Mechanisms of action of hisamine and histamine antagonists on the glomerular microcirculation in the rat.

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Abstract
Preglomerular, glomerular and postglomerular pressures and flows were measured directly before and during intra-aortic infusion of a mildly vasodepressor dose of histamine in 20 Munich-Wistar rats. As with whole kidney GFR [glomerular filtration rate], single nephron (SN) GFR remained unchanged during histamine infusion, despite significant mean increases in total renal and glomerular plasma flow (QA) rates, and in mean glomerular capillary hydraulic pressure (.hivin.PGC). These hemodynamic changes were accompanied by proportionately greater reductions in afferent than in efferent arteriolar resistances. A decline in the glomerular capillary ultrafiltration coefficient, Kf, served to offset the increases in QA and .hivin.PGC, accounting for the near-constancy of SNGFR and GFR. Infusion of diphenhydramine, but not metiamide, largely prevented these histamine-induced changes in the glomerular microcirculation, indicating that, in the Munich-Wistar rat, the action of histamine on the glomerulus is channeled largely through an H1-receptor system. Fractional clearances of uncharged dextrans with molecular ratio of 20-42 .ANG., measured in a separate group of 5 rats, were unaffected by histamine infusion. Hydrodynamic theory describing transport of macromolecules through an isoporous membrane showed that histamine did not affect glomerular pore size but did produce a major reduction in the ratio of pore area:pore length, a measure of pore density. The finding of a histamine-induced decline in Kf and the results with dextrans suggest that the fall in Kf is due largely to a functional reduction in total filtration surface area.