Under conditions of stress, sympathetic nervous activity increases, resulting in the direct vasoconstriction of afferent arterioles norepinephrine effect as well as stimulation of the adrenal medulla. The adrenal medulla, in turn, produces a generalized vasoconstriction through the release of epinephrine.
This includes vasoconstriction of the afferent arterioles, further reducing the volume of blood flowing through the kidneys. This process redirects blood to other organs with more immediate needs. Under severe stress, such as significant blood loss, the sympathetic nervous system kicks into high gear to keep the blood routed to essential organs and keep the body alive.
The strong vasoconstriction required to maintain systemic blood pressure under these severe conditions significantly reduces blood flow to the kidneys and can be damaging to the kidney tissues. If blood pressure falls, the sympathetic nerves will also stimulate the release of renin which we will discuss next. Recall that renin is an enzyme that is produced by the granular cells of the afferent arteriole at the JGA.
It enzymatically converts angiotensinogen made by the liver, freely circulating into angiotensin I. Its release is stimulated by paracrine signals from the JGA in response to decreased extracellular fluid volume. ACE is not a hormone but it is functionally important in regulating systemic blood pressure and kidney function. It is produced in the lungs but binds to the surfaces of endothelial cells in the afferent arterioles and glomerulus.
ACE is important in increasing blood pressure and this is why people with high blood pressure are sometimes prescribed ACE inhibitors to lower their blood pressure. Angiotensin II is a potent vasoconstrictor that plays an immediate role in the regulation of blood pressure. It acts systemically to cause vasoconstriction as well as constriction of both the afferent and efferent arterioles of the glomerulus.
Under the influence of Angiotensin II, the efferent arteriole constricts more strongly than the afferent arteriole, increasing GFR. In instances of blood loss or dehydration, Angiotensin II reduces both GFR and renal blood flow, thereby limiting fluid loss and preserving blood volume.
Its release is usually stimulated by decreases in blood pressure, and so the preservation of adequate blood pressure is its primary role. The GFR is influenced by hydrostatic pressure and colloid osmotic pressure. Under normal circumstances, hydrostatic pressure is significantly greater and filtration occurs.
The kidneys are innervated by sympathetic nerves of the autonomic nervous system. Sympathetic nervous activity decreases blood flow to the kidney, making more blood available to other areas of the body during times of stress. The arteriolar myogenic mechanism maintains a steady blood flow by causing arteriolar smooth muscle to contract when blood pressure increases and causing it to relax when blood pressure decreases. Tubuloglomerular feedback involves paracrine signaling at the JGA to cause vasoconstriction or vasodilation to maintain a steady rate of blood flow.
Also unbold the definintion of systemic edema. Skip to content Learning Objectives By the end of this section, you will be able to: Describe glomerular filtration, including the hydrostatic and colloid osmotic forces that favor and oppose filtration Describe glomerular filtration rate GFR and net filtration pressure NFP Predict specific factors that will increase or decrease GFR Explain the mechanisms that control renal blood flow to the glomerulus.
Explain how the kidney filters the blood to produce urine. Filterable blood components include water, nitrogenous waste, and nutrients that will be transferred into the glomerulus to form the glomerular filtrate. Non-filterable blood components include blood cells, albumins, and platelets, that will leave the glomerulus through the efferent arteriole. Glomerular filtration is caused by the force of the difference between hydrostatic and osmotic pressure though the glomerular filtration rate includes other variables as well.
Key Terms glomerulus : A small, intertwined group of capillaries within nephrons of the kidney that filter the blood to make urine. It is the primary force that drives glomerular filtration. Blood plasma enters the afferent arteriole and flows into the glomerulus, a cluster of intertwined capillaries. The visceral layer lies just beneath the thickened glomerular basement membrane and is made of podocytes that form small slits in which the fluid passes through into the nephron.
The size of the filtration slits restricts the passage of large molecules such as albumin and cells such as red blood cells and platelets that are the non-filterable components of blood. These then leave the glomerulus through the efferent arteriole, which becomes capillaries meant for kidney—oxygen exchange and reabsorption before becoming venous circulation. The positively charged podocytes will impede the filtration of negatively charged particles as well such as albumins.
The process by which glomerular filtration occurs is called renal ultrafiltration. The force of hydrostatic pressure in the glomerulus the force of pressure exerted from the pressure of the blood vessel itself is the driving force that pushes filtrate out of the capillaries and into the slits in the nephron. Osmotic pressure the pulling force exerted by the albumins works against the greater force of hydrostatic pressure, and the difference between the two determines the effective pressure of the glomerulus that determines the force by which molecules are filtered.
These factors will influence the glomeruluar filtration rate, along with a few other factors. Regulation of GFR requires both a mechanism of detecting an inappropriate GFR as well as an effector mechanism that corrects it. List the conditions that can affect the glomerular filtration rate GFR in kidneys and the manner of its regulation.
Glomerular filtration rate GFR is the measure that describes the total amount of filtrate formed by all the renal corpuscles in both kidneys per minute. The glomerular filtration rate is directly proportional to the pressure gradient in the glomerulus, so changes in pressure will change GFR. GFR is also an indicator of urine production, increased GFR will increase urine production, and vice versa. The filtration constant is based on the surface area of the glomerular capillaries, and the hydrostatic pressure is a pushing force exerted from the flow of a fluid itself; osmotic pressure is the pulling force exerted by proteins.
Many factors can change GFR through changes in hydrostatic pressure, in terms of the flow of blood to the glomerulus. GFR is most sensitive to hydrostatic pressure changes within the glomerulus. A notable body-wide example is blood volume.
The increased blood volume with its higher blood pressure will go into the afferent arteriole and into the glomerulus, resulting in increased GFR. Conversely, those with low blood volume due to dehydration will have a decreased GFR. Pressure changes within the afferent and efferent arterioles that go into and out of the glomerulus itself will also impact GFR. Vasodilation in the afferent arteriole and vasconstriction in the efferent arteriole will increase blood flow and hydrostatic pressure in the glomerulus and will increase GFR.
Conversely, vasoconstriction in the afferent arteriole and vasodilation in the efferent arteriole will decrease GFR. An example of this is a ureter obstruction to the flow of urine that gradually causes a fluid buildup within the nephrons. Osmotic pressure is the force exerted by proteins and works against filtration because the proteins draw water in.
Increased osmotic pressure in the glomerulus is due to increased serum albumin in the bloodstream and decreases GFR, and vice versa. GFR is the rate at which is this filtration occurs. GFR is one of the many ways in which homeostasis of blood volume and blood pressure may occur. In particular, low GFR is one of the variables that will activate the renin—angiotensin feedback system, a complex process that will increase blood volume, blood pressure, and GFR. Why does glucose "spill" into the urine in diabetes?
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