Abstract

Currently in renal physiology much investigative effort is being directed toward an assessment of the role of plasma colloid osmotic pressure (COP) in influencing both the rate of formation of glomerular ultrafiltrate and the rate of reabsorption of this ultrafiltrate by the renal tubules [1–4]. One important consequence of this process of ultrafiltration is that plasma undergoes a progressive increase in its protein concentration (and therefore in COP) in the course of traversing the glomerular capillary network, rising from approximately 6 g/100 ml in the afferent arteriole to values as high as 9 to 11 g/l00 ml in the efferent arteriole [1–3, 5, 6]. Thereafter, as a result of the return of reabsorbate to the postglomerular microcirculation, the concentration of protein declines from these high levels to values approaching pre-glomerular concentrations, the exact level being determined primarily by the volume of ultrafiltrate which escapes return to the renal circulation and instead leaves the kidney either as urine or lymph. At present no method is available for the direct measurement of COP in the small samples of blood which are obtainable from vessels in the postglomerular microcirculation using conventional micropuncture techniques. Instead the current approach to the estimation of COP in pre- and postglomerular blood makes use of 1) the measurement of total protein concentration in systemic and efferent arteriolar blood plasmas [1–3, 5–7], or the measurement of systemic protein concentration and the calculation of postglomerular protein concentration from simultaneous determination of filtration fraction [8], and 2) the application of one of several empirical equations which relate total protein concentration to COP [9]. The equation most frequently employed is that derived by Landis and Pappenheimer [9] for human plasma containing approximately equal concentrations of albumin and globulin (see equation 2 below).

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