Histamine H2 receptor blockade augments blood pressure responses to acute submaximal exercise in males

Hyung Woo Doh, Charles L Stebbins, Hyun Min Choi, Joonsung Park, Hosung Nho, Jong Kyung Kim

Research output: Contribution to journalArticle

Abstract

Histamine is a potent vasodilator that has been found to increase during exercise. We tested the hypothesis that histamine would attenuate blood pressure (BP), cardiac output (CO), and vascular resistance responses to short-term, submaximal dynamic exercise during H2 receptor blockade. Fourteen healthy men (20-29 years of age) were studied. Systolic (SBP), diastolic (DBP), and mean arterial (MAP) BP and heart rate (HR) were assessed at rest and during the last minute of 10 min of submaximal cycling exercise (60% of peak oxygen consumption) in the absence and presence of histamine H2 receptor blockade (ranitidine, 300 mg). Stroke volume (SV) (impedance cardiography) and plasma norepinephrine (NE) were measured, and CO, rate × pressure product (RPP), and total peripheral resistance (TPR) were calculated. Plasma levels of histamine were also measured. H2 blockade had no effects on any variables at rest. During exercise, SBP (184±3mmHg vs. 166±2mmHg), MAP (121 ± 2mmHg vs. 112±5mmHg), and RPP (25.9 ± 0.8 × 103mmHg beats/min vs. 23.5 ± 0.8 × 103mmHg/beats min) were greater during blocked conditions (P < 0.05), and an interaction was observed for TPR. SV, DBP, HR, and NE levels were unaffected by blockade. Plasma histamine increased from 1.83 ± 0.14 ng/mL at rest to 2.33 ± 0.23 ng/mL during exercise (P < 0.05) and was not affected by H2 blockade (1.56 ± 0.23 ng/mL vs. 1.70 ± 0.24 ng/mL). These findings suggest that, during submaximal exercise, histamine attenuates BP, vascular resistance, and the work of the heart via activation of H2 receptors and that these effects occurred primarily in the vasculature and not in the myocardium.

Original languageEnglish (US)
Pages (from-to)605-610
Number of pages6
JournalApplied Physiology, Nutrition and Metabolism
Volume41
Issue number6
DOIs
StatePublished - Feb 18 2016

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Histamine H2 Receptors
Histamine
Exercise
Blood Pressure
Vascular Resistance
Cardiac Output
Stroke Volume
Norepinephrine
Heart Rate
Impedance Cardiography
Pressure
Ranitidine
Vasodilator Agents
Oxygen Consumption
Myocardium
Arterial Pressure

Keywords

  • Cycling
  • Norepinephrine
  • Ranitidine
  • Rate × pressure product
  • Stroke volume

ASJC Scopus subject areas

  • Physiology
  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics
  • Physiology (medical)

Cite this

Histamine H2 receptor blockade augments blood pressure responses to acute submaximal exercise in males. / Doh, Hyung Woo; Stebbins, Charles L; Choi, Hyun Min; Park, Joonsung; Nho, Hosung; Kim, Jong Kyung.

In: Applied Physiology, Nutrition and Metabolism, Vol. 41, No. 6, 18.02.2016, p. 605-610.

Research output: Contribution to journalArticle

Doh, Hyung Woo ; Stebbins, Charles L ; Choi, Hyun Min ; Park, Joonsung ; Nho, Hosung ; Kim, Jong Kyung. / Histamine H2 receptor blockade augments blood pressure responses to acute submaximal exercise in males. In: Applied Physiology, Nutrition and Metabolism. 2016 ; Vol. 41, No. 6. pp. 605-610.
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AU - Kim, Jong Kyung

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AB - Histamine is a potent vasodilator that has been found to increase during exercise. We tested the hypothesis that histamine would attenuate blood pressure (BP), cardiac output (CO), and vascular resistance responses to short-term, submaximal dynamic exercise during H2 receptor blockade. Fourteen healthy men (20-29 years of age) were studied. Systolic (SBP), diastolic (DBP), and mean arterial (MAP) BP and heart rate (HR) were assessed at rest and during the last minute of 10 min of submaximal cycling exercise (60% of peak oxygen consumption) in the absence and presence of histamine H2 receptor blockade (ranitidine, 300 mg). Stroke volume (SV) (impedance cardiography) and plasma norepinephrine (NE) were measured, and CO, rate × pressure product (RPP), and total peripheral resistance (TPR) were calculated. Plasma levels of histamine were also measured. H2 blockade had no effects on any variables at rest. During exercise, SBP (184±3mmHg vs. 166±2mmHg), MAP (121 ± 2mmHg vs. 112±5mmHg), and RPP (25.9 ± 0.8 × 103mmHg beats/min vs. 23.5 ± 0.8 × 103mmHg/beats min) were greater during blocked conditions (P < 0.05), and an interaction was observed for TPR. SV, DBP, HR, and NE levels were unaffected by blockade. Plasma histamine increased from 1.83 ± 0.14 ng/mL at rest to 2.33 ± 0.23 ng/mL during exercise (P < 0.05) and was not affected by H2 blockade (1.56 ± 0.23 ng/mL vs. 1.70 ± 0.24 ng/mL). These findings suggest that, during submaximal exercise, histamine attenuates BP, vascular resistance, and the work of the heart via activation of H2 receptors and that these effects occurred primarily in the vasculature and not in the myocardium.

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