Norby L H, DiBona G F
J Pharmacol Exp Ther. 1975 Jun;193(3):932-40.
Left ventricular injection of meglumine diatrizoate caused an initial (1-10 minute) decrease in renal vascular resistance followed by a late (30-minute) increase in renal vascular resistance. The late renal vasoconstrictor response was not blocked by bilateral cervical vagotomy, by renal adrenergic blockade or by renal alpha adrenergic receptor blockade; it was blocked by prior extracellular fluid volume expansion and blockade of the response of the kidney to angiotensin II. There was no effect on intrarenal distribution of blood flow. In the kidney perfused at constant flow, injections of meglumine diatrizoate into the kidney resulted in early renal vasodilation (1-5 minutes) with a return to control renal vascular resistance by 7 minutes; no vasoconstriction was observed. The renal vasodilatation was not abolished by prior treatment with atropine. Vasodilator responses identical to those observed with meglumine diatrizoate were obtained with 4.5% NaCl (equiosmolar to meglumine diatrizoate); no response was obtained with 0.9% NaCl. When given into either the left ventricle or the renal artery, meglumine diatrizoate caused an early reversible depression in renal extraction of para-aminohippurate; both 0.9 and 4.5% NaCl were without effect. The renal vasodilation produced by meglumine diatrizoate initially appears to be caused by its hyperosmotic properties; the late renal vasoconstrictor response appears to be mediated via an activation of the renin-angiotensin system. The depressive effect of meglumine diatrizoate on the renal extraction of para-aminohippurate is not related to its osmotic properties but rather to an effect of the organic iodinated molecule on cellular transport of para-aminohippurate.
