cAMP and cGMP do not mediate the vasorelaxation induced by iodinated radiographic contrast media in isolated swine renal arteries.

Purpose: Vasodilatation is a frequent side effect of radiographic contrast media, partially due to a direct effect on vascular smooth muscles. Our purpose was therefore to examine any possible implication of the cyclic adenosine monophospate (cAMP) and cyclic guanosine monophosphate (cGMP) pathways in contrast media induced vasorelaxation.

Material And Methods: Isolated segments of swine renal arteries were precontracted with 10 microM phenylephrine and relaxed with iomeprol before and after blockade of the cAMP and cGMP pathways.

Iodinated radiographic contrast media inhibit the capacitative calcium entry into smooth muscle cells of the swine renal artery.

Rationale And Objectives: To investigate whether nonionic, iodinated, radiographic contrast media (RCM) could modulate calcium release from or calcium entry into smooth muscle cells of the swine renal artery.

Methods: Intracellular calcium concentrations of isolated myocytes loaded with the calcium-sensitive dye fluo-3 were analyzed using a fluorescence imaging system. Calcium signals were compared with isometric contractions of vascular segments in an organ bath.

Changes of intracellular calcium concentrations by phenylephrine in renal arterial smooth muscle cells.

In smooth muscle cells isolated from swine renal interlobar arteries, phenylephrine (PE) at concentrations of 1-10 microM produced biphasic increases of the intracellular calcium concentration. An early transient rise was followed by a maintained plateau. The maintained component was sensitive to extracellular calcium, in contrast to the early transient, which was still observed in nominally calcium-free solution.

Inhibition of L-type calcium currents in guinea pig ventricular myocytes by the kappa-opioid agonist U50488H does not involve binding to opiate receptors.

In guinea pig ventricular myocytes the kappa-opioid agonist trans(+/-)-3,3-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]- benzeneacetamide methanesulfonate salt (U50488H) inhibited L-type calcium currents (ICa) as measured by the patch clamp technique in a dose-dependent fashion. The basal, as well as the isoprenaline and 8-Br-cAMP-stimulated, ICa were found to be reduced by U50488H. The inhibition was reversible and was not prevented on preincubation with pertussis toxin or the receptor antagonists naloxone and naltrexone.