Cool head-out water immersion does not alter cerebrovascular reactivity to hypercapnia despite elevated middle cerebral artery blood velocity: A pilot study.

Episodic increases in cerebral blood flow (CBF) are thought to contribute to improved cerebrovascular function and health. Head-out water immersion (HOWI) may be a useful modality to increase CBF secondary to the hydrostatic pressure placed on the body. However, it is unclear whether water temperatures common to the general public elicit similar cerebrovascular responses. We tested the hypothesis that mean middle cerebral artery blood velocity (MCAvmean) and cerebrovascular reactivity to CO2 (CVRCO2) would be higher during an acute bout of thermoneutral (TN; 35°C) vs. cool (COOL; 25°C) HOWI. Ten healthy participants (age: 23±3 y; 4 women) completed two randomized HOWI visits. Right MCAvmean, end-tidal CO2 (PETCO2) mean arterial pressure (MAP), and MCA conductance (MCAvmean/MAP) were continuously recorded. CVRCO2 was assessed using a stepped hypercapnia protocol before (PRE), at 30 minutes of HOWI (HOWI), immediately after HOWI (POST-1), and 45 minutes after HOWI (POST-2). Absolute values are reported as mean ± SD. MCAvmean, PETCO2, MAP, and CVRCO2 were not different between conditions at any timepoint (all P≥0.17). In COOL, MCAvmean increased from PRE (61±9 cm/s) during HOWI (68±11 cm/s), at POST-1 (69±11 cm/s), and POST-2 (72±8 cm/s) (all P<0.01), and in TN from PRE to POST-1 (66±13 vs. 71±14 cm/s; P = 0.05). PETCO2 did not change over time in either condition. In COOL, MAP increased from PRE (85±5 mmHg) during HOWI (101±4 mmHg), at POST-1 (97±7 mmHg), and POST-2 (96±9 mmHg), and in TN from PRE (88±5 mmHg) at HOWI (98±7 mmHg) and POST-1 (99±8 mmHg) (all P<0.01). In COOL, CVRCO2 increased from PRE to HOWI (1.66±0.55 vs. 1.92±0.52 cm/s/mmHg; P = 0.04). MCA conductance was not different between or within conditions. These data indicate that 30 minutes of cool HOWI augments MCAvmean and that the increase in MCAvmean persists beyond cool HOWI. However, cool HOWI does not alter CVRCO2 in healthy young adults.

Hypohydration attenuates increases in creatinine clearance to oral protein loading and the renal hemodynamic response to exercise pressor reflex.

Insufficient hydration is prevalent among free living adults. This study investigated whether hypohydration alters 1) renal functional reserve, 2) the renal hemodynamic response to the exercise pressor reflex, and 3) urine-concentrating ability during oral protein loading. In a block-randomized crossover design, 22 healthy young adults (11 females and 11 males) underwent 24-h fluid deprivation (Hypohydrated) or 24-h normal fluid consumption (Euhydrated). Renal functional reserve was assessed by oral protein loading. Renal hemodynamics during the exercise pressor reflex were assessed via Doppler ultrasound. Urine-concentrating ability was assessed via free water clearance. Creatinine clearance did not differ at 150 min postprotein consumption between conditions [Hypohydrated: 246 mL/min, 95% confidence interval (CI): 212-280; Euhydrated: 231 mL/min, 95% CI: 196-265, P = 0.2691] despite an elevated baseline in Hypohydrated (261 mL/min, 95% CI: 218-303 vs. 143 mL/min, 95% CI: 118-168, P < 0.0001). Renal artery vascular resistance was not different at baseline (P = 0.9290), but increases were attenuated in Hypohydrated versus Euhydrated at the end of handgrip (0.5 mmHg/cm/s, 95% CI: 0.4-0.7 vs. 0.8 mmHg/cm/s 95% CI: 0.6-1.1, P = 0.0203) and end occlusion (0.2 mmHg/cm/s, 95% CI: 0.1-0.3 vs. 0.4 mmHg/cm/s 95% CI: 0.3-0.6, P = 0.0127). There were no differences between conditions in free water clearance at 150 min postprotein (P = 0.3489). These data indicate that hypohydration 1) engages renal functional reserve and attenuates the ability to further increase creatinine clearance, 2) attenuates increases in renal artery vascular resistance to the exercise pressor reflex, and 3) does not further enhance nor impair urine-concentrating ability during oral protein loading.NEW & NOTEWORTHY Insufficient hydration is prevalent among free living adults. This study found that hypohydration induced by 24-h fluid deprivation engaged renal functional reserve and that oral protein loading did not further increase creatinine clearance. Hypohydration also attenuated the ability to increase renal vascular resistance during the exercise pressor reflex. In addition, hypohydration neither enhanced nor impaired urine-concentrating ability during oral protein loading. These data support the importance of mitigating hypohydration in free living adults.

