Norepinephrine Stimulates Inositol Trisphosphate Formation in Rat Pulmonary Arteries

Abstract

Although the discovery of the “phosphoinositide effect” occurred over 35 years ago, its mechanisms were explored only over the last decade. It now is clear that hydrolysis of phosphoinositides generates second messengers for multiple cellular functions when receptors are activated by a wide array of hormones and agonists in a variety of cell types (for review see Rana and Hokin, 1990). Early studies focused on the role of phosphoinositides on regulation of secretion or control of release of secretory cell contents (Hokin and Hokin, 1953, 1960; Freinkel, 1957; Hokin et al., 1958, 1963; Axen et al., 1983). In recent years, studies of the physiological effects of phosphoinositide hydrolysis have extended to such cell types and tissues as cerebral cortical slices (Kendall and Nahorski, 1984), sympathetic ganglia (Bone et al., 1984), adrenal glomerulosa cells (Kojima et al., 1986), rod outer segments (Brown et al., 1987), epithelium (Anderson and Welsh, 1990), leukocytes (Bradford and Rubin, 1986), skeletal muscle (Volpe et al., 1985), and smooth muscle (Akhtar and Abdel-Latif, 1980; Bielkiewicz-vollrath et al., 1987).