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

Area of Science:

• Cardiovascular Physiology
• Skeletal Muscle Afferents
• Neurogenic Reflexes

Background:

• Bradykinin is a peptide involved in various physiological processes.
• Skeletal muscle afferents play a role in cardiovascular regulation.
• Prostaglandins are known mediators of inflammation and pain.

Purpose of the Study:

• To investigate the cardiovascular response to bradykinin stimulation of skeletal muscle afferents.
• To determine the role of prostaglandins in mediating this cardiovascular response.

Main Methods:

• Intra-arterial injection of bradykinin into the gracilis muscle of cats.
• Measurement of hemodynamic parameters (mean arterial pressure, left ventricular end-diastolic pressure, maximal dP/dt, heart rate, mean aortic flow).
• Denervation of the gracilis muscle and inhibition of prostaglandin synthesis (using indomethacin) to assess the role of these factors.

Main Results:

• Bradykinin injection reflexly increased mean arterial pressure, left ventricular end-diastolic pressure, maximal dP/dt, heart rate, and mean aortic flow.
• These responses were abolished after gracilis muscle denervation.
• Indomethacin treatment significantly reduced the increases in mean arterial pressure and maximal dP/dt.
• Prostaglandin E2 (PGE2) administration partially restored the bradykinin-induced increase in mean arterial pressure and augmented other responses.

Conclusions:

• Bradykinin, at low doses, can reflexly activate the cardiovascular system via skeletal muscle afferents.
• Prostaglandins are crucial for the complete manifestation of bradykinin-induced cardiovascular adjustments.
• The observed hemodynamic pattern resembles that of static exercise, suggesting a potential role for bradykinin in exercise-induced cardiovascular reflexes.