AJP - Renal Physiology, Vol 244, Issue 2 95-104, Copyright © 1983 by American Physiological Society
Hormonal modulation of glomerular function
L. D. Dworkin, I. Ichikawa and B. M. Brenner
Glomeruli contain receptors for many hormones. Binding of angiotensin II
(ANG II) or antidiuretic hormone (ADH) to glomerular mesangial cells
elicits a contractile response. Other hormones induce synthesis of cyclic
nucleotides (cAMP, cGMP). Glomeruli also synthesize several prostaglandins,
renin, and ANG II. Micropuncture studies in Munich-Wistar rats have
examined the effects of vasoactive drugs and hormones on the filtration
process. Several vasodilators increase renal plasma flow in the dog and
rat, but GFR remains relatively unchanged due to an offsetting fall in the
ultrafiltration coefficient (Kf). Vasoconstrictor substances such as ANG II
and norepinephrine cause declines in renal plasma flow and Kf, but GFR
remains constant due to an increase in the transcapillary hydraulic
pressure gradient. Antidiuretic peptides and parathyroid hormone also
reduce Kf. Glomerular mesangial cells may regulate Kf by contracting and
reducing glomerular capillary surface area. ANG II and ADH directly
stimulate mesangial cell contraction in vitro. Other hormones appear to
cause contraction by inducing local ANG II synthesis. These hormonal
pathways are implicated in the pathogenesis of altered glomerular function
in diverse forms of renal injury.
