Renal blood flow

Typical 24 h indices Filtered Nan-Filtered Cl-Filtered HCO-3 Filtered Kn-Renal blood flow Renal plasma flow Glomerular filtrate Urinary volume... 

The kidneys are an important pathway for elimination of drugs, and any impairment of renal function (e.g. decreased renal blood flow, renal damage) can cause marked increases in plasma concentrations of drugs eliminated primarily by renal mechanisms. 

Yu M. A peek at renal blood flow, renal function, and oxygen consumption with epinephrine and dopamine therapy. Crit Care Med 2000 28 1661-1663. 

Minoxidil (loniten) is efficacious in patients with the most severe and drug-resistant forms of hypertension. A small fraction of minoxidil is metabolized by hepatic sulfotransferase to the active molecule, minoxidil N-O sulfate. Minoxidil sulfate activates the ATP-modulated channel in smooth muscle, causing hyperpolarization and relaxation of arteriolar smooth muscle. Minoxidil produces arteriolar vasodilation with essentially no effect on capacitance vessels. Minoxidil preferentially increases blood flow to skin, skeletal muscle, the GI tract, and the heart. The disproportionate increase in blood flow to the heart may have a metabolic basis, in that administration of minoxidil is associated with a reflex increase in myocardial contractility and in cardiac output. The cardiac output can increase by as much as three- to fourfold, primarily due to enhanced venous return to the heart. The increased venous return probably results from enhanced flow in vascular beds with a fast response for venous return to the heart. The adrenergic increase in myocardial contractility contributes to the increased cardiac output, but is not the predominant factor. The renal effects of minoxidil are complex it dilates renal arteries, but systemic hypotension produced by the drug actually can decrease renal blood flow. Renal function usually improves in patients who take minoxidil for the treatment of hypertension, especially if renal dysfunction is secondary to hypertension. Minoxidil potently stimulates renin secretion, an effect mediated by renal sympathetic stimulation. 

Long-lasting vasoconstriction is produced by the ETs in almost all arteries and veins and several studies have shown that ET-1 causes a reduction in renal blood flow and urinary sodium excretion. ET-1 has been reported to be a potent mitogen in fibroblasts and aortic smooth muscle cells and to cause contraction of rat stomach strips, rat colon and guinea pig ileum. In the central nervous system, ETs have been shown to modulate neurotransmitter release. 

Kidney Function. Prostanoids influence a variety of kidney functions including renal blood flow, secretion of renin, glomerular filtration rate, and salt and water excretion. They do not have a critical role in modulating normal kidney function but play an important role when the kidney is under stress. Eor example, PGE2 and -I2 are renal vasodilators (70,71) and both are released as a result of various vasoconstrictor stimuli. They thus counterbalance the vasoconstrictor effects of the stimulus and prevent renal ischemia. The renal side effects of NSAIDS are primarily observed when normal kidney function is compromised. 

Moreover, digitahs has indirect effects on the circulation, which in normal hearts results in a small increase in arterial pressure, peripheral resistance, and cardiac output (114). The effects of digitahs on the circulation of an individual experiencing congestive heart failure are much more dramatic, however. The increased cardiac output, for example, increases renal blood flow which can reheve in part the edema of CHF associated with salt and water retention (114). 

Verapamil (Table 1), the first slow channel calcium blocker synthesized to selectively inhibit the transmembrane influx of calcium ions into cells, lowers blood pressure in hypertensive patients having good organ perfusion particularly with increased renal blood flow. Sustained-release verapamil for once a day dosing is available for the treatment of hypertension. Constipation is a prominent side effect. Headache, dizziness, and edema are frequent and verapamil can sometimes cause AV conduction disturbances and AV block. Verapamil should not be used in combination with -adrenoceptor blockers because of the synergistic negative effects on heart rate and contractile force. 

