Measurement of Renal Hemodynamics by Doppler Ultrasound during Sympathetic Activation while Heat Stressed
Authors: Benati Julia M , Chapman Christopher L , Johnson Blair D , Lema Penelope C , Gideon Elizabeth A , Abdul‐Rashed Jabril L , Solis Fernando E , Schlader Zachary J 
Published: June 2021

P‐aminohippurate clearance demonstrates that passive heat stress increases renal vascular resistance (RVR) in proportion to increases in core temperature. These heat stress evoked elevations in RVR are exacerbated during exercise, a sympathetic stimulus. Passive heat stress attenuates the vascular response to the cold pressor test (CPT), a non‐exercise sympathoexcitatory maneuver. However, the effect of passive heating on renal vascular responsiveness to a non‐exercise sympathoexcitatory stimulus is unknown.

Purpose

Test the hypothesis that passive heat stress augments increases in RVR during the CPT compared to normothermia.

Methods

Eight healthy adults (aged 22 ± 1 y, 3 F) completed a CPT by immersing their right hand in an agitated ice slurry mixture for 2 min during normothermia (Normothermia), and after intestinal temperature increased by 1.3 ± 0.1°C following passive heating with a water perfused suit (Heated). Mean arterial pressure (MAP, finger photoplethysmography), heart rate (HR, 3 lead ECG) and renal blood velocity (RBV) were measured at 1 min pre‐CPT, and at 1 and 2 min into the CPT (T1 and T2). RBV was assessed in the distal segment of the right renal artery during the same phase of the respiratory cycle via Doppler ultrasound (GE Vivid 7 Dimension). The coronal approach was utilized using a linear‐array transducer with a 2.5–3.5 MHz pulsed frequency, and participants assumed the left lateral recumbent position. All measurements were obtained by the same sonographer with the focal zone set to the artery's depth, and the transducer held in the same location at an insonation angle <60°. RVR was calculated as MAP/RBV. RBV and RVR were averaged across 2–4 beats. Data are presented as the absolute change from pre‐CPT (mean ± SD) unless otherwise stated.

Results

Pre‐CPT, MAP was lower (76 ± 8 vs 84 ± 7 mmHg; P<0.01) and HR was higher (101 ± 14 vs 60 ± 6 bpm; P<0.01) in Heated. RBV was lower (Heated: 31.3 ± 5.0 Normothermia: 34.9 ± 2.4 cm · s−1; P=0.05), but RVR did not differ (Heated: 2.5 ± 0.7, Normothermia: 2.4 ± 0.2 mmHg · cm−1 · s‐1; P=0.67) between Normothermia and Heated pre‐CPT. Elevations in MAP (T1: 22 ± 12; T2: 26 ± 13 mmHg) and HR (T1: 16 ± 8; T2: 13 ± 6 bpm) during Normothermia differed from the MAP (T1: 5 ± 3; T2: 2 ± 2 mmHg) and HR (T1: 3 ± 11; T2: 1 ± 10 bpm) response evoked by the CPT during Heated (P<0.01). Changes in RBV during the CPT did not differ between Heated and Normothermia at T1 (Heated: −2.5 ± 6.2; Normothermia: −4.0 ± 4.9 cm · s−1, P=0.94) or T2 (Heated: 0.9 ± 5.8; Normothermia: −4.0 ± 4.9 cm · s−1, P=0.97). Changes in RVR did not differ between Heated and Normothermia at T1 (Heated: 0.4 ± 0.6, Normothermia: 1.1 ± 1.0 mmHg · cm−1 · s‐1; P=0.10), but were lower in Heated at T2 (0.0 ± 0.4, vs 1.1 ± 1.0 mmHg · cm−1 · s‐1; P<0.02).

Conclusion

These data indicate that passive heat stress attenuates Doppler ultrasound derived measures of renal vascular responsiveness to the CPT, a non‐exercising sympathoexcitatory stimulus.

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.