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      Renal Myogenic Response : Kinetic Attributes and Physiological Role

      1 , 1 , 1
      Circulation Research
      Ovid Technologies (Wolters Kluwer Health)

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          Abstract

          The kinetic attributes of the afferent arteriole myogenic response were investigated using the in vitro perfused hydronephrotic rat kidney. Equations describing the time course for pressure-dependent vasoconstriction and vasodilation, and steady-state changes in diameter were combined to develop a mathematical model of autoregulation. Transfer functions were constructed by passing sinusoidal pressure waves through the model. These findings were compared with results derived using data from instrumented conscious rats. In each case, a reduction in gain and increase in phase were observed at frequencies of 0.2 to 0.3 Hz. We then examined the impact of oscillating pressure signals. The model predicted that pressure signals oscillating at frequencies above the myogenic operating range would elicit a sustained vasoconstriction the magnitude of which was dependent on peak pressure. These predictions were directly confirmed in the hydronephrotic kidney. Pressure oscillations presented at frequencies of 1 to 6 Hz elicited sustained afferent vasoconstrictions and the magnitude of the response depended exclusively on the peak pressure. Elevated systolic pressure elicited vasoconstriction even if mean pressure was reduced. These findings challenge the view that the renal myogenic response exists to maintain glomerular capillary pressure constant, but rather imply a primary role in protecting against elevated systolic pressures. Thus, the kinetic features of the afferent arteriole allow this vessel to adjust tone in response to changes in systolic pressures presented at the pulse rate. We suggest that the primary function of this mechanism is to protect the glomerulus from the blood pressure power that is normally present at the pulse frequency.

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          The case for intrarenal hypertension in the initiation and progression of diabetic and other glomerulopathies.

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            Paracrine regulation of the renal microcirculation.

            There has been an explosive growth of interest in the multiple interacting paracrine systems that influence renal microvascular function. This review first discusses the membrane activation mechanisms for renal vascular control. Evidence is provided that there are differential activating mechanisms regulating pre- and postglomerular arteriolar vascular smooth muscle cells. The next section deals with the critical role of the endothelium in the control of renal vascular function and covers the recent findings related to the role of nitric oxide and other endothelial-derived factors. This section is followed by an analysis of the roles of vasoactive paracrine systems that have their origin from adjoining tubular structures. The interplay of signals between the epithelial cells and the vascular network to provide feedback regulation of renal hemodynamics is developed. Because of their well-recognized contributions to the regulation of renal microvascular function, three major paracrine systems are discussed in separate sections. Recent findings related to the role of intrarenally formed angiotensin II and the prominence of the AT1 receptors are described. The possible contribution of purinergic compounds is then discussed. Recognition of the emerging role of extracellular ATP operating via P2 receptors as well as the more recognized functions of the P1 receptors provides fertile ground for further studies. In the next section, the family of vasoactive arachidonic acid metabolites is described. Possibilities for a myriad of interacting functions operating both directly on vascular smooth muscle cells and indirectly via influences on endothelial and epithelial cells are discussed. Particular attention is given to the more recent developments related to hemodynamic actions of the cytochrome P-450 metabolites. The final section discusses unique mechanisms that may be responsible for differential regulation of medullary blood flow by locally formed paracrine agents. Several sections provide perspectives on the complex interactions among the multiple mechanisms responsible for paracrine regulation of the renal microcirculation. This plurality of regulatory interactions highlights the need for experimental strategies that include integrative approaches that allow manifestation of indirect as well as direct influences of these paracrine systems on renal microvascular function.
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              Hemodynamic theory of progressive renal disease: a 10-year update in brief review.

              Experimental studies have suggested that glomerular hypertension is ultimately damaging to the kidney. Prevention of glomerular hypertension by dietary protein restriction or antihypertensive therapy lessens glomerular injury in several experimental models of chronic renal disease. Glomerular hypertension and hyperfiltration also occur in humans with diabetes mellitus, solitary or remnant kidneys, and various forms of acquired renal disease. Clinical studies are beginning to show that dietary protein restriction and antihypertensive therapy may slow progression in these disorders. Large multicenter trials are currently under way to better define the effects of these therapeutic maneuvers on the progression of chronic renal disease.
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                Author and article information

                Journal
                Circulation Research
                Circulation Research
                Ovid Technologies (Wolters Kluwer Health)
                0009-7330
                1524-4571
                June 28 2002
                June 28 2002
                : 90
                : 12
                : 1316-1324
                Affiliations
                [1 ]From the Smooth Muscle Research Group (R.L., L.C.), Department of Pharmacology and Therapeutics, The University of Calgary, Calgary, Alberta, Canada; and the Division of Nephrology and Hypertension (A.B.), Department of Medicine, Loyola University, Chicago, Hines Veteran’s Administration Medical Center, Maywood, Ill.
                Article
                10.1161/01.RES.0000024262.11534.18
                12089070
                60123f85-534a-4f4f-85a1-468e4d1bef46
                © 2002
                History

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