Asset Details
Do you wish to reserve the book?
In vitro and in vivo studies on nitrate tolerance in rat
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
In vitro and in vivo studies on nitrate tolerance in rat
Do you wish to request the book?
In vitro and in vivo studies on nitrate tolerance in rat
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Dissertation
In vitro and in vivo studies on nitrate tolerance in rat
2006
Overview
This research represents an effort to bridge a critical gap in the knowledge regarding the phenomenon of nitrate tolerance. The first objective was designed to determine if hydrogen peroxide plays a role in the development of nitrate tolerance. Based on current data, one could conclude that nitrate tolerance was associated with decreased endogenous' formation of hydrogen peroxide, which attenuates nitrate tolerance development. Superoxide dismutase mimetics may reduce nitrate tolerance, in part, by increasing the formation of hydrogen peroxide. I have also tested the hypothesis that endogenous calcitonin gene-related peptide (CGRP) affects the process of nitrate tolerance development in blood vessels. The results suggested that nitroglycerin releases CGRP from sensory nerves during the process of desensitization to nitrovasodilators and that interference with either the release or action of endogenous CGRP during this period enhances the extent to which nitrate tolerance occurs. It was further tested whether nitrate tolerance induces a compensatory response involving potassium channels in nitroglycerin-induced smooth muscle relaxation. Findings from these studies provide evidence that (1) an increased expression of large-conductance, calcium-activated potassium channels, BKCa channels may be a mechanism for the NTG-enhanced BKCa current in aortic smooth muscle cells of nitrate-tolerant rats, and (2) the upregulation of BKCa channels in arterial muscle membranes in nitrate tolerance is regarded as a compensatory mechanism for maintaining the vascular relaxation. The results of these studies have definitely improved understanding of the altered cellular mechanisms in nitrate tolerance. Moreover, this information may have important therapeutic implications, inasmuch as the results obtained may suggest new strategies for the development of novel nitrates and like drugs that do not cause tolerance.
