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Am J Physiol Renal Physiol 254: F184-F190, 1988;
0363-6127/88 $5.00
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AJP - Renal Physiology, Vol 254, Issue 2 184-F190, Copyright © 1988 by American Physiological Society

ARTICLES

Renal adrenergic effector mechanisms: glomerular sites for prostaglandin interaction

J. C. Pelayo
Department of Pediatrics, University of Colorado Health Sciences Center, School of Medicine, Denver 80262.

Micropuncture experiments were performed in Munich-Wistar rats to ascertain the renal microcirculatory sites at which prostaglandins interact with the renal nerve and angiotensin II. Renal nerve stimulation (RNS) of 3 Hz alone decreased single-nephron glomerular filtration rate (SNGFR) by 30%, the consequence of 10 and 35% reductions in the glomerular capillary hydrostatic pressure difference (delta P) and the single-nephron plasma flow (SNPF), respectively. Pre- and postglomerular vascular resistances increased. RNS during prostaglandin inhibition (indomethacin) resulted in a 70% reduction in SNGFR, secondary to 1) a further diminution in delta P and in SNPF, via heightened pre- and postglomerular vasoconstriction and 2) a marked decline in the glomerular ultrafiltration coefficient (LpA), from 0.058 +/- 0.006 to 0.027 +/- 0.002 nl.s-1.mmHg-1.g kidney wt-1 (P less than 0.005). Acute angiotensin II inhibition (MK-421 and [Sar1,Ala8]angiotensin II) in rats pretreated with indomethacin partially attenuated the effects of RNS on vascular resistances and therefore on delta P, SNPF, and SNGFR and prevented the reduction in LpA. Thus vasodilatory prostaglandins act as local modulators of both renal nerve and angiotensin II constrictive actions on glomeruli and renal microcirculation.


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