Kidney vasculature

US due to its ability to detect flow within vasculature on the micron level. Contrast-enhanced Doppler has proven successful in the detection and diagnosis of cancers, " detection of inflammation precursors, and brain imaging. Figure 3 shows an example of contrast-enhanced Doppler of a rabbit kidney using a poly(laaic-co-glycolic acid) (PLGA), air-filled UCA developed in our laboratory. After injection, UCAs within the kidney vasculature become apparent, providing substantial contour detection. 

Renal angiography (administration of intravenous contrast dye to assess the vasculature of the kidney)... 

Hypertension is the most common cardiovascular disease in fact, nearly 25% of adults in the U.S. are considered hypertensive. Hypertension is defined as a consistent elevation in blood pressure such that systolic/diastolic pressures are >140/90 mmHg. Over time, chronic hypertension can cause pathological changes in the vasculature and in the heart. As a result, hypertensive patients are at increased risk for atherosclerosis, aneurysm, stroke, myocardial infarction, heart failure, and kidney failure. There are several categories of antihypertensive agents ... 

Assuming the capsular pressures opposing the movement of water out of the blood and into the top of the nephron are constant, the net filtration pressure is due largely to the blood pressure. Any fall in blood pressure can have a dramatic effect on the efficiency of filtration and therefore clearance of waste materials. So important is the pressure within the renal vasculature that the kidney is critical in regulating systemic blood pressure via the renin-angiotensin-aldosterone (RAA) axis, a physiological process which relies on transport mechanisms within the renal tubules. 

Mechanism of Action An alpha-adrenergic agonist that stimulates alphaj-adrenergic receptors. Inhibits sympatheticcardioaccelerat or and vasoconstrictor center to heart, kidneys, peripheral vasculature. Therapeutic Effect Decreases systolic, diastolic blood pressure (BP). Chronic use decreases peripheral vascular resistance. Pharmacohinetics Well absorbed from gastrointestinal (GI) tract. Widely distributed. Protein binding 90%. Metabolized in liver. Excreted in urine and feces. Not removed by hemodialysis. Half-life 6 hr. 

Intravenous administration of dopamine promotes vasodilation of renal, splanchnic, coronary, cerebral, and perhaps other resistance vessels, via activation of Di receptors. Activation of the Di receptors in the renal vasculature may also induce natriuresis. The renal effects of dopamine have been used clinically to improve perfusion to the kidney in situations of oliguria (abnormally low urinary output). The activation of presynaptic D2 receptors suppresses norepinephrine release, but it is unclear if this contributes to cardiovascular effects of dopamine. In addition, dopamine activates Bj receptors in the heart. At low doses, peripheral resistance may decrease. At higher rates of infusion, dopamine activates vascular a. receptors, leading to vasoconstriction, including in the renal vascular bed. Consequently, high rates of infusion of dopamine may mimic the actions of epinephrine. 

AM is widely distributed in the body. The highest concentrations are found in the adrenal glands, hypothalamus, and anterior pituitary, but high levels are also present in the kidneys, lungs, cardiovascular system, and gastrointestinal tract. AM in plasma apparently originates in the heart and vasculature. 

Acute exposure to inorganic lead can cause reversible damage to the kidneys, manifested as tubular dysfunction. Chronic exposure to lead, however, causes permanent interstitial nephropathy, which involves tubular cell atrophy, pathological changes in the vasculature, and fibrosis. The most pronounced changes occur in the proximal tubules. Indeed, lead-protein complexes are seen as inclusion bodies in tubular cells, and the mitochondria in such cells have been shown to be altered with impaired oxidative phosphorylation. Clearly, this will influence the function of the proximal tubular cells in reabsorption and secretion of solutes and metabolites. Consequently, one indication of renal dysfunction is amino aciduria, glycosuria, and impairment of sodium reabsorption. 

FIGURE 21-1 Schematic diagram of the possible mechanisms in essential hypertension. Various factors interact to turn on sympathetic outflow to the kidneys, heart, and peripheral vasculature, resulting in elevated blood pressure. Hypertension also causes structural and functional changes in the vasculature that help maintain the elevated pressure. 

Peripheral vasculature and certain organs with a functional renin-angiotensin system (heart, kidneys]... 

The renal system consists of the kidneys and their vasculature and innervation, the kidneys each draining through a ureter into a single median urinary bladder, and the latter draining to the exterior via a single duct, the urethra. The kidney has three major anatomical areas the cortex, the medulla, and the papilla. 

If the underlying disease causes cardiac function to deteriorate despite expansion of plasma volume, the kidney continues to retain salt and water, which then leaks from the vasculature and becomes interstitial or pulmonary edema. At this point, diuretic use becomes necessary to reduce the accumulation of edema, particularly that which is in the lungs. Reduction of pulmonary vascular congestion with diuretics may actually improve oxygenation and thereby improve myocardial function. Edema associated with heart failure is generally managed with loop diuretics. In some instances, salt and water retention may become so severe that a combination of thiazides and loop diuretics is necessary. 

G. A. McDonald, G. Zhu, Y. Li, I. Kovesdi, T. J. Wickham, and V. P. Sukhatme, Efficient adenoviral gene transfer to kidney cortical vasculature utilizing a fiber modified vector, J. Gene Med. 7 103 (1999). 

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