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• W3023132906 abstract "This chapter focuses on the physiology of PTHrP in vascular smooth muscle, cardiovascular system, and central nervous system. In all smooth muscle cell beds studied to date, induction of PTHrP expression occurs in close association with normal physiological stimuli. Application of PTHrP to precontracted smooth muscle preparations induces relaxant activity, precisely mimicking the actions described previously for PTH. The ability of PTHrP to modulate vascular smooth muscle cell growth suggests that the protein might function during the development of the cardiovascular system. Although the cardiovascular system appears to develop normally in the PTHrP knockout mouse, homologous deletion of the PTH1R receptor results in a higher incidence of early fetal death at approximately embryonic day 9–10, coincident with development of the heart and major blood vessels. Transgenic mice expressing high levels of PTHrP and its receptor in vascular smooth muscle, created by crossing the ligand and receptor overexpressing mice, die at day E9.5 with severe thinning of the ventricle and disruption of ventricular trabeculae. PTHrP exerts its vasodilatory actions by activating the PTH1R. This receptor is expressed in rat vascular smooth muscle beds, and relaxation of aortic preparations is accompanied by an increased accumulation of cAMP. The hot spots for PTHrP gene expression are neuronal populations that have a number of features in common, including high-density L-VSCC expression as well as high-density expression of excitatory amino acid receptors and a known susceptibility to excitotoxicity." @default.
• W3023132906 created "2020-05-13" @default.
• W3023132906 creator A5025822097 @default.
• W3023132906 date "2002-01-01" @default.
• W3023132906 modified "2023-10-16" @default.
• W3023132906 title "Vascular, Cardiovascular, and Neurological Actions of Parathyroid-Related Protein" @default.
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• W3023132906 doi "https://doi.org/10.1016/b978-012098652-1.50132-3" @default.
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