Cardiovascular and mood responses to an acute bout of cold water immersion.

Cold water immersion (CWI) may provide benefits for physical and mental health. Our purpose was to investigate the effects of an acute bout of CWI on vascular shear stress and affect (positive and negative). Sixteen healthy adults (age: 23 ± 4 y; (9 self-reported men and 7 self-reported women) completed one 15-min bout of CWI (10 °C). Self-reported affect (positive and negative) was assessed at pre-CWI (Pre), 30-min post-immersion, and 180-min post-immersion in all participants. Brachial artery diameter and blood velocity were measured (Doppler ultrasound) at Pre, after 1-min and 15-min of CWI, and 30-min post-immersion (n = 8). Total, antegrade, and retrograde shear stress, oscillatory shear index (OSI), and forearm vascular conductance (FVC) were calculated. Venous blood samples were collected at Pre, after 1-min and 15-min of CWI, 30-min post-immersion, and 180-min post-immersion (n = 8) to quantify serum ß-endorphins and cortisol. Data were analyzed using a one-way ANOVA with Fisher's least significance difference and compared to Pre. Positive affect did not change (ANOVA p = 0.450) but negative affect was lower at 180-min post-immersion (p < 0.001). FVC was reduced at 15-min of CWI and 30-min post-immersion (p < 0.020). Total and antegrade shear and OSI were reduced at 30-min post-immersion (p < 0.040) but there were no differences in retrograde shear (ANOVA p = 0.134). ß-endorphins did not change throughout the trial (ANOVA p = 0.321). Cortisol was lower at 180-min post-immersion (p = 0.014). An acute bout of CWI minimally affects shear stress patterns but may benefit mental health by reducing negative feelings and cortisol levels.

Acute kidney injury biomarkers and hydration assessments following prolonged mild hypohydration in healthy young adults.

