Prostaglandins activate phosphoinositide metabolism in rat aorta

Excitatory Amino Acid Agonist‐Antagonist Interactions at 2‐Amino‐4‐Phosphonobutyric Acid‐Sensitive Quisqualate Receptors Coupled to Phosphoinositide Hydrolysis in Slices of Rat Hippocampus

“…When interactions among excitatory amino acids were examined, nonadditive effects were consistently observed. Nonadditive stimulation of phosphoinositide hydrolysis has also been reported to occur with combinations of nonexcitatory amino acid agonists that do not act on the same receptor (Suba and Roth, 1987). Thus, taken alone, the lack of additive responses among the excitatory amino acids in this study may not be conclusive evidence for interaction at the same receptor site.…”

Ryanodine reveals multiple contractile and relaxant mechanisms in vascular smooth muscle: simultaneous measurements of mechanical activity and of cytoplasmic free Ca2+ level with fura‐2

“…However, activation of PI turnover per se is not always a necessary condition for contraction in the aorta (Suba & Roth, 1987). If the sustained contraction in the absence of extracellular Ca2 + is induced by activation of protein kinase C (PKC) through diacylglycerol production (Itoh et al, 1986;Chiu et al, 1987a,b;Khalil & van Breemen, 1988; but see Inagaki et al, 1987), the contraction should necessitate increased PI turnover.…”

Differing calcium sensitivities of human cerebral and digital arteries, human metatarsal veins, and rat aorta.

“…It has therefore been inferred that contractile responses to U46619 are being largely mediated through the release of internal calcium stores. Since arachidonic acid is a component of phosphatidylinositol, which breaks down to inositol triphosphate (IP3), the postulated second messenger responsible for releasing calcium from intracellular stores, it is tempting to speculate that U46619 may be stimulating IP3 formation by interfering with the recycling of phosphatidylinositol in a manner similar to that of prostaglandins (Suba & Roth, 1987).…”