Dynamic interaction between myogenic and TGF mechanisms in afferent arteriolar blood flow autoregulation

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Abstract
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% ΔAAD/s; respectively) yet different maximum vasoconstrictive magnitude (−11.28 ± 0.1 vs. −7.02 ± 0.9% ΔAAD;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% ΔAAD) and kinetics (−0.01% ΔAAD/s) of the TGF-independent system were markedly blunted whereas the TGF-intact system exhibited continued vasoconstriction with slower kinetics (−0.20% ΔAAD/s) until a steady-state plateau was reached (−25.9 ± 0.4% ΔAAD). Thus the TGF mechanism plays a role in both direct mediation of vasoconstriction and in modulation of the myogenic response.