The high prevalence of inadequate hydration (e.g., hypohydration and underhydration) is concerning given that extreme heat increases excess hospitalizations for fluid/electrolyte disorders and acute kidney injury (AKI). Inadequate hydration may also be related to renal and cardiometabolic disease development. This study tested the hypothesis that prolonged mild hypohydration increases the urinary AKI biomarker product of insulin-like growth factor-binding protein 7 and tissue inhibitor of metalloproteinase-2 ([IGFBP7·TIMP-2]) compared with euhydration. In addition, we determined the diagnostic accuracy and optimal cutoffs of hydration assessments for discriminating positive AKI risk ([IGFBP·TIMP-2] >0.3 (ng/mL)2/1,000). In a block-randomized crossover design, 22 healthy young adults (11 females and 11 males) completed 24 h of fluid deprivation (hypohydrated group) or 24 h of normal fluid consumption (euhydrated group) separated by ≥72 h. Urinary [IGFBP7·TIMP-2] and other AKI biomarkers were measured following the 24-h protocols. Diagnostic accuracy was assessed via receiver operating characteristic curve analysis. Urinary [IGFBP7·TIMP-2] [1.9 (95% confidence interval: 1.0-2.8) vs. 0.2 (95% confidence interval: 0.1-0.3) (ng/mL)2/1,000, P = 0.0011] was markedly increased in hypohydrated versus euhydrated groups. Urine osmolality (area under the curve: 0.91, P < 0.0001) and urine specific gravity (area under the curve: 0.89, P < 0.0001) had the highest overall performance for discriminating positive AKI risk. Optimal cutoffs with a positive likelihood ratio of 11.8 for both urine osmolality and specific gravity were 952 mosmol/kgH2O and 1.025 arbitrary units. In conclusion, prolonged mild hypohydration increased urinary [IGFBP7·TIMP-2] in males and females. Urinary [IGFBP7·TIMP-2] corrected to urine concentration was elevated in males only. Urine osmolality and urine specific gravity may have clinical utility for discriminating positive AKI risk following prolonged mild hypohydration.NEW & NOTEWORTHY This study found that prolonged mild hypohydration in healthy young adults increased the Food and Drug Administration approved acute kidney injury (AKI) biomarker urinary insulin-like growth factor-binding protein 7 and tissue inhibitor of metalloproteinase-2 [IGFBP7·TIMP-2]. Urine osmolality and specific gravity demonstrated an excellent ability to discriminate positive AKI risk. These findings emphasize the importance of hydration in protecting renal health and lend early support for hydration assessment as an accessible tool to assess AKI risk.

Acute beetroot juice consumption does not alter cerebral autoregulation or cardiovagal baroreflex sensitivity during lower-body negative pressure in healthy adults.

Introduction: Beetroot juice (BRJ) improves peripheral endothelial function and vascular compliance, likely due to increased nitric oxide bioavailability. It is unknown if BRJ alters cerebrovascular function and cardiovagal baroreflex control in healthy individuals. Purpose: We tested the hypotheses that BRJ consumption improves cerebral autoregulation (CA) and cardiovagal baroreflex sensitivity (cBRS) during lower-body negative pressure (LBNP). Methods: Thirteen healthy adults (age: 26 ± 4 years; 5 women) performed oscillatory (O-LBNP) and static LBNP (S-LBNP) before (PRE) and 3 h after consuming 500 mL of BRJ (POST). Participants inhaled 3% CO2 (21% O2, 76% N2) during a 5 min baseline and throughout LBNP to attenuate reductions in end-tidal CO2 tension (PETCO2). O-LBNP was conducted at ∼0.02 Hz for six cycles (-70 mmHg), followed by a 3-min recovery before S-LBNP (-40 mmHg) for 7 min. Beat-to-beat middle cerebral artery blood velocity (MCAv) (transcranial Doppler) and blood pressure were continuously recorded. CA was assessed using transfer function analysis to calculate coherence, gain, and phase in the very-low-frequency (VLF; 0.020-0.070 Hz) and low-frequency bands (LF; 0.07-0.20 Hz). cBRS was calculated using the sequence method. Comparisons between POST vs. PRE are reported as mean ± SD. Results: During O-LBNP, coherence VLF was greater at POST (0.55 ± 0.06 vs. 0.46 ± 0.08; P < 0.01), but phase VLF (P = 0.17) and gain VLF (P = 0.69) were not different. Coherence LF and phase LF were not different, but gain LF was lower at POST (1.03 ± 0.20 vs. 1.12 ± 0.30 cm/s/mmHg; P = 0.05). During S-LBNP, CA was not different in the VLF or LF bands (all P > 0.10). Up-cBRS and Down-cBRS were not different during both LBNP protocols. Conclusion: These preliminary data indicate that CA and cBRS during LBNP in healthy, young adults is largely unaffected by an acute bolus of BRJ.

Cerebral vascular function following the acute consumption of caffeinated artificially- and sugar sweetened soft drinks in healthy adults.

