Renal Vasoconstrictor, but Not Vasodilator, Responses are Modified by Mild Passive Heat Stress in Humans

Abstract

Purpose The effect of heat stress on renal vascular control is not well studied. For instance, moderate passive heat stress attenuates the renal segmental artery vasoconstrictor response to the cold pressor test (CPT), a sympathoexcitatory stimulus. Whether this occurs with mild passive heat stress is unknown. Additionally, the vasodilatory response of the kidneys has never been studied during heat stress. Oral protein loading is a common approach used to elicit increases in renal blood flow. The purpose of this study was to test the hypothesis that both renal segmental artery vasoconstriction and vasodilation are attenuated during mild passive heat stress. Methods Twelve healthy adults (26 ± 1 y, 3 females) completed two experimental visits where they underwent passive heat stress or a normothermic time control trial in a randomized crossover design. In the heat stress trial, core temperature was increased ~0.5°C within the first hour and was maintained thereafter. Subjects completed a CPT one hour into heat stress which involved subjects immersing their right hand in an agitated ice slurry for 2 min. One hour post-CPT, subjects ingested a whey protein shake (1.2 g of protein/kg of body weight mixed with water). Renal segmental artery blood velocity (BV, Doppler ultrasound) and beat-to-beat blood pressure (Penaz method) were measured pre-CPT, in the final minute of CPT, pre-protein, and 150 min post-protein. Segmental artery vascular resistance (VR) was calculated as mean arterial pressure (MAP) divided by segmental artery BV. Data are presented as mean ± SD. Results Core temperature was higher pre-CPT (37.6 ± 0.5 vs 37.1 ± 0.5°C, P<0.01) and pre-protein (37.7 ± 0.4 vs 37.0 ± 0.4°C, P<0.01), and body fluid loss was greater (3.0 ± 0.9% vs. 1.5 ± 0.4%, P<0.01) in heat stress compared to normothermia. MAP did not differ pre-CPT between heat stress (80 ± 11 mmHg) and normothermia (84 ± 9 mmHg, P=0.76), but during the CPT was lower during heat stress (88 ± 18 vs. 113 ± 14 mmHg, P<0.01). Segmental BV did not differ pre-CPT between heat stress (22 ± 3 cm/s) and normothermia (22 ± 4 cm/s, P=0.99) or during the CPT (P = 0.56). Segmental VR pre-CPT did not differ between heat stress (3.8 ± 0.6 mmHg/cm/s) and normothermia (4.0 ± 0.7 mmHg/cm/s, P=0.91) but was lower in heat stress during the CPT (5.7 ± 1.1 vs. 4.6 ± 1.5 mmHg/cm/s, P=0.01). MAP did not differ pre-protein between heat stress (83 ± 9 mmHg) and normothermia (85 ± 9 mmHg, P=0.93), or post-protein (P=0.94). Segmental BV did not differ pre-protein between heat stress (22 ± 3 cm/s) and normothermia (22 ± 3 cm/s, P=0.99), or post-protein (P=0.36). Segmental VR was not different pre-protein between heat stress (3.9 ± 0.8 mmHg/cm/s, P=0.97) and normothermia (3.9 ± 0.6 mmHg/cm/s). Segmental VR decreased post-protein (P=0.03) but did not differ between heat stress (3.4 ± 0.9 mmHg/cm/s) and normothermia (3.5 ± 0.5 mmHg/cm/s, P=0.98). Conclusion Compared to normothermia, renal segmental artery vasoconstriction during a sympathetic stimulus is attenuated, but renal segmental artery vasodilation following a protein load is not affected by mild passive heat stress.