# N-methyl-D-aspartate receptors (NMDAr) participates in renal hemodynamic regulation and blood pressure homeostasis

> **NIH NIH K01** · EMORY UNIVERSITY · 2021 · $115,272

## Abstract

Abstract
Internationally, hypertension is the leading single risk factor for mortality. However, in more than 90% of
hypertensive patients, the cause is unknown. There is a critical need to understand the mechanisms behind
the origins of hypertension to enable the development of new therapies. Connecting tubule-glomerular
feedback (CNTGF) is an epithelial sodium channel (ENaC)-dependent kidney feedback mechanism that
facilitates sodium excretion under certain physiological situations by inducing vasodilation. It has been
previously demonstrated that amino acids, mediated by the N-methyl-D-aspartate receptors (NMDAr), can
induce renal vasodilation. The NMDAr-induced vasodilation mechanism is unknown. Dr. Romero’s long-term
objectives are to explore the consequences of impaired vasodilation in the kidney as a cause of hypertension
and develop a program to thoroughly understand some of the causes of human hypertension. The main
hypothesis is that the mechanisms of NMDAr-mediated vasodilation and CNTGF are closely related and that
impairments of these biological pathways induce hypertension. The hypothesis will be addressed through the
following specific aims. AIM I: To determine the mechanism of NMDAr-induced renal vasodilation. We will
evaluate the role of NMDAr in CNTGF-induced vasodilation in vitro using microperfusion, and in-vivo using
NMDAr NR2C null mice. Aim II: To determine the mechanism by which NMDAr interacts with ENaC.
Using tubule microperfusion, electrophysiology, confocal imaging techniques, and proteoteomic approaches,
we will explore the molecular signaling associated with the interaction between NMDAr and ENaC which
induces the vasodilation. Aim III: To test the effect of NMDAr on blood pressure and renal
hemodynamics. We will evaluate the role of NMDA on blood pressure and renal hemodynamics by treating
ENaC channel gain-in-function mice (Liddle syndrome) with NMDAr inhibitors. The objective and hypothesis of
this proposal align with those of the NHLBI that promote the prevention and treatment of heart and blood
diseases by stimulating basic discoveries about the causes of diseases. Dr. Romero’s development plan
during these funding years include: 1) Increasing his research experience by consolidating the microperfusion
technique and exploring two new areas relating to electrophysiology and proteomics while expanding his
critical thinking and laboratory management skills; 2) Increasing his teaching and mentoring experience; 3)
Further developing his communication skills and publication record. Dr. Romero will be guided by Dr. Wall as a
principal mentor as well as Dr. Eaton and Dr. Hoover as a co-mentors. In addition, an advisory committee will
be supporting the development of this plan. Dr. Romero’s career goal is to be an independently funded
principal investigator in a highly ranked U.S. university to study renal hemodynamics and tubular transport
interactions and their roles in hypertension. This career development plan will b...

## Key facts

- **NIH application ID:** 10105015
- **Project number:** 1K01HL155235-01
- **Recipient organization:** EMORY UNIVERSITY
- **Principal Investigator:** Cesar Andres Romero
- **Activity code:** K01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $115,272
- **Award type:** 1
- **Project period:** 2021-01-07 → 2025-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10105015

## Citation

> US National Institutes of Health, RePORTER application 10105015, N-methyl-D-aspartate receptors (NMDAr) participates in renal hemodynamic regulation and blood pressure homeostasis (1K01HL155235-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10105015. Licensed CC0.

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