing them to do facultative waterThe universal solvent essential for life. reabsorptionThe process of fluid moving back into capillaries from surrounding tissues due to colloid osmotic p.  This increases your blood volume (or keeps it the same) and increases your blood pressure.   Aldosterone targets the same cells, making them reabsorb sodium, which further increases the amount of water reabsorption can cause.  So, the combined effect of these two hormones is also very powerful.  All of this increases blood pressure.  For most people with essential hypertension, the first drug you might try is an ACE inhibitor.  Actually, no, you might get on a diuretic first.  You might consider a drug like captopril. Or, any of those other ones ending in –pril.  These drugs are ACE inhibitors.  They stop the angiotensin converting enzyme in the lungs.  This prevents all these blood pressure raising effects of angiotensin II. 

Side note – I take BP drugs occasionally. This happens when I have a high pressure issue with one of my eyes.  The first time this happened, I got catopril.  It caused this horrible, unavoidable, hacking cough.  I found out that this is common for people who just don’t tolerate the –pril drugs.  I have found some literature, although not a lot, that hypothesizes the cough comes from abnormal activity of the angiotensin converting enzyme in the lungs.