Chronic consumption of sugar- and artificially-sweetened beverages (SSB and ASB) are associated with an increased risk of stroke but it is unclear how acute consumption influences cerebral vascular function. Purpose: We hypothesized that: (1) acute consumption of SSB and ASB would augment dynamic cerebral autoregulation (dCA) and attenuate cerebral vascular reactivity to hypercapnia (CVRCO2) compared to water; and (2) dCA and CVRCO2 would be attenuated with SSB compared to ASB and water. Methods: Twelve healthy adults (age: 23 ± 2 years, four females) completed three randomized trials where they drank 500 ml of water, SSB (Mountain Dew®), or ASB (Diet Mountain Dew®). We measured mean arterial pressure (MAP), middle and posterior cerebral artery blood velocities (MCAv and PCAv), and end-tidal CO2 tension (PETCO2). Cerebral vascular conductance was calculated as cerebral artery blood velocity/MAP (MCAc and PCAc). Twenty min after consumption, participants completed a 5 min baseline, and in a counterbalanced order, a CVRCO2 test (3%, 5%, and 7% CO2 in 3 min stages) and a dCA test (squat-stand tests at 0.10 Hz and 0.05 Hz for 5 min each) separated by 10 min. CVRCO2 was calculated as the slope of the linear regression lines of MCAv and PCAv vs. PETCO2. dCA was assessed in the MCA using transfer function analysis. Coherence, gain, and phase were determined in the low frequency (LF; 0.07-0.2 Hz) and very low frequency (VLF; 0.02-0.07 Hz). Results: MCAv and MCAc were lower after SSB (54.11 ± 12.28 cm/s, 0.58 ± 0.15 cm/s/mmHg) and ASB (51.07 ± 9.35 cm/s, 0.52 ± 1.0 cm/s/mmHg) vs. water (62.73 ± 12.96 cm/s, 0.67 ± 0.11 cm/s/mmHg; all P < 0.035), respectively. PCAc was also lower with the ASB compared to water (P = 0.007). MCA CVRCO2 was lower following ASB (1.55 ± 0.38 cm/s/mmHg) vs. water (2.00 ± 0.57 cm/s/mmHg; P = 0.011) but not after SSB (1.90 ± 0.67 cm/s/mmHg; P = 0.593). PCA CVRCO2 did not differ between beverages (P > 0.853). There were no differences between beverages for coherence (P ≥ 0.295), gain (P ≥ 0.058), or phase (P ≥ 0.084) for either frequency. Discussion: Acute consumption of caffeinated SSB and ASB resulted in lower intracranial artery blood velocity and conductance but had a minimal effect on cerebral vascular function as only MCA CVRCO2 was altered with the ASB compared to water.

Hot head-out water immersion does not acutely alter dynamic cerebral autoregulation or cerebrovascular reactivity to hypercapnia.

Recurring hot head-out water immersion (HOWI) enhances peripheral vascular function and cerebral blood velocity during non-immersion conditions. However, it is unknown if an acute bout of hot HOWI alters cerebrovascular function. Using two experimental studies, we tested the hypotheses that dynamic cerebral autoregulation (dCA) and cerebrovascular reactivity (CVR) are improved during an acute bout of hot (HOT; 39 °C) vs. thermoneutral (TN; 35 °C) HOWI. Eighteen healthy participants (eight females) completed the dCA study, and 14 participants (6 females) completed the CVR study. Both studies consisted of two randomized (TNdCA vs. HOTdCA; TNCVR vs. HOTCVR) 45minute HOWI visits. Middle cerebral artery blood velocity (MCAvmean) was continuously recorded. dCA was assessed using a respiratory impedance device and analyzed via transfer gain and phase in the low-frequency band. CVR was assessed using stepped hypercapnia. Assessments were completed PRE and 30 minutes into HOWI. Values are reported as a change (Δ) from PRE (mean ± SD). There were no differences at PRE for either study. ΔMCAvmean was greater in TNdCA (TNdCA: 4 ± 4 vs. HOTdCA: -3 ± 5 cm/s; P < 0.01) and TNCVR (TNCVR: 5 ± 4 vs. HOTCVR: -1 ± 6 cm/s; P < 0.01) during HOWI. ΔGain was greater in HOTdCA during HOWI (TNdCA: -0.09 ± 0.15 vs. HOTdCA: 0.10 ± 0.17 cm/s/mmHg; P = 0.04). ΔPhase (P > 0.84) and ΔCVR (P > 0.94) were not different between conditions. These data indicate that hot and thermoneutral water immersion do not acutely alter cerebrovascular function in healthy, young adults.

