Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597554
Title: Role of natriuretic peptides in the response of vascular smooth muscle to injury
Author: Chen, Q.
Awarding Body: University of Cambridge
Current Institution: University of Cambridge
Date of Award: 1997
Availability of Full Text:
Full text unavailable from EThOS.
Please contact the current institution’s library for further details.
Abstract:
Vascular smooth muscle cell (VSMC) proliferation with neointima formation is the key feature of restenosis after successful percutaneous transluminal coronary angioplasty (PTCA), which severely limits the clinical benefits of a major option in the treatment of coronary heart disease. To date, the prevention and therapy of restenosis in humans remain limited or unsuccessful. Natriuretic peptides (NP) are powerful inhibitors of VSMC proliferation in vitro. However, the mechanisms by which NP inhibit VSMC proliferation are still nuclear, and neither are the in vivo effects of NP on VSMC proliferation known. This dissertation is addressed to the study of the interaction of the NP system with VSMC under pathological conditions of arterial injury. Normal VSMC from different species or different arteries all expressed NP receptors (NPR), although in different subtypes. Normal rat carotid arteries expressed type-A NPR (NPR-A), whereas normal rabbit ear central arteries expressed exclusively type-B NPR (NPR-B). Despite this difference in normal arteries, neointimal VSMC in both rat and rabbit arteries expressed the same subtype of NPR, type-C (NPR-C) implying the involvement of NPR-C in the regulation of arterial response to injury. In the rabbit model of arterial injury, the media of damaged arteries also expressed NPR-C besides the NPR-B that already exists in normal arteries. Time course experiments of NPR expression in this model showed that NPR-C were upregulated between 5 and 7 days after arterial injury. Affinity cross-linking demonstrated that the molecular weights of reduced NPR-A, NPR-B and NPR-C in arteries were 120, 130 and 64 kDa, respectively. Second messenger assays showed that NPR-A and NPR-B in the normal arteries were coupled with cGMP system, whereas NPR-C was not found to be coupled to the cGMP nor to the cAMP system.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.597554  DOI: Not available
Share: