Do the peripheral chemoreceptors contribute to exercise blood pressure in people with a family history of hypertension?

Physiology 2019 (Aberdeen, UK) (2019) Proc Physiol Soc 43, C055

Oral Communications: Do the peripheral chemoreceptors contribute to exercise blood pressure in people with a family history of hypertension?

A. Smets1*, P. Ramasawmy1*, K. Hope1, Z. Adams1, T. Hinton1, R. Baker1, A. Nightingale1, E. C. Hart1

1. Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, United Kingdom.

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People with a family history of hypertension (FH+) have a greater rise in blood pressure (BP) during exercise compared to people without FH (FH-). The peripheral chemoreceptors, particularly the carotid body, play a role in the pressor response to exercise [1]. The carotid bodies have been implicated in the aetiology of hypertension, thus, it is possible the carotid bodies play a role in the excessive BP response to exercise in people with FH+. Therefore, we aimed to establish whether inhibiting the carotid body during submaximal steady state exercise (via hyperoxia), could blunt the rise in systolic BP (SBP) in people with FH+ (n=9, age; 23±1 years, body mass index (BMI); 21.4 ± 1.6 kg/m2) vs. people with FH- (n=9, age; 21±1 years (P=0.004), BMI; 21.9 ± 2.1 kg/m2 (P=0.59) . FH+ was defined as people with 1° or 2° relatives with a diagnosis of hypertension. People were excluded if they could not find out their family history. Chemoreflex sensitivity (CRS) at rest was measured using poikilocapnic intermittent hypoxia. This involved measuring the minute ventilation response to desaturation via short bursts of nitrogen [2] . An incremental exercise test was completed on a bike ergometer to measure peak oxygen consumption (VO2 peak). On a separate day, participants were asked to complete two 5 min bouts of exercise at 60% of their VO2 peak. One was completed under normoxic conditions (room air) and the other was completed during hyperoxic conditions (0.80 fraction of inspired O2 to inhibit the carotid body). The order was counterbalanced and separated by a 20 min rest. BP was measured using an automated cuff at baseline, 3 and 5 mins during each exercise bout. Group difference in CRS was assessed using an unpaired Student’s T-test and differences in SBP between FH+ and FH- during submaximal exercise in normoxia and hyperoxia were measured using a two-way ANOVA. Data are mean ± SD. We found that there was no difference in CRS between the groups (FH+; -0.41 ± 0.85 L/min/% vs. FH-; -0.35 ± 0.37 L/min%, P=0.84). However, during normoxic submaximal exercise there was a greater change in SBP in FH+ vs. the FH- group (56 ± 21 mmHg vs. 35 ± 19 mmHg; P=0.05), but there was no group interaction effect by gas on the absolute SBP during exercise (P=0.07), although there was a moderate effect size (eta2=0.59). In summary, resting CRS is not different in people with FH+ vs FH-. The change in SBP during exercise is higher in people in people with FH+, however, it is not clear whether the carotid body plays a role in this.



Where applicable, experiments conform with Society ethical requirements.

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