Acute Beetroot Juice Ingestion Does Not Alter Renal Hemodynamics during Normoxia and Mild Hypercapnia in Healthy Young Adults.

Arterial hypercapnia reduces renal perfusion. Beetroot juice (BRJ) increases nitric oxide bioavailability and may improve renal blood flow. We tested the hypothesis that acute consumption of BRJ attenuates both decreases in blood velocity and increases in vascular resistance in the renal and segmental arteries during acute hypercapnia. In fourteen healthy young adults, blood velocity and vascular resistance were measured with Doppler ultrasound in the renal and segmental arteries during five minutes of breathing a carbon dioxide gas mixture (CO2) before and three hours after consuming 500 mL of BRJ. There was no difference between pre- and post-BRJ consumption in the increase in the partial pressure of end-tidal CO2 during CO2 breathing (pre: +4 ± 1 mmHg; post: +4 ± 2 mmHg, p = 0.4281). Segmental artery blood velocity decreased during CO2 breathing in both pre- (by -1.8 ± 1.9 cm/s, p = 0.0193) and post-BRJ (by -2.1 ± 1.9 cm/s, p = 0.0079), but there were no differences between pre- and post-consumption (p = 0.7633). Segmental artery vascular resistance increased from room air baseline during CO2 at pre-BRJ consumption (by 0.4 ± 0.4 mmHg/cm/s, p = 0.0153) but not post-BRJ (p = 0.1336), with no differences between pre- and post-consumption (p = 0.7407). These findings indicate that BRJ consumption does not attenuate reductions in renal perfusion during acute mild hypercapnia in healthy young adults.

Voluntary Cooling during Exercise Is Augmented in People with Multiple Sclerosis Who Experience Heat Sensitivity.

INTRODUCTION: We tested the hypothesis that people with multiple sclerosis (MS) who experience heat sensitivity voluntarily engage in cool-seeking behavior during exercise to a greater extent than healthy controls. METHODS: In a 27.0°C ± 0.2°C, 41% ± 2% RH environment, seven participants with relapsing-remitting MS who exhibited heat sensitivity and seven healthy controls completed two randomized trials cycling for 40 min (EX) at 3.5 W·kg-1 metabolic heat production, followed by 30 min recovery (REC). In one trial, participants were restricted from engaging in cooling (CON). In the other trial, participants voluntarily pressed a button to receive 2 min of ~2°C water perfusing a top (COOL). Mean skin and core temperatures and mean skin wettedness were recorded continuously. Total time in cooling provided an index of cool-seeking behavior. RPE, total symptom scores (MS only), and subjective fatigue (MS only) were recorded every 10 min. RESULTS: Core temperature (+0.5°C ± 0.1°C) and skin wettedness (+0.53 ± 0.02 a.u.) increased but were not different between groups or trials at end exercise (P = 0.196) or end recovery (P = 0.342). Mean skin temperature was reduced in COOL compared with CON at end exercise (P ≤ 0.002), with no differences between groups (P ≥ 0.532). MS spent more total time in cooling during EX (MS, 13 ± 3 min; healthy, 7 ± 4 min; P < 0.001) but not REC (MS, 2 ± 1 min; healthy, 0 ± 1 min; P = 0.496). RPE was greater at end exercise in MS (P = 0.001). Total symptom scores increased during exercise (P = 0.005) but was not different between trials (P = 0.321), whereas subjective fatigue was not attenuated in the cooling trial (P = 0.065). CONCLUSION: Voluntary cooling is augmented in MS but does not consistently mitigate perceptions of heat-related symptoms or subjective fatigue.

Sugar-sweetened soft drink consumption acutely decreases spontaneous baroreflex sensitivity and heart rate variability.

In healthy humans, fructose-sweetened water consumption increases blood pressure variability (BPV) and decreases spontaneous cardiovagal baroreflex sensitivity (cBRS) and heart rate variability (HRV). However, whether consuming commercially available soft drinks containing high levels of fructose elicits similar responses is unknown. We hypothesized that high-fructose corn syrup (HFCS)-sweetened soft drink consumption increases BPV and decreases cBRS and HRV to a greater extent compared with artificially sweetened (diet) and sucrose-sweetened (sucrose) soft drinks and water. Twelve subjects completed four randomized, double-blinded trials in which they drank 500 mL of water or commercially available soft drinks matched for taste and caffeine content. We continuously measured beat-to-beat blood pressure (photoplethysmography) and R-R interval (ECG) before and 30 min after drink consumption during supine rest for 5 min during spontaneous and paced breathing. BPV was evaluated using standard deviation (SD), average real variability (ARV), and successive variation (SV) methods for systolic and diastolic blood pressure. cBRS was assessed using the sequence method. HRV was evaluated using the root mean square of successive differences (RMSSD) in R-R interval. There were no differences between conditions in the magnitude of change from baseline in SD, ARV, and SV (P ≥ 0.07). There were greater reductions in cBRS during spontaneous breathing in the HFCS (-3 ± 5 ms/mmHg) and sucrose (-3 ± 5 ms/mmHg) trials compared with the water trial (+1 ± 5 ms/mmHg, P < 0.03). During paced breathing, HFCS evoked greater reductions in RMSSD compared with water (-26 ± 34 vs. +2 ± 26 ms, P < 0.01). These findings suggest that sugar-sweetened soft drink consumption alters cBRS and HRV but not BPV.

Blunted Cardiac Parasympathetic Activation in Student Athletes With a Remote History of Concussion: A Pilot Study.

Introduction: Blunted cardiac autonomic nervous system (ANS) responses, quantified using heart rate variability (HRV), have been reported after sport-related concussion (SRC). Research suggests this persists beyond clinical recovery. This study compared cardiac parasympathetic responses in student athletes with a remote history of SRC (> 1-year ago, Concussion History: CH) with those who reported no lifetime history of SRC (Concussion Naïve: CN). Design: Retrospective nested case-control. Setting: University laboratory. Patients or Other Participants: CH (n = 9, 18.3 ± 2 years, 44% male, median 2 years since injury) were student athletes with a remote history of concussion(s) from more than 1 year ago. CN (n = 21, 16.7 ± 3 years, 67% male) were student athletes with no lifetime history of concussion. Exclusion criteria included taking medications that could affect ANS function, history of concussion within the past year, persistent concussion symptoms, lifetime history of moderate to severe brain injury, and lifetime history of more than 3 concussions. Material and Methods: Participants performed the Face Cooling (FC) test for 3-min after 10-min of supine rest while wearing a 3-lead electrocardiogram in a controlled environment. Outcome Measures: Heart rate (HR), R-R interval (RRI), root mean square of the successive differences (RMSSD) of RRI, high frequency (HF) and low frequency to HF (LF:HF) ratios. Results: At baseline, CH had a lower resting HR than CN (62.3 ± 11 bpm vs. 72.9 ± 12, p = 0.034). CH had a different HR response to FC than CN (+8.9% change from baseline in CH vs. -7.5% in CN, p = 0.010). CH also had a smaller RMSSD increase to FC than CN (+31.8% change from baseline in CH vs. +121.8% in CN, p = 0.048). There were no significant group differences over time in RRI (p = 0.106), HF (p = 0.550) or LF:HF ratio (p = 0.053). Conclusion: Asymptomatic student athletes with a remote history of concussion had a blunted cardiac parasympathetic response to FC when compared with athletes with no lifetime history of concussion. These data suggest that an impaired autonomic response to a physiological stressor persists after clinical recovery from SRC for longer than previously reported.