Hydralazine. Hydrala2iae causes vasodilation ia all primary vascular beds and has more pronounced effects on capacitance than on resistance blood vessels. Despite the hypotension it produces, hydrala2iae iacreases renal blood flow and cardiac output. PRA iacreases with its use. Tachycardia, headache, di22iaess, and water and sodium retention are principal side effects of hydrala2iae therapy. 

The clinical performance of a hemodialy2er is usually described in terms of clearance, a term having its roots in renal physiology, which is defined as the rate of solute removal divided by the inlet flow concentration as shown in equation 7, where Cl is clearance in ml,/min and all other terms are as defined previously except that, in deference to convention, flow rates are now expressed in minutes rather than seconds and feed side (/) is now synonymous with blood flow on the luminal side. 

Under normal conditions, ca 25% of the resting cardiac output passes through the kidney. Blood flowing through the renal artery and the afferent... 

Methybcanthine Diuretics. The mild diuretic effect of drinking coffee, from caffeine, and tea, mainly from theophylline, has been recogni2ed for along time. But the methylxanthines (Table 5) are of very limited efficacy when used as diuretics. The excretion of sodium and chloride ions are increased, but the potassium excretion is normal. Methylxanthines do not alter the urinary pH. Even though the methylxanthines have been demonstrated to have minor direct effects in the renal tubules, it is beUeved that they exert their diuretic effects through increased renal blood flow and GER (71). 

In the kidney, ANG II reduces renal blood flow and constricts preferentially the efferent arteriole of the glomerulus with the result of increased glomerular filtration pressure. ANG II further enhances renal sodium and water reabsorption at the proximal tubulus. ACE inhibitors thus increase renal blood flow and decrease sodium and water retention. Furthermore, ACE inhibitors are nephroprotective, delaying the progression of glomerulosclerosis. This also appears to be a result of reduced ANG II levels and is at least partially independent from pressure reduction. On the other hand, ACE inhibitors decrease glomerular filtration pressure due to the lack of ANG II-mediated constriction of the efferent arterioles. Thus, one important undesired effect of ACE inhibitors is impaired glomerular filtration rate and impaired kidney function. 

In the kidney, bradykinin increases renal blood flow, whereas glomerular filtration rate remains unaffected. 

As a general rule, increases of renal blood flow and/ or glomerular filtration rate (GFR) correlate rather well with increased urinary excretion of solutes and water. The underlying causes for this correlation are not fully understood, but they reflect incomplete adjustments of tubular reabsorption to an increase of tubular electrolyte load. 

As to be expected from a peptide that has been highly conserved during evolution, NPY has many effects, e.g. in the central and peripheral nervous system, in the cardiovascular, metabolic and reproductive system. Central effects include a potent stimulation of food intake and appetite control [2], anxiolytic effects, anti-seizure activity and various forms of neuroendocrine modulation. In the central and peripheral nervous system NPY receptors (mostly Y2 subtype) mediate prejunctional inhibition of neurotransmitter release. In the periphery NPY is a potent direct vasoconstrictor, and it potentiates vasoconstriction by other agents (mostly via Yi receptors) despite reductions of renal blood flow, NPY enhances diuresis and natriuresis. NPY can inhibit pancreatic insulin release and inhibit lipolysis in adipocytes. It also can regulate gut motility and gastrointestinal and renal epithelial secretion. 

Decreased serum proteins Decreased renal mass, blood flow, and glomerular filtration rate... 

West JR, Smith HW, Chasis H. 1948. Glomemlar filtration rate, effective renal blood flow, and maximal tubular excretory capacity in infancy. J Pediatr 32 10-18. 

Discontinue medications that may decrease renal blood flow... 

Finally, poor CO may contribute to diuretic resistance. In these patients, it may become necessary to add vasodilators or inotropes to enhance perfusion to the kidneys. Care must be taken, as vasodilators can decrease renal blood flow despite increasing CO through dilation of central and peripheral vascular beds. 

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