Effect of healthy aging on renal vascular responses to local cooling and apnea

Patel, Hiren; Mast, Jessica; Sinoway, Lawrence I.; Muller, Matthew D.

doi:10.1152/japplphysiol.00089.2013

Cited by 32 publications

(42 citation statements)

References 72 publications

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“…It is well established that face cooling elicits a pressor response in humans for up to 180 s (1,3,7,11,14,15,18,19,21,22). Data from the present study extend these findings and show that face cooling-induced increases in blood pressure can be sustained for at least 15 min (Fig.…”

Section: Face Cooling Elicits Sustained Increases In Blood Pressuresupporting

confidence: 86%

“…It is well known that face cooling elicits robust increases in sympathetic nerve activity (11,15,21) and, thus, vascular resistance in the peripheral (11,16), visceral (6,19), and cerebral (3) vasculatures. Ultimately, these responses elevate blood pressure (1,3,7,11,14,15,18,19,21,22), as cardiac output remains largely unaffected by face Values are expressed as means Ϯ SD. RMSSD, root mean square of successive differences of the R-R interval; PU, perfusion units.…”

Section: Face Cooling Elicits Sustained Increases In Blood Pressurementioning

confidence: 99%

“…Cooling of the forehead and cheeks evokes a similar, yet less pronounced, response in humans (1,3,7,11,14,15,18,19,21,22), which occurs secondary to stimulation of the cold afferents of the trigeminal nerve (10,17). Face cooling in humans simultaneously stimulates the parasympathetic and sympathetic nervous systems, evoking bradycardia and peripheral vasoconstriction (1,3,7,11,14,15,18,19,21,22). In humans, reductions in heart rate are not sufficient to reduce cardiac output (3).…”

mentioning

confidence: 99%

“…In humans, reductions in heart rate are not sufficient to reduce cardiac output (3). Therefore, blood pressure increases as a result of systemic peripheral vasoconstriction (1,3,7,11,14,15,18,19,21,22).…”

mentioning

confidence: 99%

“…The hemodynamic responses to face cooling in humans have only been studied up to 180 s in duration (1,3,7,11,14,15,18,19,21,22). Thus, it is unknown whether the relative hypertensive responses elicited by face cooling, in addition to the temporal dynamics of parasympathetic and sympathetic activation, are sustained beyond 180 s. The diving reflex in diving mammals and birds persists for the duration of the dive (4).…”

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confidence: 99%

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Sustained increases in blood pressure elicited by prolonged face cooling in humans

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Coleman

Sackett

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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We tested the hypothesis that increases in blood pressure are sustained throughout 15 min of face cooling. Two independent trials were carried out. In the Face-Cooling Trial, 10 healthy adults underwent 15 min of face cooling where a 2.5-liter bag of ice water (0 ± 0°C) was placed over their cheeks, eyes, and forehead. The Sham Trial was identical except that the temperature of the water was 34 ± 1°C. Primary dependent variables were forehead temperature, mean arterial pressure, and forearm vascular resistance. The square root of the mean of successive differences in R-R interval (RMSSD) provided an index of cardiac parasympathetic activity. In the Face Cooling Trial, forehead temperature fell from 34.1 ± 0.9°C at baseline to 12.9 ± 3.3°C at the end of face cooling ( P < 0.01). Mean arterial pressure increased from 83 ± 9 mmHg at baseline to 106 ± 13 mmHg at the end of face cooling ( P < 0.01). RMSSD increased from 61 ± 40 ms at baseline to 165 ± 97 ms during the first 2 min of face cooling ( P ≤ 0.05), but returned to baseline levels thereafter (65 ± 49 ms, P ≥ 0.46). Forearm vascular resistance increased from 18.3 ± 4.4 mmHg·ml−1·100 g tissue−1·min at baseline to 26.6 ± 4.0 mmHg·ml−1·100 g tissue−1·min at the end of face cooling ( P < 0.01). There were no changes in the Sham Trial. These data indicate that increases in blood pressure are sustained throughout 15 min of face cooling, and face cooling elicits differential time-dependent parasympathetic and likely sympathetic activation.

