R.R. Warner

Bio: R.R. Warner is an academic researcher from Harvard University. The author has contributed to research in topics: Reabsorption & Microprobe. The author has an hindex of 6, co-authored 9 publications receiving 941 citations.

Ultramicroanalysis: x-ray spectrometry by electron probe excitation.

Abstract: UItramicroanalysis is the chemical analysis of very small amounts of material. In usual descriptions of ultra microanalytical methods, the minimum amount of sample needed for quantitative or even qualitative analysis is in the microliter volume range. Using these uItramicroanalytical methods, each chemical element is identified by a different reaction, more or less specific, more or less time consuming (1, 2). In this chapter we review a new ultramicroanalytical method, based on X-ray spectrometry by electron beam excitation [electron probe microanalysis (EPA)). EP A permits analysis of the chemical element content of liquid samples in the picoliter volume range 00-12 liter), and of cell and tissue samples in the femtoliter range (10-15 liter), at least five orders of magnitude smaller than in conventional ultramicroanalysis. Moreover, by using EPA, all the elements of the periodic table after boron can be quantitatively analyzed by the same method within the same sample with an absolute specificity. To fully exploit the capabilities of X-ray spectrometry by electron probe excita­ tion in biology, it is necessary to develop general methods of biological sample preparation. We do not attempt to review all the specific biological applications of EPA; instead, we outline the general methods of preparation that can be utilized and the general categories of biological samples that can be studied by EPA. We make large use of our particular experience, emphasizing the methods that can be routinely used, the difficulties encountered, and the perspectives offered. For more comprehensive descriptions of EPA of biological samples, the reader can refer to several recent reviews or books (3-8).

Isosmotic volume reabsorption in rat proximal tubule.

Abstract: A theoretical model incorporation both active and passive forces has been developed for fluid reabsorption from split oil droplets in rat intermediate and late proximal tubule. Of necessity, simplifying assumptions have been introduced; we have assumed that the epithelium can be treated as a single membrane and that the membrane "effective" HCO3 permeability is near zero. Based on this model with its underlying assumptions, the following conclusions are drawn. Regardless of the presence or absence of active NaCl transport, fluid reabsorption from the split oil droplet is isosmotic. The reabsorbate osmolarity can be affected by changes in tubular permeability parameters and applied forces but is not readily altered from an osmolarity essentially equal to that of plasma. In a split droplet, isosmotic flow need not be a special consequence of active Na transport, is not the result of a particular set of permeability properties, and is not merely a trivial consequence of a very high hydraulic conductivity; isosmotic flow can be obtained with hydraulic conductivity nearly an order of magnitude lower than that previously measured in the rat proximal convoluted tubule. Isosmotic reabsorption is, in part, the result of the interdependence of salt and water flows, their changing in parallel, and thus their ratio, the reabsorbate concentration being relatively invariant. Active NaCl transport can cause osmotic water flow by reducing the luminal fluid osmolarity. In the presence of passive forces the luminal fluid can be hypertonic to plasma, and active NaCl transport can still exert its osmotic effect on volume flow. There are two passive forces for volume flow: the Cl gradient and the difference in effective osmotic pressure; they have an approximately equivalent effect on volume flow. Experimentally, we have measured volume changes in a droplet made hyperosmotic by the addition of 50 mM NaCl; the experimental results are predicted reasonably well by our theoretical model.

A circulating inhibitor of (Na+ + K+) ATPase associated with essential hypertension

Abstract: The aetiology of essential hypertension, a disease prevalent in cultured societies, is unknown. However, much evidence suggests that abnormal sodium metabolism has a critical role—this has led to the hypothesis that an increase in the circulating concentration of an inhibitor of (Na+ + K+) ATPase is responsible for the increased peripheral vascular resistance in essential hypertension1. Evidence for relatively high levels of a Na+ pump inhibitor in essential hypertension has come from bioassay and cytochemical assays of plasma and urine from normotensive and hypertensive individuals2,3. There is also evidence for increased plasma levels of a Na+ pump inhibitor in some animal models (for example, renal and deoxycorticosterone acetate (DOCA) models) of hypertension4. Nevertheless, direct biochemical determination of (Na+ + K+) ATPase inhibition by this substance has not yet been reported. We demonstrate here, with a kinetic (Na+ + K+) ATPase assay, a highly significant correlation between levels of a plasma inhibitor of (Na+ + K+)ATPase activity and mean arterial blood pressure (MAP) in normotensive and hypertensive individuals. These data provide evidence for the involvement of a circulating Na+ pump inhibitor in the genesis of essential hypertension. Moreover, our assay methods may be useful for the isolation and characterization of this inhibitor.