Treadmill exercise-induced stress causes a rise of blood histamine in normotensive but not in primary hypertensive humans

Campos, H. A.; Montenegro, Martha; Velasco, Manuel; Romero, Eduardo; Álvarez, Rolando; Urbina, Adalberto

doi:10.1016/s0014-2999(99)00598-1

Cited by 10 publications

(7 citation statements)

References 14 publications

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“…Numerous substances and certain conditions have been suggested to cause mast cells and basophils to release histamine (2). It has been suggested that exercise causes histamine release; however, this is difficult to assess in humans because red blood cells actively take up histamine (9). Histamine levels have been measured in arterial and venous whole blood as well as venous plasma during and after high-intensity exercise (9,15,25,26,39).…”

Section: Discussionmentioning

confidence: 99%

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H₂-receptor-mediated vasodilation contributes to postexercise hypotension

McCord¹,

Beasley²,

Halliwill³

2006

Journal of Applied Physiology

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The early (approximately 30 min) postexercise hypotension response after a session of aerobic exercise is due in part to H1-receptor-mediated vasodilation. The purpose of this study was to determine the potential contribution of H2-receptor-mediated vasodilation to postexercise hypotension. We studied 10 healthy normotensive men and women (ages 23.7 +/- 3.4 yr) before and through 90 min after a 60-min bout of cycling at 60% peak O2 uptake on randomized control and H2-receptor antagonist days (300 mg oral ranitidine). Arterial pressure (automated auscultation), cardiac output (acetylene washin) and femoral blood flow (Doppler ultrasound) were measured. Vascular conductance was calculated as flow/mean arterial pressure. Sixty minutes postexercise on the control day, femoral (delta62.3 +/- 15.6%, where Delta is change; P < 0.01) and systemic (delta13.8 +/- 5.3%; P = 0.01) vascular conductances were increased, whereas mean arterial pressure was reduced (Delta-6.7 +/- 1.1 mmHg; P < 0.01). Conversely, 60 min postexercise with ranitidine, femoral (delta9.4 +/- 9.2%; P = 0.34) and systemic (delta-2.8 +/- 4.8%; P = 0.35) vascular conductances were not elevated and mean arterial pressure was not reduced (delta-2.2 +/- 1.3 mmHg; P = 0.12). Furthermore, postexercise femoral and systemic vascular conductances were lower (P < 0.05) and mean arterial pressure was higher (P = 0.01) on the ranitidine day compared with control. Ingestion of ranitidine markedly reduces vasodilation after exercise and blunts postexercise hypotension, suggesting H2-receptor-mediated vasodilation contributes to postexercise hypotension.

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Section: Discussionmentioning

confidence: 99%

“…Histamine can also be synthesized (but not stored) in some tissues by histidine decarboxylase. Histamine levels have been shown to increase during and after exercise (9,15,25), but it is unclear whether histamine contributes to exercise hyperemia. However, there does seem to be activation of H 1 receptors immediately (ϳ30 min) after exercise (36).…”

mentioning

confidence: 99%

H₂-receptor-mediated vasodilation contributes to postexercise hypotension

McCord¹,

Beasley²,

Halliwill³

2006

Journal of Applied Physiology

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“…Numerous substances and certain conditions have been suggested to cause mast cells and basophils to release histamine (Atkinson et al 1992). It has been suggested that exercise causes histamine release; however, this is difficult to assess in humans as red blood cells actively take up histamine (Campos et al 1999). Histamine levels have been measured in arterial and venous whole blood as well as venous plasma during and after high‐intensity exercise (Duner & Pernow, 1958; Harries et al 1979; Hartley et al 1981; Morgan et al 1983; Campos et al 1999).…”

