Departments of Internal Medicine, Neuroscience, and Pharmacology, Francois M. Abboud Cardiovascular Center, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA.
Address correspondence to: Frank M. Faraci, Department of Internal Medicine, 3296 CBRB, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242-1081, USA. Phone: 319.335.7640; Email: firstname.lastname@example.org.
Published September 15, 2021 - More info
Hypertension is a leading cause of cognitive impairment and dementias. Such loss of brain health has a vascular component, but the mechanisms involved are poorly defined. In this issue of the JCI, Koide et al. provide evidence that end-organ effects of hypertension on capillary endothelium and inward-rectifier K+ channels (Kir2.1) impair integrated propagation of electrical signals and vasodilation upstream, resulting in reduced neurovascular coupling (NVC) despite neural activation. NVC was partly restored by amlodipine, but not losartan. Moreover, NVC was improved by eplerenone in the presence of losartan, suggesting a role for aldosterone. These findings support the concept that endothelial cells and Kir2.1 are potential therapeutic targets to prevent or reverse the loss of NVC and the vascular component of cognitive deficits that occur with increased frequency during hypertension.
A subscription is required for you to read this article in full. If you are a subscriber, you may sign in to continue reading.
Click here to sign into your account.
Please select one of the subscription options, which includes a low-cost option just for this article.
If you are at an institution or library and believe you should have access, please check with your librarian or administrator (more information).
Please try these troubleshooting tips.