Cardiac reflex effects of intracoronary bradykinin in humans

Saul Schaefer, Richard A. Valente, Lawrence J. Laslett, John C. Longhurst

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Background: Endogenous production of bradykinin (BK) has been postulated to cause hemodynamic changes and cardiac pain during myocardial ischemia, presumably because of the stimulation of cardiac afferent fibers. Methods: To test the hypothesis that BK results in cardiac reflex responses and can cause the sensation of angina, 10 patients with and without coronary atherosclerosis had BK injected into their right (RCA) and left (LCA) coronary arteries in graded concentrations up to 105 m. Patients were monitored for hemodynamic changes and the presence and quality of pain. Results: Intracoronary BK ID'5 m caused a significant reduction in blood pressure in most patients with either injection into the RCA or LCA (RCA: 151 ±10/90 ±5 mm Hg to 119 ±11/70 ±6 mm Hg, LCA: 161 ±11/88 ±6 mm Hg to 118 ±10/65 ±6 mm Hg) that began 12 to 14 seconds after injection. Injection into the LCA also resulted in a signifi-cant increase in heart rate (69 ±4 to 81 ±7 beats/minute), while injection into the RCA did not. Pain occurred after changes in blood pressure in all but one patient, which was present in 5 of 9 patients with RCA injection and 8 of 9 patients with LCA injection, and was often associated with flushing and nausea. Pain caused by BK was not similar to previous clinical ischémie pain in the patients with coronary atherosclerosis. Conclusions: The absence of a chronotropic response associated with arterial hypotension following injection of BK into the RCA is consistent with activation of cardiac vagal afférents in the left ventricle. The latency and quality of pain in these patients following injection of BK suggests that, while BK is nociceptive, it likely is not the cause of angina in patients with myocardial ischemia.

Original languageEnglish (US)
Pages (from-to)160-167
Number of pages8
JournalJournal of Investigative Medicine
Volume44
Issue number4
StatePublished - 1996

Fingerprint

Bradykinin
Reflex
Injections
Pain
Blood pressure
Hemodynamics
Myocardial Ischemia
Coronary Artery Disease
Blood Pressure
Hypotension
Nausea
Heart Ventricles
Chemical activation
Coronary Vessels
Heart Rate
Fibers

Keywords

  • Afférents
  • Angina
  • Bradykinin
  • Myocardial ischemia
  • Reflexes

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Schaefer, S., Valente, R. A., Laslett, L. J., & Longhurst, J. C. (1996). Cardiac reflex effects of intracoronary bradykinin in humans. Journal of Investigative Medicine, 44(4), 160-167.

Cardiac reflex effects of intracoronary bradykinin in humans. / Schaefer, Saul; Valente, Richard A.; Laslett, Lawrence J.; Longhurst, John C.

In: Journal of Investigative Medicine, Vol. 44, No. 4, 1996, p. 160-167.

Research output: Contribution to journalArticle

Schaefer, S, Valente, RA, Laslett, LJ & Longhurst, JC 1996, 'Cardiac reflex effects of intracoronary bradykinin in humans', Journal of Investigative Medicine, vol. 44, no. 4, pp. 160-167.
Schaefer, Saul ; Valente, Richard A. ; Laslett, Lawrence J. ; Longhurst, John C. / Cardiac reflex effects of intracoronary bradykinin in humans. In: Journal of Investigative Medicine. 1996 ; Vol. 44, No. 4. pp. 160-167.
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abstract = "Background: Endogenous production of bradykinin (BK) has been postulated to cause hemodynamic changes and cardiac pain during myocardial ischemia, presumably because of the stimulation of cardiac afferent fibers. Methods: To test the hypothesis that BK results in cardiac reflex responses and can cause the sensation of angina, 10 patients with and without coronary atherosclerosis had BK injected into their right (RCA) and left (LCA) coronary arteries in graded concentrations up to 105 m. Patients were monitored for hemodynamic changes and the presence and quality of pain. Results: Intracoronary BK ID'5 m caused a significant reduction in blood pressure in most patients with either injection into the RCA or LCA (RCA: 151 ±10/90 ±5 mm Hg to 119 ±11/70 ±6 mm Hg, LCA: 161 ±11/88 ±6 mm Hg to 118 ±10/65 ±6 mm Hg) that began 12 to 14 seconds after injection. Injection into the LCA also resulted in a signifi-cant increase in heart rate (69 ±4 to 81 ±7 beats/minute), while injection into the RCA did not. Pain occurred after changes in blood pressure in all but one patient, which was present in 5 of 9 patients with RCA injection and 8 of 9 patients with LCA injection, and was often associated with flushing and nausea. Pain caused by BK was not similar to previous clinical isch{\'e}mie pain in the patients with coronary atherosclerosis. Conclusions: The absence of a chronotropic response associated with arterial hypotension following injection of BK into the RCA is consistent with activation of cardiac vagal aff{\'e}rents in the left ventricle. The latency and quality of pain in these patients following injection of BK suggests that, while BK is nociceptive, it likely is not the cause of angina in patients with myocardial ischemia.",
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AB - Background: Endogenous production of bradykinin (BK) has been postulated to cause hemodynamic changes and cardiac pain during myocardial ischemia, presumably because of the stimulation of cardiac afferent fibers. Methods: To test the hypothesis that BK results in cardiac reflex responses and can cause the sensation of angina, 10 patients with and without coronary atherosclerosis had BK injected into their right (RCA) and left (LCA) coronary arteries in graded concentrations up to 105 m. Patients were monitored for hemodynamic changes and the presence and quality of pain. Results: Intracoronary BK ID'5 m caused a significant reduction in blood pressure in most patients with either injection into the RCA or LCA (RCA: 151 ±10/90 ±5 mm Hg to 119 ±11/70 ±6 mm Hg, LCA: 161 ±11/88 ±6 mm Hg to 118 ±10/65 ±6 mm Hg) that began 12 to 14 seconds after injection. Injection into the LCA also resulted in a signifi-cant increase in heart rate (69 ±4 to 81 ±7 beats/minute), while injection into the RCA did not. Pain occurred after changes in blood pressure in all but one patient, which was present in 5 of 9 patients with RCA injection and 8 of 9 patients with LCA injection, and was often associated with flushing and nausea. Pain caused by BK was not similar to previous clinical ischémie pain in the patients with coronary atherosclerosis. Conclusions: The absence of a chronotropic response associated with arterial hypotension following injection of BK into the RCA is consistent with activation of cardiac vagal afférents in the left ventricle. The latency and quality of pain in these patients following injection of BK suggests that, while BK is nociceptive, it likely is not the cause of angina in patients with myocardial ischemia.

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