Influence of angiotensin II and telmisartan on in vivo high-resolution renal arterial impedance in rats

Angiotensin II (ANG II) is known to play an important role in regulating renal hemodynamics. We sought to quantify this effect in an in vivo rat model with high-resolution renal arterial (RA) impedance. This study examines the effects of ANG II and its type 1 receptor blocker telmisartan (TELM) on RA impedance. In baroreflex-deactivated rats, we measured RA pressure (P-r) and blood flow (F-r) during random ventricular pacing to induce pressure fluctuation at three different mean P-r (60, 80, and 100 mmHg). We then estimated RA impedance as the transfer function from F-r to P-r. The RA impedance was found to align with a three-element Windkessel model consisting of proximal (R-p) and distal (R-d) resistance and compliance (C). Our study showed R-d reflected the composite characteristics of afferent and efferent arterioles. R-d increased with increasing P-r under the baseline condition with a slope of 1.03 +/- 0.21 (x 10(-1)) min<middle dot>mL(-1). ANG II significantly increased the slope by 0.72 +/- 0.29 (x 10(-1)) min<middle dot>mL(-1) (P < 0.05) without affecting the intercept. TELM significantly reduced the intercept by 34.49 +/- 4.86 (x 10(-1)) mmHg<middle dot>min<middle dot>mL(-1) (P < 0.001) from the baseline value of 37.93 +/- 13.36 (x 10(-1)) mmHg<middle dot>min<middle dot>mL(-1), whereas it did not affect the slope. In contrast, R-p was less sensitive than R-d to ANG II or TELM, suggesting R-p may represent the characteristics of elastic large arteries. Our findings provide valuable insights into the influence of ANG II on the dynamics of the renal vasculature. NEW & NOTEWORTHY This present method of quantifying high-resolution renal arterial impedance could contribute to elucidating the characteristics of renal vasculature influenced by physiological mechanisms, renal diseases, or pharmacological effects. The present findings help construct a lumped-parameter renal hemodynamic model that reflects the influence of angiotensin II.