Paradoxical inhibition of vasoconstrictor and vasodilator responses by hypertonic mannitol in isolated arterial smooth muscle.
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V S Krishnamurty
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Inhibitory effect of hypertonic mannitol on vasoconstrictor and vasodilator responses of isolated coronary arteries.
The effect of hypertonic mannitol on pressor responses to vasoactive agents was studied in isolated canine coronary arteries perfused with physiologic salt solution at a constant flow. When perfusion pressure was increased with 60 mM KCl, mannitol (50 mosM) consistently caused a decrease in perfusion pressure that lasted for at least 1 h. Withdrawal of mannitol from the perfusion media was associated with a vasoconstrictor response that was not prevented by alpha- or beta-adrenoceptor blockade or by the presence of either nitroglycerin or norepinephrine. Hypertonic mannitol also reduced the responsiveness of the isolated smooth muscle preparations to several different mechanistically unrelated vasodilator agents. The mechanism(s) responsible for the paradoxical ability of hypertonic mannitol to reduce vascular responsiveness to both vasoconstrictor and vasodilator interventions in isolated canine coronary arteries is not known, but future studies should be directed at elucidating it as well as determining whether similar phenomena occur in vivo.
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Influence of mannitol on contractile responses of isolated perfused arteries.
The influence of hyperosmotic mannitol on vascular smooth muscle contractile responses was examined in isolated arterial preparations. Vasoconstrictor effects of norepinephrine (NE) and potassium chloride (K+) in the perfused central artery of the rabbit's ear and in perfused mesenteric arteries of cats were significantly inhibited by infusion with Krebs bicarbonate solution made hyperosmotic with mannitol (50-200 mosM increase). Similarly, the magnitude and duration of vasoconstrictor responses to transmural stimulation of the central ear artery of the rabbit were decreased by hyperosmotic mannitol (50 mosM). Mannitol (50 mosM) produced a decrease in perfusion pressure when perfusion pressure was maintained at an increased level by K+ (60 mM). Mannitol-induced vasodilatation was not affected by ethacrynic acid (1.5 X 10(-5) M), beta adrenergic blockade or by the development of tachyphylaxis to the vasodilator effects of nitroglycerin. The concentration of cyclic adenosine-monophosphate was not changed by mannitol. Isotonic mannitol also inhibited NE-induced contractile responses. These data indicate that hyperosmotic mannitol produces vasodilatation in isolated arterial smooth muscle by a mechanism(s) that appears dissimilar from that of several other vasodilator substances and suggest that hypertonicity may not be the only factor involved in the vasodilator effect of mannitol.
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