In large part, this is due to the autoregulatory nature of smooth muscle. When you stretch it, it contracts. Thus, when blood pressure goes up, smooth muscle in the afferent arterioles contracts to limit any increase in blood flow and filtration rate. When blood pressure drops, the same capillaries relax to maintain blood flow and filtration rate.
The net result is a relatively steady flow of blood into the glomerulus and a relatively steady filtration rate in spite of significant systemic blood pressure changes. One third of this is 10, and when you add this to the diastolic pressure of 80, you arrive at a calculated mean arterial pressure of 90 mm Hg.
Therefore, if you use mean arterial pressure for the GBHP in the formula for calculating NFP, you can determine that as long as mean arterial pressure is above approximately 60 mm Hg, the pressure will be adequate to maintain glomerular filtration. Blood pressures below this level will impair renal function and cause systemic disorders that are severe enough to threaten survival.
This condition is called shock. It is vital that the flow of blood through the kidney be at a suitable rate to allow for filtration and yet not too fast to overwhelm the reabsorbing potential of the nephron tubule. This rate determines how much solute is retained or discarded, how much water is retained or discarded, and ultimately, the osmolarity of blood and the blood pressure of the body.
Glomerular filtration has to be carefully and thoroughly controlled because the simple act of filtrate production can have huge impacts on body fluid homeostasis and systemic blood pressure. Due to these two very distinct physiological needs, the body employs two very different mechanisms to regulate GFR.
The kidney can control itself locally through intrinsic controls, also called renal autoregulation. These intrinsic control mechanisms maintain filtrate production so that the body can maintain fluid, electrolyte, and acid-base balance and also remove wastes and toxins from the body. There are also control mechanisms that originate outside of the kidney, the nervous and endocrine systems, and are called extrinsic controls. The nervous system and hormones released by the endocrine systems function to control systemic blood pressure by increasing or decreasing GFR to change systemic blood pressure by changing the fluid lost from the body.
The kidneys are very effective at regulating the rate of blood flow over a wide range of blood pressures. Your blood pressure will decrease when you are relaxed or sleeping. It will increase when exercising. Yet, despite these changes, the filtration rate through the kidney will change very little. This is due to two internal autoregulatory mechanisms that operate without outside influence: the myogenic mechanism and the tubuloglomerular feedback mechanism. The myogenic mechanism regulating blood flow within the kidney depends upon a characteristic shared by most smooth muscle cells of the body.
When you stretch a smooth muscle cell, it contracts; when you stop, it relaxes, restoring its resting length. This mechanism works in the afferent arteriole that supplies the glomerulus and can regulate the blood flow into the glomerulus.
When blood pressure increases, smooth muscle cells in the wall of the arteriole are stretched and respond by contracting to resist the pressure, resulting in little change in flow.
This vasoconstriction of the afferent arteriole acts to reduce excess filtrate formation, maintaining normal NFP and GFR. Reducing the glomerular pressure also functions to protect the fragile capillaries of the glomerulus. When blood pressure drops, the same smooth muscle cells relax to lower resistance, increasing blood flow. The vasodilation of the afferent arteriole acts to increase the declining filtrate formation, bringing NFP and GFR back up to normal levels.
The tubuloglomerular feedback mechanism involves the juxtaglomerular JG cells, or granular cells, from the juxtaglomerular apparatus JGA and a paracrine signaling mechanism utilizing ATP and adenosine. These juxtaglomerular cells are modified, smooth muscle cells lining the afferent arteriole that can contract or relax in response to the paracrine secretions released by the macula densa. This mechanism stimulates either contraction or relaxation of afferent arteriolar smooth muscle cells, which regulates blood flow to the glomerulus Table Recall that the DCT is in intimate contact with the afferent and efferent arterioles of the glomerulus.
The increased fluid movement more strongly deflects single nonmotile cilia on macula densa cells. This increased osmolarity of the filtrate, and the greater flow rate within the DCT, activates macula densa cells to respond by releasing ATP and adenosine a metabolite of ATP.
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.
This system is also activated by low blood pressure itself, and sympathetic nervous stimulation, in addition to low GFR. Tubular reabsorption is the process by which solutes and water are removed from the tubular fluid and transported into the blood.
The fluid filtered from blood, called filtrate, passes through the nephron, much of the filtrate and its contents are reabsorbed into the body. Reabsorption is a finely tuned process that is altered to maintain homeostasis of blood volume, blood pressure, plasma osmolarity, and blood pH.
Reabsorbed fluids, ions, and molecules are returned to the bloodstream through the peri-tubular capillaries, and are not excreted as urine. Tubular secretion : Diagram showing the basic physiologic mechanisms of the kidney and the three steps involved in urine formation. Namely filtration, reabsorption, secretion, and excretion.
Reabsorption in the nephron may be either a passive or active process, and the specific permeability of the each part of the nephron varies considerably in terms of the amount and type of substance reabsorbed. The mechanisms of reabsorption into the peri-tubular capillaries include:.
These processes involve the substance passing though the luminal barrier and the basolateral membrane, two plasma membranes of the kidney epithelial cells, and into the peri-tubular capillaries on the other side. Some substances can also pass through tiny spaces in between the renal epithelial cells, called tight junctions. As filtrate passes through the nephron, its osmolarity ion concentration changes as ions and water are reabsorbed.
Finally, in the distal convoluted tubule and collecting duct, a variable amount of ions and water are reabsorbed depending on hormonal stimulus.
The final osmolarity of urine is therefore dependent on whether or not the final collecting tubules and ducts are permeable to water or not, which is regulated by homeostasis. Reabsorption throughout the nephron : A diagram of the nephron that shows the mechanisms of reabsorption. Hydrogen, creatinine, and drugs are removed from the blood and into the collecting duct through the peritubular capillary network. Tubular secretion is the transfer of materials from peritubular capillaries to the renal tubular lumen; it is the opposite process of reabsorption.
This secretion is caused mainly by active transport and passive diffusion. Usually only a few substances are secreted, and are typically waste products. Note that the kidneys filter much more fluid than the amount of urine that is actually excreted about 1. This is essential for the kidneys to rapidly remove waste and toxins from the plasma efficiently. Reabsorption is the movement of water and solutes from the tubule back into the plasma.
Reabsorption of water and specific solutes occurs to varying degrees over the entire length of the renal tubule. Bulk reabsorption, which is not under hormonal control, occurs largely in the proximal tubule.
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