Portuguese man-of-war (Physalia physalis)venom has profound effects on the cardiovascular system of man and animals. The venom produces vascular relaxation in norepinephrine precontracted, intact rabbit femoral arterial rings by stimulating vasodilatory prostaglandin synthesis in the endothelium. This action does not depend on endotheliumderived relaxing factor (EDRF). P. physalis venom produces a vascular constriction on KC1 depolarized, intact rings. This is completely inhibited by dibenzyline and yohimbine. Increased membrane permeability to calcium may be involved in direct vascular smooth muscle stimulation. The venom has a positive inotropic effect on rat atrial preparations, which is intensified by increased extracellular calcium concentration. P. physalis venom markedly increases calcium influx of cultured embryonic chick heart cells in a dose dependent manner by activating L type calcium channels. The increased calcium influx is consistent with the positive inotropic action on the cultured heart cells observed under the microscope. This effect is completely inhibited by diltiazem and verapamil. Sodium influx of cultured embryonic chick heart cells is moderately increased (about one sixth of increased calcium influx) under the influence of P. physalis venom. Flecainide (a sodium channel blocker) and verapamil do not inhibit the increased sodium influx. The venom may accelerate sodium/calcium exchange directly and/or indirectly by increased calcium influx, the major mechanism for the embryonic chick heart to eliminate excessive cytoplasmic free calcium. Rubidium (an analog of potassium) influx is not affected by P. physalis venom at lower dose levels. A high concentration of the venom, nevertheless, decreases rubidium influx, implicating an inhibition of the Na+, K+-pump. Greatly increased contraction of the cultured heart cells associated with a large calcium influx may result in energy depletion, hence, inhibition of the Na+, K+-pump. The increased calcium influx of the cultured heart cells appears to be highly correlated with an increased efflux of rubidium. Stimulation of calcium-dependent potassium channels is an indirect effect of the venom. Activation of ATP-sensitive potassium channels may also contribute to the increased rubidium efflux when ATP depletion occurs under the condition of greatly increased contraction in the presence of a high venom concentration. P. physalis venom does not affect 2-deoxy-D-glucose uptake by cultured embryonic chick heart cells. However, at extremely high doses the uptake of the glucose is reduced. Glucose transport and metabolism may be disturbed by the excessive cytoplasmic calcium caused by P. physalis venom.
Ramon R. Gonzalez
David A. Hessinger
Ian M. Fraser
Marvin A. Peters
Robert A. Chilson
Doctor of Philosophy (PhD)
Year Degree Awarded
Date (Title Page)
Library of Congress/MESH Subject Headings
Portuguese Man-of-war; Venoms; Marine Toxins; Cardiovascular System -- pathology
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This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights.
Luo, Eva, "Molecular Mechanisms of Physalia Physalis Venom Modulation of Cardiac and Vascular Functions" (1990). Loma Linda University Electronic Theses, Dissertations & Projects. 907.
Loma Linda University Electronic Theses and Dissertations
Loma Linda University. Del E. Webb Memorial Library. University Archives