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.
Learning Objectives Describe the myogenic and tubuloglomerular feedback mechanisms and explain how they affect urine volume and composition Describe the function of the juxtaglomerular apparatus. Sympathetic Nerves The kidneys are innervated by the sympathetic neurons of the autonomic nervous system via the celiac plexus and splanchnic nerves. Autoregulation The kidneys are very effective at regulating the rate of blood flow over a wide range of blood pressures. Arteriole Myogenic Mechanism The myogenic mechanism regulating blood flow within the kidney depends upon a characteristic shared by most smooth muscle cells of the body.
Chapter Review The kidneys are innervated by sympathetic nerves of the autonomic nervous system. Review Questions Q. Answer: B. Answer: A. Which of these three paracrine chemicals cause vasodilation?
ATP B. Answer: C. The net result of the increased blood flow, the decreased diffusion distance, and the increased total capillary surface area is a more rapid delivery of oxygen and other metabolic substrates to the tissue cells and a more rapid removal of metabolic waste products from the tissue. Metabolic control of blood flow involves negative feedback.
The accumulation of metabolic products and the lack of oxygen initiate vasodilation, which increases blood flow. The increased blood flow removes the accumulating metabolic products and delivers additional oxygen. A new balance is reached when the increased blood flow closely matches the increased metabolic needs of the tissue.
Figure summarizes the major features of metabolic control of blood flow. Reactive hyperemia is a temporary increase above normal in the flow of blood to a tissue after a period when blood flow was restricted. In this case the increased flow hyperemia is a response reaction to a period of inadequate blood flow. Mechanical compression of blood vessels is one cause of inadequate blood flow, and release of that mechanical compression elicits reactive hyperemia.
This can be easily demonstrated in any accessible nonpigmented epithelial tissue. For example, press a finger against nonpigmented skin hard enough to occlude the blood flow. Maintain the pressure for about 1 minute, and then release. After release of the pressure, the previously compressed skin will appear darker redder for a short time, because blood flow will become greater than normal after the compression is released.
The same metabolic control mechanisms that account for active hyperemia also explain reactive hyperemia. During the period when mechanical compression restricts blood flow, metabolism continues in the compressed tissue; metabolic products accumulate, and the local concentration of oxygen decreases.
These metabolic effects cause dilation of the arterioles and a decrease in arteriolar resistance. Figure compares active and reactive hyperemia. Metabolic control mechanisms also participate in the phenomenon known as blood flow autoregulation.
Autoregulation is evident in denervated organs and organs in which local control of blood flow is predominant over neural and humoral control e. Figure summarizes an experiment that demonstrates autoregulation in the brain. These stable responses are plotted in the bottom graph. The remainder of the bottom graph is obtained in a similar way; that is, perfusion pressure is set artificially to various levels, ranging from 40 to mm Hg, and the resulting steady-state levels of blood flow are plotted.
Over a considerable range of perfusion pressure about 60 to mm Hg , relatively little change occurs in steady-state blood flow to the brain; that is, brain blood flow is autoregulated. The range of perfusion pressures over which flow remains relatively constant is called the autoregulatory range. Autoregulation fails at very high and very low perfusion pressures. Extremely high pressures result in marked increases in blood flow, and extremely low pressures result in marked decreases in blood flow.
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