Enhancement of vascular function by modulation of endogenous nitric oxide production or activity
AssigneeThe Board of Trustees of the Leland Stanford Junior University
InventorsJohn P. Cooke, Victor J. Dzau, Gary H. Gibbons
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Abstract
Vascular function and structure is maintained or improved by long term administration of physiologically acceptable compounds which enhance the level of endogenous nitric oxide or other intermediates in the NO induced relaxation pathway in the host. Alternatively, or in combination, other compounds may be administered which provide for short term enhancement of nitric oxide, either directly or by physiological processes.
Claims21
A method of inhibiting adherence of leukocytes to vascular endothelial cells of a mammalian host, said method comprising:
- administering a genetic construct comprising a gene encoding nitric oxide synthetase operably linked to a promoter to vascular endothelial cells at a site for leukocyte adherence, wherein said construct is administered intravascularly directly to said site and wherein said nitric oxide synthetase is expressed in vascular endothelial cells to enhance nitric oxide levels at said site and thereby inhibit said adherence of leukocytes at said site.
A method of improving NO-dependent vasodilation in a vasculature of a mammalian host, said method comprising:
- administering a genetic construct comprising a gene encoding nitric oxide synthetase operably linked to a promoter to cells at a site for reduced NO-dependent vasodilation wherein said construct is administered intravascularly directly to said site and wherein said nitric oxide synthetase is expressed at said site to enhance the level of nitric oxide in the vasculature and improve NO-dependent vasodilation at said site.
A method of inhibiting expression of a molecule involved in leukocyte accumulation on a vessel wall in a vascular system of a mammalian host, said method comprising:
- administering a genetic construct expressing a nitric oxide synthetase operably linked to a promoter to cells of a vessel wall at a site for leukocyte accumulation, wherein said construct is administered intravascularly directly to said site and wherein expression of the nitric oxide synthetase enhances the level of nitric oxide at said site thereby inhibiting expression of a molecule involved in leukocyte accumulation at said site.
Dependencies are inferred from the claim text.