Bradykinin-induced chemoreflexes from skeletal muscle: Implications for the exercise reflex

Charles L Stebbins, J. C. Longhurst

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Abstract

We examined the cardiovascular response to bradykinin stimulation of skeletal muscle afferents and the effect of prostaglandins on this response. Intra-arterial injection of 1 μg bradykinin into the gracilis muscle of cats reflexly increased mean arterial pressure by 16 ± 2 mmHg, left ventricular end-diastolic pressure by 1.6 ± 0.6 mmHg, maximal dP/dt by 785 ± 136 mmHg/s, heart rate by 11 ± 2 beats/min, and the mean aortic flow by 22 ± 3 ml/min. The hemodynamic responses were abolished following denervation of the gracilis muscle. The increases in mean arterial pressure and maximal dP/dt were reduced by 68 and 45%, respectively, following inhibition of prostaglandin synthesis with indomethacin (2-8 mg/kg iv). Treatment with prostaglandin E2 (PGE2, 15-25 μg ia) restored the initial increase in mean arterial pressure, but not dP/dt, caused by bradykinin stimulation. Injection of PGE2 (15-30 μg ia) into the gracilis, without prior treatment with indomethacin, augmented the bradykinin-induced increases in mean arterial pressure and dP/dt. We conclude that small doses of bradykinin injected into skeletal muscle are capable of reflexly activating the cardiovascular system and that prostaglandins are necessary for the full manifestation of the corresponding hemodynamic response. The pattern of hemodynamic adjustment following bradykinin injection into skeletal muscle is very similar to that induced by static exercise. Therefore, it is possible that intense exercise provides a stimulus for this bradykinin-induced reflex in vivo.

Original languageEnglish (US)
Pages (from-to)56-63
Number of pages8
JournalJournal of Applied Physiology
Volume59
Issue number1
StatePublished - 1985

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ASJC Scopus subject areas

  • Endocrinology
  • Physiology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

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