Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Chronic delayed cerebral vasospasm has a major impact on morbidity and mortality related to aneurysmal subarachnoid hemorrhage. Reduced concentrations of endothelium-derived NO, an important vasodilator, and increased levels of endothelin-1, one of the most potent vasoconstrictors, are important contributory factors. This review discusses the relevant mechanisms in cerebral vasospasm.
Despite treatment being available for angina in the form of β-blockers and calcium-channel blockers, these drugs are contraindicated in some patients. PharmacologicalIfinhibition could prove a promising alternative for protection from angina through heart-rate slowing. This review discusses the early mechanisms and early clinical use of ivabradine as a specific bradycardic agent.