Bradykinin has no acute effect on the response of forearm blood flow to sympathetic stimulation in man

M. J. Cullen, J. R. Cockcroft, D. J. Webb

Research output: Contribution to journalArticleResearchpeer-review

Abstract

1. Six healthy male subjects received 0.9% (w/v) NaCl (saline) followed by incremental doses of bradykinin (1, 3 and 10 pmol/min), via the left brachial artery. Blood flow and the response of blood flow to lower-body negative pressure were measured in both forearms during infusion of saline and each dose of bradykinin. 2. Bradykinin produced a moderate and dose-dependent increase in blood flow in the infused, but not the non-infused, forearm. Lower-body negative pressure produced an approximately 15-20% reduction in blood flow in both forearms, and this response was unaffected by local infusion of bradykinin. 3. Bradykinin, in contrast to angiotensin II, had no acute effect on peripheral sympathetic responses to lower-body negative pressure. We conclude that, in forearm resistance vessels in man, withdrawal of angiotensin II, rather than accumulation of bradykinin, is likely to account for the attenuation of peripheral sympathetic responses after acute administration of a converting-enzyme inhibitor.

LanguageEnglish
Pages399-401
Number of pages3
JournalClinical Science
Volume78
Issue number4
Publication statusPublished - 1990
Externally publishedYes

Fingerprint

Bradykinin
Forearm
Lower Body Negative Pressure
Angiotensin II
Brachial Artery
Enzyme Inhibitors
Healthy Volunteers

Keywords

  • Angiotensin II
  • Bradykinin
  • Converting enzyme
  • Sympathetic nervous system

Cite this

Cullen, M. J. ; Cockcroft, J. R. ; Webb, D. J. / Bradykinin has no acute effect on the response of forearm blood flow to sympathetic stimulation in man. In: Clinical Science. 1990 ; Vol. 78, No. 4. pp. 399-401.
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Bradykinin has no acute effect on the response of forearm blood flow to sympathetic stimulation in man. / Cullen, M. J.; Cockcroft, J. R.; Webb, D. J.

In: Clinical Science, Vol. 78, No. 4, 1990, p. 399-401.

Research output: Contribution to journalArticleResearchpeer-review

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AU - Cockcroft, J. R.

AU - Webb, D. J.

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N2 - 1. Six healthy male subjects received 0.9% (w/v) NaCl (saline) followed by incremental doses of bradykinin (1, 3 and 10 pmol/min), via the left brachial artery. Blood flow and the response of blood flow to lower-body negative pressure were measured in both forearms during infusion of saline and each dose of bradykinin. 2. Bradykinin produced a moderate and dose-dependent increase in blood flow in the infused, but not the non-infused, forearm. Lower-body negative pressure produced an approximately 15-20% reduction in blood flow in both forearms, and this response was unaffected by local infusion of bradykinin. 3. Bradykinin, in contrast to angiotensin II, had no acute effect on peripheral sympathetic responses to lower-body negative pressure. We conclude that, in forearm resistance vessels in man, withdrawal of angiotensin II, rather than accumulation of bradykinin, is likely to account for the attenuation of peripheral sympathetic responses after acute administration of a converting-enzyme inhibitor.

AB - 1. Six healthy male subjects received 0.9% (w/v) NaCl (saline) followed by incremental doses of bradykinin (1, 3 and 10 pmol/min), via the left brachial artery. Blood flow and the response of blood flow to lower-body negative pressure were measured in both forearms during infusion of saline and each dose of bradykinin. 2. Bradykinin produced a moderate and dose-dependent increase in blood flow in the infused, but not the non-infused, forearm. Lower-body negative pressure produced an approximately 15-20% reduction in blood flow in both forearms, and this response was unaffected by local infusion of bradykinin. 3. Bradykinin, in contrast to angiotensin II, had no acute effect on peripheral sympathetic responses to lower-body negative pressure. We conclude that, in forearm resistance vessels in man, withdrawal of angiotensin II, rather than accumulation of bradykinin, is likely to account for the attenuation of peripheral sympathetic responses after acute administration of a converting-enzyme inhibitor.

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