Prazosin-stimulated release of hepatic triacylglyceride lipase from primary cultured rat hepatocytes is involved in the regulation of cAMP-dependent protein kinase through activation of the Ca2+/calmodulin-dependent protein kinase-II

Abstract

These results suggested that prazosin-stimulated HTGL release from hepatocytes was caused by activation of PKA associated with stimulation of CaMK-II activity through a signal cascade from PLC.

The Proline 7 Substitution in the Preproneuropeptide Y Is Associated with Higher Hepatic Lipase Activity In Vivo

“…Carriers of the 7Pro allele were found to have a decreased basal but enhanced peripheral NPY release upon sympathetic stimulation [36, 37]. Catecholamines on the other hand as well as alpha-adrenergic stimulation have an inhibitory effect on HL secretion, and inhibition of alpha-adrenergic signalling stimulates the release of HL from hepatocytes [38–40]. These data lead us to speculate that the link between NPY and HL might be the peripheral sympathetic system (Figure 2).…”

Prazosin inhibits the growth and mobility of osteosarcoma cells

“…potential anti-tumor effects (9). Prazosin [1-(4-amino-6,7-dimethoxy-quinazolin-2-yl)-4-(2-furoyl) piperazine], an α1-adrenoceptor antagonist, had generally been used as a sympatholytic drug for the treatment of hypertension and posttraumatic stress disorder (PTSD) (9)(10)(11). Recently however, Lin et al demonstrated that Prazosin also displays an anti-proliferative effect in prostate cancer cells; it accomplished this by inducing apoptosis via resulting in DNA damage stress (12).…”