High-fructose corn syrup-sweetened soft drink consumption increases vascular resistance in the kidneys at rest and during sympathetic activation.

We first tested the hypothesis that consuming a high-fructose corn syrup (HFCS)-sweetened soft drink augments kidney vasoconstriction to sympathetic stimulation compared with water (study 1). In a second study, we examined the mechanisms underlying these observations (study 2). In study 1, 13 healthy adults completed a cold pressor test, a sympathoexcitatory maneuver, before (preconsumption) and 30 min after drinking 500 mL of decarbonated HFCS-sweetened soft drink or water (postconsumption). In study 2, venous blood samples were obtained in 12 healthy adults before and 30 min after consumption of 500 mL water or soft drinks matched for caffeine content and taste, which were either artificially sweetened (Diet trial), sucrose-sweetened (Sucrose trial), or sweetened with HFCS (HFCS trial). In both study 1 and study 2, vascular resistance was calculated as mean arterial pressure divided by blood velocity, which was measured via Doppler ultrasound in renal and segmental arteries. In study 1, HFCS consumption increased vascular resistance in the segmental artery at rest (by 0.5 ± 0.6 mmHg·cm-1·s-1, P = 0.01) and during the cold pressor test (average change: 0.5 ± 1.0 mmHg·cm-1·s-1, main effect: P = 0.05). In study 2, segmental artery vascular resistance increased in the HFCS trial (by 0.8 ± 0.7 mmHg·cm-1·s-1, P = 0.02) but not in the other trials. Increases in serum uric acid were greater in the HFCS trial (0.3 ± 0.4 mg/dL, P ≤ 0.04) compared with the Water and Diet trials, and serum copeptin increased in the HFCS trial (by 0.8 ± 1.0 pmol/L, P = 0.06). These findings indicate that HFCS acutely increases vascular resistance in the kidneys, independent of caffeine content and beverage osmolality, which likely occurs via simultaneous elevations in circulating uric acid and vasopressin.

Renal and segmental artery hemodynamic response to acute, mild hypercapnia.

Profound increases (>15 mmHg) in arterial carbon dioxide (i.e., hypercapnia) reduce renal blood flow. However, a relatively brief and mild hypercapnia can occur in patients with sleep apnea or in those receiving supplemental oxygen therapy during an acute exacerbation of chronic obstructive pulmonary disease. We tested the hypothesis that a brief, mild hypercapnic exposure increases vascular resistance in the renal and segmental arteries. Blood velocity in 14 healthy adults (26 ± 4 yr; 7 women, 7 men) was measured in the renal and segmental arteries with Doppler ultrasound while subjects breathed room air (Air) and while they breathed a 3% CO2, 21% O2, 76% N2 gas mixture for 5 min (CO2). The end-tidal partial pressure of CO2 ([Formula: see text]) was measured via capnography. Mean arterial pressure (MAP) was measured beat to beat via the Penaz method. Vascular resistance in the renal and segmental arteries was calculated as MAP divided by blood velocity. [Formula: see text] increased with CO2 (Air: 45 ± 3, CO2: 48 ± 3 mmHg, P < 0.01), but there were no changes in MAP (P = 0.77). CO2 decreased blood velocity in the renal (Air: 35.2 ± 8.1, CO2: 32.2 ± 7.3 cm/s, P < 0.01) and segmental (Air: 24.2 ± 5.1, CO2: 21.8 ± 4.2 cm/s, P < 0.01) arteries and increased vascular resistance in the renal (Air: 2.7 ± 0.9, CO2: 3.0 ± 0.9 mmHg·cm-1·s, P < 0.01) and segmental (Air: 3.9 ± 1.0, CO2: 4.4 ± 1.0 mmHg·cm-1·s, P < 0.01) arteries. These data provide evidence that the kidneys are hemodynamically responsive to a mild and acute hypercapnic stimulus in healthy humans.