Section: Discussionmentioning

confidence: 99%

H₁ receptor‐mediated vasodilatation contributes to postexercise hypotension

Lockwood

Wilkins

Halliwill

2005

The Journal of Physiology

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In normally active individuals, postexercise hypotension after a single bout of aerobic exercise is due to an unexplained peripheral vasodilatation. Histamine has been shown to be released during exercise and could contribute to postexercise vasodilatation via H 1 receptors in the peripheral vasculature. The purpose of this study was to determine the potential contribution of an H 1 receptor-mediated vasodilatation to postexercise hypotension. We studied 14 healthy normotensive men and women (ages 21.9 ± 2.1 years) before and through to 90 min after a 60 min bout of cycling at 60%V O 2 peak on randomized control and H 1 receptor antagonist days (540 mg oral fexofenadine hydrochloride; Allegra). Arterial blood pressure (automated auscultation) and femoral blood flow (Doppler ultrasound) were measured in the supine position. Femoral vascular conductance was calculated as flow/pressure. Fexofenadine had no effect on pre-exercise femoral vascular conductance or mean arterial pressure (P > 0.5). At 30 min postexercise on the control day, femoral vascular conductance was increased (∆ +33.7 ± 7.8%; P < 0.05 versus pre-exercise) while mean arterial pressure was reduced (∆ −6.5 ± 1.6 mmHg; P < 0.05 versus pre-exercise). In contrast, at 30 min postexercise on the fexofenadine day, femoral vascular conductance was not elevated (∆ +10.7 ± 9.8%; P = 0.7 versus pre-exercise) and mean arterial pressure was not reduced (∆ −1.7 ± 1.2 mmHg; P = 0.2 versus pre-exercise). Thus, ingestion of an H 1 receptor antagonist markedly reduces vasodilatation after exercise and blunts postexercise hypotension. These data suggest H 1 receptor-mediated vasodilatation contributes to postexercise hypotension.

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“…Interestingly, they also reported no effects of this exercise protocol on blood or plasma concentrations of histamine (McCord et al 2006). In contrast, exercise of shorter duration (i.e., 6-12 min) has been shown to induce increases in blood histamine levels (Campos et al 1999). Thus, it is possible that production of histamine during exercise wanes over time.…”

Section: Discussionmentioning

confidence: 92%

“…Since histamine increases during short term dynamic exercise (Campos et al 1999) and has been shown to play a role in mediating post-exercise hypotension (Lockwood et al 2005;McCord et al 2006), it may also contribute to hyperemic and blood pressure responses to exercise. Presumably, potential effects could be mediated, at least in part, via stimulation of peripheral H 2 receptors as they are instrumental in mediating histamine-induced vascular responses (Hill, 1990;Brown and Roberts 2001) that include reductions in blood pressure and vascular resistance (Black et al 1975).…”

Section: Introductionmentioning

confidence: 99%

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

Doh

Stebbins

Choi

et al. 2016

Appl. Physiol. Nutr. Metab.

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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 ± 3 mm Hg vs. 166 ± 2 mm Hg), MAP (121 ± 2 mm Hg vs. 112 ± 5 mm Hg), and RPP (25.9 ± 0.8 × 10(3) mm Hg·beats/min vs. 23.5 ± 0.8 × 10(3) mm Hg/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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Treadmill exercise-induced stress causes a rise of blood histamine in normotensive but not in primary hypertensive humans

Cited by 10 publications

References 14 publications

H₂-receptor-mediated vasodilation contributes to postexercise hypotension

H₂-receptor-mediated vasodilation contributes to postexercise hypotension

H₁ receptor‐mediated vasodilatation contributes to postexercise hypotension

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

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Treadmill exercise-induced stress causes a rise of blood histamine in normotensive but not in primary hypertensive humans

Cited by 10 publications

References 14 publications

H2-receptor-mediated vasodilation contributes to postexercise hypotension

H2-receptor-mediated vasodilation contributes to postexercise hypotension

H1 receptor‐mediated vasodilatation contributes to postexercise hypotension

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

Contact Info

Product

Resources

About

H₂-receptor-mediated vasodilation contributes to postexercise hypotension

H₂-receptor-mediated vasodilation contributes to postexercise hypotension

H₁ receptor‐mediated vasodilatation contributes to postexercise hypotension

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