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Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana 70112
The dynamic activity of
afferent arteriolar diameter (AAD) and blood flow (AABF) responses to a
rapid step increase in renal arterial pressure (100-148 mmHg) was
examined in the kidneys of normal Sprague-Dawley rats
(n = 11) before [tubuloglomerular feedback (TGF)-intact] and after interruption of distal tubular flow
(TGF-independent). Utilizing the in vitro blood-perfused juxtamedullary
nephron preparation, fluctuations in AAD and erythrocyte velocity were
sampled by using analog-to-digital computerized conversion, video
microscopy, image shearing, and fast-frame, slow-frame techniques.
These assessments enabled dynamic characterization of the autonomous
actions and collective interactions between the myogenic and TGF
mechanisms at the level of the afferent arteriole. The TGF-intact and
TGF-independent systems exhibited common initial (0-24 vs.
0-13 s, respectively) response slope kinetics (
0.53 vs. 0.47%
AAD/s; respectively) yet different maximum vasoconstrictive
magnitude (11.28 ± 0.1 vs. 7.02 ± 0.9% AAD;
P < 0.05, respectively). The initial AABF responses
similarly exhibited similar kinetics but differing magnitudes. In
contrast, during the sustained pressure input (13-97 s), the maximum vasoconstrictor magnitude (7.02 ± 0.9% AAD) and
kinetics (0.01% AAD/s) of the TGF-independent system were
markedly blunted whereas the TGF-intact system exhibited continued
vasoconstriction with slower kinetics (0.20% AAD/s) until a
steady-state plateau was reached (25.9 ± 0.4% AAD). Thus
the TGF mechanism plays a role in both direct mediation of
vasoconstriction and in modulation of the myogenic response.
renal hemodynamics; frequency analysis; vascular resistance; myogenic response; dynamic analysis; tubuloglomerular feedback
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