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Section: Face Cooling Elicits Sustained Increases In Blood Pressuresupporting

confidence: 86%

Section: Face Cooling Elicits Sustained Increases In Blood Pressurementioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Sustained increases in blood pressure elicited by prolonged face cooling in humans

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Coleman

Sackett

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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Forearm vascular responses to mental stress in healthy older adults

2013

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Forearm vascular conductance (FVC) increases in response to mental stress (verbal mental arithmetic) in young people. However, the effect of healthy aging and mental stress on FVC is unknown. In this study, we tested the hypothesis that FVC and cutaneous vascular conductance (CVC) would be attenuated in older adults compared to young adults. In 13 young (27 ± 1 year) and 11 older (62 ± 1 year) subjects, we quantified heart rate (HR), mean arterial pressure (MAP), FVC (Doppler ultrasound), and CVC (laser Doppler flowmetry) in response to a 3‐min bout of mental stress in the supine posture. Changes from baseline were compared between groups and physiological variables were also correlated. Older adults had a blunted HR response to mental stress (Δ = 7 ± 2 vs. 14 ± 2 beats/min) but ΔMAP was comparable between groups (Δ = 11 ± 2 mmHg vs. 9 ± 1). During the third minute of mental stress, the %ΔFVC (−2 ± 5 vs. 31 ± 12%) and %ΔCVC (2 ± 6 vs. 31 ± 15%) were both impaired in older adults compared to young subjects. There was no relationship between ΔHR and %ΔCVC in either group, but there was a positive relationship between ΔHR and %ΔFVC in both young subjects (R = 0.610, P < 0.027) and older subjects (R = 0.615, P < 0.044), such that larger tachycardia was associated with higher forearm vasodilation. These data indicate that older adults have impaired forearm vasodilation in response to mental stress.

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Effect of oxidative stress on sympathetic and renal vascular responses to ischemic exercise

et al. 2013

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Reactive oxygen species (ROS), produced acutely during skeletal muscle contraction, are known to stimulate group IV muscle afferents and accentuate the exercise pressor reflex (EPR) in rodents. The effect of ROS on the EPR in humans is unknown. We conducted a series of studies using ischemic fatiguing rhythmic handgrip to acutely increase ROS within skeletal muscle, ascorbic acid infusion to scavenge free radicals, and hyperoxia inhalation to further increase ROS production. We hypothesized that ascorbic acid would attenuate the EPR and that hyperoxia would accentuate the EPR. Ten young healthy subjects participated in two or three experimental trials on separate days. Beat-by-beat measurements of heart rate (HR), mean arterial pressure (MAP), muscle sympathetic nerve activity (MSNA), and renal vascular resistance index (RVRI) were measured and compared between treatments (saline and ascorbic acid; room air and hyperoxia). At fatigue, the reflex increases in MAP (31 ± 3 versus 29 ± 2 mmHg), HR (19 ± 3 versus 20 ± 3 bpm), MSNA burst rate (21 ± 4 versus 23 ± 4 burst/min), and RVRI (39 ± 12 versus 44 ± 13%) were not different between saline and ascorbic acid. Relative to room air, hyperoxia did not augment the reflex increases in MAP, HR, MSNA, or RVRI in response to exercise. Muscle metaboreflex activation and time/volume control experiments similarly showed no treatment effects. While contrary to our initial hypotheses, these findings suggest that ROS do not play a significant role in the normal reflex adjustments to ischemic exercise in young healthy humans.

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Effect of healthy aging on renal vascular responses to local cooling and apnea

Cited by 32 publications

References 72 publications

Sustained increases in blood pressure elicited by prolonged face cooling in humans

Sustained increases in blood pressure elicited by prolonged face cooling in humans

Forearm vascular responses to mental stress in healthy older adults

Effect of oxidative stress on sympathetic and renal vascular responses to ischemic exercise

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