Acetylstrophanthidin does not enhance the reflex pressor response to static muscular contraction.
Cardiac glycosides have been shown to enhance the sensitivity of the reflex cardiovascular responses to stimulation of mechanoreceptors in the heart, carotid sinus and aorta. Little is known, however, about the effect of glycosides on the reflex cardiovascular responses to the contraction-induced stimulation of afferent endings in hindlimb skeletal muscle. We therefore examined the reflex heart rate and arterial pressure responses to static contraction of the hindlimb muscles before and after femoral arterial injection of two doses of acetylstrophanthidin (20 and 80 micrograms/kg). Neither of the two doses enhanced the reflex cardiovascular responses to contraction, although the larger of the two significantly increased femoral venous potassium concentrations from 3.4 +/- 0.2 to 3.8 +/- 0.1 mM. Although injection of the two doses as well as injection of a very large dose of acetylstrophanthidin (400 micrograms/kg) increased baseline mean arterial pressure, these effects were probably caused by the vasoconstrictor action of this agent and not by a chemoreflex, because the increase was not attenuated by denervation of the hindlimb.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D002415:Cats; D006339:Heart Rate / Q000187:drug effects*; D008465:Mechanoreceptors / Q000187:drug effects / Q000502:physiology*; D009119:Muscle Contraction / Q000187:drug effects*; D011188:Potassium / Q000097:blood; D012018:Reflex / Q000187:drug effects; D013116:Spinal Cord / Q000502:physiology; D013327:Strophanthidin / Q000031:analogs & derivatives* / Q000494:pharmacology
D013327:Strophanthidin; C004681:acetylstrophanthidin; D011188:Potassium