In young spontaneously hypertensive rats, a rapidly acting intrarenal control mechanism provides efficient renal blood flow autoregulation independent of tubuloglomerular feedback.
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Findings in hypertensive rat models suggest preserved autoregulation post-obstruction independent of TGF; extends mechanistic insights but leaves open human applicability.
Experiments were conducted in 8-wk-old spontaneously hypertensive rats to determine whether tubuloglomerular feedback is essential for the autoregulation of renal blood flow. Autoregulation curves were obtained by measuring mean renal arterial blood pressure and flow during graded aortic occlusion. Renal vascular admittance was calculated from recordings of pulsatile renal arterial blood pressure and flow during induced atrial fibrillation. After a control period, acute ureteral obstruction was used to suppress tubuloglomerular feedback, as confirmed by measuring stop-flow pressure responses to rapid perfusion of Henle's loop. Ureteral obstruction did not impair steady-state autoregulation. During both the control and obstruction periods, the admittance gain was less than 1 at frequencies below 0.2 Hz, indicating dynamic autoregulatory activity. The control admittance contained two gain shoulders and two phase maxima, suggesting the presence of two control systems with response half-times of 1 and 10 s. During ureteral obstruction, the low-frequency shoulder and maximum disappeared, indicating that the slower system was no longer active. However, the high-frequency shoulder and maximum persisted, suggesting continued activity of the faster system. Collectively, these observations indicate the existence of a rapidly acting intrarenal control mechanism, in young spontaneously hypertensive rats, that may provide efficient autoregulation without assistance from tubuloglomerular feedback.
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Daniels et al. (1990) studied this question.
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