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and the remainder in the thick ascending limb of Henle s loop, distal convoluted tubule, and collecting-duct system. Overall, reabsorption is normally 97 99%. Calcium reabsorption in the proximal tubule and thick ascending limb of Henle s loop is largely passive and paracellular, and the electrochemical forces driving it are dependent directly or indirectly on sodium reabsorption as they are for so many other substances. In contrast, calcium reabsorption in the more distal segments is active and transcellular. It uses the same mechanism as in the GI tract, ie, entrance via calcium-specific channels, diffusion bound to calbindins and exit across the basolateral membrane actively by a combination of Ca-ATPase and Na-Ca antiport activity (Figure 10 1). The distal tubule is the site of endocrine control of renal calcium handling. The amount of calcium excreted in the urine is, on average, equal to the net addition of new calcium to the body via the GI tract; thus, the kidneys help maintain a stable balance of total-body calcium. However, the change in renal excretion in response to changes in dietary input is much less than the equivalent responses to dietary sodium, water, or potassium. For example, only about 5% of an increment in dietary calcium appears in the urine, whereas virtually all of an increased ingestion of water or sodium soon appears in the urine. The reason is that most of the dietary increment never gains entry to the blood because it fails

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If it is possible to single out one substance as being the most important in the control of sodium excretion and blood pressure, then that substance would be angiotensin II It is a potent vasoconstrictor and a mediator of multiple actions in the kidneys that affect sodium excretion Thus, it affects blood pressure directly as a vasoconstrictor and indirectly via regulation of renal sodium excretion There are many local RAS in individual tissues, including the kidneys, brain, and the heart There is also a global or systemic RAS which we normally consider to be the major renal regulator of blood pressure All RAS, whether global or local, consist of a large protein substrate called angiotensinogen, several enzymes and several products The key product is angiotensin II When angiotensin II binds to cell surface receptors, it initiates actions that affect blood pressure and excretion of sodium.

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The first key enzyme in all RAS is renin It acts on angiotensinogen to produce a small (10-amino-acid) product called angiotensin I Angiotensin I is acted upon by another enzyme, angiotensin-converting enzyme (ACE), to produce the highly active 8-amino-acid peptide angiotensin II In the global RAS, the source of angiotensinogen circulating in the blood is the liver The source of circulating renin is the granule cells in the kidney Renin is secreted both into the interstitium of the kidney and into the lumen of the afferent arterioles, where it acts on circulating angiotensinogen to produce circulating angiotensin I ACE, which is expressed on the luminal surface of endothelial cells in many parts of the vasculature, particularly in the lungs, then converts angiotensin I to angiotensin II We will describe the regulation of RAS in terms of the global system, in part because more is known about it.

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Investigators agree, however, that locally produced angiotensin II (and some related peptides) is the more important source in terms of regulating the kidneys because the levels of angiotensin II in renal tissues are far higher than can be accounted for by a systemic source It is presumed that global angiotensin II arriving in the renal blood supply acts synergistically with local angiotensin II as a regulator of function Circulating levels of angiotensinogen are usually fairly high and ACE activity usually converts most angiotensin I into angiotensin II Therefore, the primary determinant of circulating levels of angiotensin II is the amount of renin available to convert angiotensinogen to angiotensin I Consequently, to understand angiotensin II regulation of blood pressure, we require an understanding of the regulation of renin secretion What determines how much renin is secreted Two primary regulators have been described.

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In tissues where movement of dissolved gas (CO2 and O2) is quite rapid, a substantial amount of these gases may move through aquaporins.

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