Glomerular hemodynamic responses to pregnancy in rats with severe reduction of renal mass

A Deng, C Baylis - Kidney international, 1995 - Elsevier
A Deng, C Baylis
Kidney international, 1995Elsevier
Glomerular hemodynamic responses to pregnancy in rats with severe reduction of renal
mass. These studies investigate glomerular hemodynamic responses to pregnancy in rats
with 5/6th reduction of renal mass of four weeks duration. Both preglomerular and efferent
arteriolar resistances (RA and RE) fell significantly at midterm although single nephron
glomerular filtration rate (SNGFR) and glomerular plasma flow (QA) were unchanged versus
virgins. In late pregnant rats with reduction of renal mass, the gestational fall in RA and RE …
Glomerular hemodynamic responses to pregnancy in rats with severe reduction of renal mass. These studies investigate glomerular hemodynamic responses to pregnancy in rats with 5/6th reduction of renal mass of four weeks duration. Both preglomerular and efferent arteriolar resistances (RA and RE) fell significantly at midterm although single nephron glomerular filtration rate (SNGFR) and glomerular plasma flow (QA) were unchanged versus virgins. In late pregnant rats with reduction of renal mass, the gestational fall in RA and RE was maintained and GFR, RPF, SNGFR and QA were higher compared to virgins. The gestational renal vasodilation was prolonged in this model of hypertension versus normals and a peripheral vasodilation is also indicated by the late fall in blood pressure. In virgins with 5/6th reduction of renal mass, PGC; is elevated but in pregnant rats PGC fell towards term. The value of Kf was doubled in late pregnancy compared to virgins. All three groups of rats with reduction of renal mass showed similar proteinuria and similar levels of focal glomerular sclerosis, suggesting that pregnancy did not exacerbate the glomerular damage in this model of hypertension and renal disease. A decrease in hematocrit in late pregnancy compared with both virgin and midterm pregnancy indicated a plasma volume expansion. We conclude that when superimposed on hypertension with glomerular damage due to 5/6th reduction of renal mass, pregnancy induced gestational renal and peripheral vasodilation and plasma volume expansion. Since pregnancy was antihypertensive and lowered PGC, there was no hemodynamic basis for pregnancy-associated exacerbation of damage in this model of glomerular injury.
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