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Biomedical subjects

I Ichikawa

Publications and source records attributed to I Ichikawa.

173 records · Page 10Linked to original sources
PubMed1977

Dynamics of glomerular ultrafiltration. IX. Effects of plasma protein concentration.

Experiments were carried out on 42 Munich-Wistar rats with surface glomeruli accessible to micropuncture to investigate the effects of reduction in systemic plasma protein concentration. CA, and thus afferent oncotic pressure, IIA, on the determinants of glomerular ultrafiltration. In animals in which CA was reduced by a variety of maneuvers, observed values for single-nephron GFR were lower than values predicted by the Starling relation, when the latter were calculated assuming that the observed increase in the net driving pressure for ultrafiltration (due to the reduction in IIA) was the only factor perturbed. In all experimental conditions where CA was reduced, rats were invariably observed to be at filtration pressure disequilibrium, permitting calculation of unique values of the ultrafiltration coefficient, Kt. In all low-CA groups, mean values of Kf were uniformly lower than values obtainedin normoproteinemic control animals. The failure of SNGFR to rise to predicted values when CA is reduced is therefore due to the concomitant reduction in Kf. No morphological basis for this reduction in Kf was discerned.

Animals↗
PubMed1977

Evidence for glomerular actions of ADH and dibutyryl cyclic AMP in the rat.

Experiments were performed on 54 chronically water diuretic Munich-Wistar rats to investigate the effects of various antidiuretic peptides on the determinants of glomerular ultrafiltration. Transition from water diuresis to antidiuresis, induced either by intravenous infusion of 1) exogenous peptides (Pitressin, synthetic arginine vasopressin, or synthetic [1-deamino,4-valine]-8-D-arginine vasopressin) or 2) dibutyryl cyclic AMP, or by stimulation of endogenous ADH release by acute, mild arterial hemorrhage, was associated with near-constant or decreased values for single nephron (SN) and total kidney GFR. Nevertheless, the glomerular transcapillary hydraulic pressure difference (deltaP) uniformly increased with antidiuresis, due to consistent reductions in Bowman's space hydraulic pressure rather than to increases in glomerular capillary hydraulic pressure, the former a consequence of the fall in urine flow rate. In all antidiuretic states, the rats were uniformly observed to be at filtration pressure disequilibrium, permitting calculation of unique values of the glomerular ultrafiltration coefficient (Kf). These values of Kf in antidiuresis were invariably lower than the values obtained during water diuresis. Whether these effects of ADH and DBcAMP on deltaP and Kf represent physiological influences in the control of GFR remains uncertain; their offsetting effects in the present studies usually failed to alter GFR appreciably.

Animals↗
PubMedDate not supplied

In vivo influence of prostaglandin I2 on systemic and renal circulation in the rat.

The effect of prostaglandin I2 and two other vasodilator agents, acetylcholine and sodium nitroprusside, on systemic and renal circulation was studied in 29 adult euvolemic Sprague-Dawley rats. Intra-aortic infusion of prostaglandin I2 (3.6 micrograms/kg/hr; n = 6 rats) produced significant vasodilation (p less than 0.05), as indicated by an average reduction in total peripheral vascular resistance of 24.8 +/- 2.0%, while renal vascular resistance remained essentially unchanged. Essentially identical findings were obtained in a separate group of six rats pretreated with intravenous administration of saralasin (0.5 mg/kg/hr). In contrast, in another group of six rats pretreated with saralasin, intraaortic infusion of acetylcholine (0.35 mg/kg/hr), which caused a reduction in total peripheral vascular resistance (21.4 +/- 3.8%) comparable to that induced by prostaglandin I2, produced a significant fall in renal vascular resistance (average, 27.7 +/- 5.0%) and, hence, an increase in renal blood flow (average, 26.2 +/- 2.9%). The effect of sodium nitroprusside (0.4 mg/kg/hr i.v.) was intermediate between those of prostaglandin I2 and acetylcholine: both renal vascular resistance and total peripheral vascular resistance fell mildly. These results indicate that prostaglandin I2, given in a dose sufficient to cause systemic vasodilation, fails to induce any discernible renal vasodilative response and that this absence of renal vasodilation by prostaglandin I2 in vivo is not due, as previously postulated, to the highly efficient offsetting influence of intrarenal angiotensin II release.

Acetylcholine↗