Effect of dopamine on the tubuloglomerular feedback mechanism
Schnermann, J.; Todd, K.M.; Briggs, J.P.
American Journal of Physiology 258(4 Pt 2): F790-F798
1990
ISSN/ISBN: 0002-9513 PMID: 2330978 Document Number: 360584
Experiments were performed in anesthetized rats to examine whether infusion dopamine is associated with a reduction in the tubuloglomerular feedback (TGF) response of stop-flow pressure (PSF) and early proximal flow rate (.ovrhdot.VEP) to increases of loop of Henle flow. The purpose of these studies was to test further the validity of the proposal that renal vasodilatation is a nonspecific cause for diminished TGF responsiveness. When femoral arterial pressure was kept constant with a suprarenal aortic clamp, intravenous infusion of dopamine at rates of 4, 15, 35, and 75 .mu.g .cntdot. kg-1 .cntdot. min-1 induced a 10.9, 23.4, 31.3, and 30.1% decrease in renal vascular resistance. Maximum PSF and .ovrhdot.VEP responses were significantly reduced at all dose levels of dopamine, whereas .ovrhdot.V1/2, the flow rate required to produce the half-maximum response, was not altered. TGF blunting occurred within < 10 min after starting the dopamine infusion. Peritubular infusion of dopamine reduced maximum PSF responses from 8.8 .+-. 0.7 to 4.6 .+-. 0.53 mmHg at 10-4 M (P < 0.01) and from 6.0 .+-. 1.19 to 3.6 .+-. 0.55 mmHg at 10-3 M (P < 0.05). The results are consistent with the notion that renal vasodilatation may modify TGF responses by preventing the full vasoconstrictor response to changes in luminal NaCl concentration.