Numerous Errors

Abstract

In Figure 4 in his review article (1), Schleusner shows a smooth muscle cell in the uterus and signal transduction mechanisms. Unfortunately, there are numerous errors in the accompanying text. The s-adrenergic receptor in the uterus is the s2-adrenoceptor. This matters because the pharmacological agents used are 2-adrenoceptor agonists ([2], page 433). There are different G proteins. The G protein involved in the signal transduction of the s2-adrenoceptor is the stimulatory Gs protein ([2]], page 320). The represented oxytocin receptors and prostaglandin receptors also act through G proteins—in particular, Gq proteins. Also, for these receptors, phospholipase C as an effector is missing. There is not only one prostaglandin receptor, but it needs to be specified that prostaglandin F2α induces a contraction of the smooth muscle cells through the FP-receptor ([2]], page 445). The receptors are represented by different symbols. The prostaglandin receptor suggests a channel-like structure with one pore and two receptor units. This is erroneous. Prostaglandin receptors are not among the group of the ligand-controlled ion channels but among the group of G-protein-linked receptors. All depicted receptors should have been represented with 7 transmembrane domains ([2]], page 64–66). There is no molecule with the name “inosidol phosphate.” The molecule that mobilizes Ca2+ from intracellular stores is called inosidol-1,4,5-trisphosphate and originates from the breakdown of phosphatidylinositol-4,5-bisphosphate through phospholipase C ([2]], page 64–66). The soluble guanylyl cyclase as a receptor for NO-pharmacological agents is lacking from the figure. Guanylyl cyclase synthesizes cGMP from GTP. Guanylyl cyclase should have been included in the figure because cAMP-synthesizing adenylyl cyclase is also shown ([2], page 535). Calcium channel antagonists of the dihydropyridine type, such as nifedipine, inhibit the Ca2+ influx through voltage-dependent calcium channels located in the plasma membrane, not the release of calcium from intracellular stores ([2]], page 505). Indomethacine is obsolete because of its high rate of adverse side effects and should be replaced with substances that are better tolerated , such as ibuprofen ([2]], page 211–12).