In certain physiologic (low sodium intake) or pathologic conditions (decrease in volume of circulating blood because of hemorrhage or reduction in renal perfusion owing to compression of the renal arteries), juxtaglomerular cells are responsible for activating the renin–angiotensin–aldosterone system (RAAS). This system plays an important role in maintaining sodium homeostasis and renal hemodynamics. The granules of the juxtaglomerular cells contain an aspartyl protease, called renin, which is synthesized, stored, and released into the bloodstream from the modified smooth muscle cells. In the blood, renin catalyzes the hydrolysis of a circulating 2-globulin, angiotensinogen, to produce the  decapeptide angiotensin I. Then,  Angiotensin I is converted to the active octapeptide angiotensin II by angiotensin-converting enzyme (ACE) present on the endothelial cells of lung capillaries.
 Angiotensin II stimulates the synthesis and release of the hormone aldosterone from the zona glomerulosa of the adrenal gland (see page 766).
 Aldosterone, in turn, acts on collecting ducts to increase reabsorption of sodium and concomitant reabsorption of water, thereby raising blood volume and pressure.
with suspected renal disease. It typically includes several measurement of physical, biochemical, and microscopic urine characteristics such as pH, specific gravity (indirect measurement of ion concentration), bilirubin, concentration of intermediate compounds derived from the fatty acid metabolism known as ketone bodies, hemoglobin, and con-centration of the proteins. Important part of this analysis in-cludes the determination of the amount of protein excreted in the urine. The excretion of excessive amounts of protein (i.e., proteinuria [albuminuria]) is an important  diagnostic sign of renal disease. Normally, less than 150 mg of protein is of protein almost always indicates renal disease, extreme exercise, such as jogging, or severe dehydration may pro-duce increased proteinuria in individuals without renal dis-ease. Microscopic examination of the urine may reveal presence of red and white blood cells, mineral crystals, and pathogenic agents such as bacteria or fungi. Often these elements are enclosed within the cylindrical structures called urinary casts. The matrix of urinary cast is formed by an 85kilodalton protein, uromodulin (Tamm-Horsfall protein) that precipitate in the lumen of distal convoluted tubes and collecting ducts during a disease process.
 FOLDER 20.3 Clinical Correlation: Examination of the Urine—Urinalysis
Urinalysis is an important part of the examination of  patients excreted in the urine each day. Although excessive excretion
For years, cardiologists and nephrologists believed that chronic essential hypertension, the most common form of hypertension, was somehow related to an abnor-mality in the RAAS. However, 24-hour urine renin levels in such patients were usually normal. Not until a factor in the venom of a South American snake was shown to be a potent inhibitor of angiotensin-converting enzyme (ACE) in the lung did investigators have both a clue to the cause of chronic essential hypertension and a new series of drugs with which to treat this common disease. The “lesion” in chronic essential hypertension is now be-lieved to be excessive production of angiotensin II in the lung. Development of the so-called ACE inhibitors—captopril, enalapril, and related derivatives of the original snake venom factor—has revolutionized the treatment of chronic essential hypertension. These antihypertensive drugs do not cause the often-dangerous side effects of the diuretics and -blockers that were previously the most commonly used drugs for control of this condition.