When is sympathetic stimulation of glomerular filtration important

The concentration of plasma solutes in the glomerulus is greater than the concentration of the filtrate in the glomerular capsule since the filtration membrane limits the size of particles crossing the membrane. This pressure acting to draw water into the glomerulus is called blood colloid osmotic pressure.

The absence of proteins in the glomerular space the lumen within the glomerular capsule results in a capsular osmotic pressure near zero. Glomerular filtration occurs when glomerular blood hydrostatic pressure exceeds the hydrostatic pressure of the glomerular capsule and the blood colloid osmotic pressure.

The sum of all of the influences, both osmotic and hydrostatic, results in a net filtration pressure NFP. Glomerular hydrostatic pressure is typically about 55 mmHg pushing fluid into the glomerular capsule.

This outward pressure is countered by a typical capsular hydrostatic pressure of about 15 mmHg and a blood colloid osmotic pressure of 30 mmHg. To calculate the value of NFP:. A proper concentration of solutes in the blood is important in maintaining osmotic pressure both in the glomerulus and systemically. There are disorders in which too much protein passes through the filtration slits into the kidney filtrate. This excess protein in the filtrate leads to a deficiency of circulating plasma proteins.

Together, blood colloid osmotic pressure decreases, resulting in an increase in urine volume potentially causing dehydration. As you can see, there is a low net pressure across the filtration membrane. Intuitively, you should realize that minor changes in osmolarity of the blood or changes in capillary blood pressure result in major changes in the amount of filtrate formed at any given point in time. The kidney is able to cope with a wide range of blood pressures.

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.

ATP and adenosine act locally as paracrine factors to stimulate the myogenic juxtaglomerular cells of the afferent arteriole to constrict, slowing blood flow into the glomerulus. This vasoconstriction causes less plasma to be filtered, which decreases the glomerular filtration rate GFR , which gives the tubule more time for NaCl reabsorption.

Conversely, when GFR decreases, less NaCl is in the filtrate, and most will be reabsorbed before reaching the macula densa, which will result in decreased ATP and adenosine, allowing the afferent arteriole to dilate and increase GFR. Thus, increased angiotensin II levels that occur with a low-sodium diet or volume depletion help preserve GFR and maintain normal excretion of metabolic waste products such as urea and creatinine that depend on glomerular filtration for their excretion; at the same time, the angiotensin II—induced constriction of efferent arterioles increases tubular reabsorption of sodium and water, which helps restore blood volume and blood pressure.

An autacoid that de-creases renal vascular resistance and is released by the vascular endothelium throughout the body is endothe-lial-derived nitric oxide. A basal level of nitric oxideproduction appears to be important for maintaining vasodilation of the kidneys. This allows the kidneys to excrete normal amounts of sodium and water. There-fore, administration of drugs that inhibit this normal formation of nitric oxide increases renal vascular resistance and decreases GFR and urinary sodium excretion, eventually causing high blood pressure.

In some hypertensive patients, impaired nitric oxide pro-duction could be the cause of increased renal vaso-constriction and increased blood pressure. Although these vasodilators do not appear to be of major importance in regulating renal blood flow or GFR in normal conditions, they may dampen the renal vasoconstrictor effects of the sympathetic nerves or angiotensin II, especially their effects to constrict the afferent arterioles.

By opposing vasoconstriction of afferent arterioles, the prostaglandins may help prevent excessive reduc-tions in GFR and renal blood flow. Under stressful conditions, such as volume depletion or after surgery, the administration of nonsteroidal anti-inflammatory agents, such as aspirin, that inhibit prostaglandin syn-thesis may cause significant reductions in GFR. Developed by Therithal info, Chennai.

Toggle navigation BrainKart. Author : Arthur C. Guyton, John E. Hall Posted On : Physiologic Control of Glomerular Filtration and Renal Blood Flow The determinants of GFR that are most variable and subject to physiologic control include the glomerular hydrostatic pressure and the glomerular capillary colloid osmotic pressure. Sympathetic Nervous System Activation Decreases GFR Essentially all the blood vessels of the kidneys, includ-ing the afferent and the efferent arterioles, are richly innervated by sympathetic nerve fibers.

Related Topics Abnormalities of Micturition. Determinants of the GFR. Renal Blood Flow.