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Mechanisms of Central Sodium Sensing and Salt-Sensitive Hypertension

Award Number: F32HL158149
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 01/03/2022
PERIOD OF PERFORMANCE END DATE: 08/11/2024

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Mechanisms of Central Sodium Sensing and Salt-Sensitive Hypertension - PROJECT SUMMARY/ABSTRACT Excessive dietary sodium consumption is ubiquitous in the United States and is a large contributor to hypertension and cardiovascular disease. This is especially problematic for Black adults, who are known to have high rates of salt-sensitive hypertension. Although the mechanisms underlying salt-sensitive hypertension are poorly understood in humans, rodent studies document a neurohumoral component. Rodent studies have identified specialized sodium chloride (NaCl)-sensing neurons in the circumventricular organs (CVOs) in the brain (which lack a complete blood brain barrier (BBB)), that mediate NaCl-induced changes in sympathetic nerve activity (SNA), arginine vasopressin (AVP), and regulation of blood pressure (BP). Recent data suggests Na+-K+-2Cl- co-transporter (NKCC2) is not kidney specific but is in fact expressed in brain regions that regulate whole body NaCl and water homeostasis. Interestingly, Black adults have greater basal level NKCC2 renal activity, but it is unknown if these differences are present in sodium sensing areas of the brain. The objective of this F32 is to determine if NKCC2 contributes toward NaCl-sensitivity in a population that is more prone to salt- sensitive hypertension, Black adults. We seek to translate the prior rodent findings to humans by assessing neuronal activation (using blood oxygen level dependent functional magnetic resonance imaging, BOLD fMRI) as well as SNA, AVP, and BP during an acute hypernatremic stimulus, with and without an NKCC2 antagonist. This will enable us to isolate the role of NKCC2 in NaCl sensitivity in Black and White adults. The overall hypothesis is that Black adults have increased central sodium sensing and neurohumoral BP responses due to greater NKCC2 activity in the brain. Accordingly, the first specific aim is to determine if NKCC2 contributes to the differences observed in the neurohumoral regulation of blood pressure to acute hypernatremia between Black and White adults. We hypothesize that the NKCC2 antagonist furosemide will attenuate the increase in SNA, AVP, and BP during hypertonic saline infusion more in Black compared to White adults. The second specific aim is to determine if there are differences in sodium sensing areas in the brain that are influenced by NKCC2 between Black and White adults. We hypothesize that furosemide will attenuate the increase in BOLD fMRI signal during hypertonic saline infusion more in Black compared to White adults. This comprehensive assessment of sodium sensing and neurohumoral regulation of BP in response to hypertonic saline infusion, with and without a NKCC2 antagonist, will provide novel information on the mechanisms contributing to salt- sensitive BP. Understanding the central origins of sodium sensing and salt-sensitivity may lead to novel therapeutic approaches to combat hypertension, a costly public health problem. Innovative and translational approaches such as those employed in this proposal are needed to advance the field.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2025 ( Subtotal = -$43,684 )
2025	2024	UNIVERSITY OF DELAWARE	550 S COLLEGE AVE	NEWARK	DE	19713	NEW CASTLE	USA	Cardiovascular Diseases Research	001	3	6/17/2025	NON-COMPETING CONTINUATION	-$43,684
2025	2024	UNIVERSITY OF DELAWARE	550 S COLLEGE AVE	NEWARK	DE	19713	NEW CASTLE	USA	Cardiovascular Diseases Research	000	3	3/20/2025	NON-COMPETING CONTINUATION	$0
														Subtotal = -$43,684

Issue Date FY: 2024 ( Subtotal = $76,756 )
2024	2024	UNIVERSITY OF DELAWARE	220 HULLIHEN HALL	NEWARK	DE	19716	NEW CASTLE	USA	Cardiovascular Diseases Research	001	3	8/29/2024	NON-COMPETING CONTINUATION	$4,964
2024	2024	UNIVERSITY OF DELAWARE	220 HULLIHEN HALL	NEWARK	DE	19716	NEW CASTLE	USA	Cardiovascular Diseases Research	000	3	12/25/2023	NON-COMPETING CONTINUATION	$71,792
														Subtotal = $76,756

Issue Date FY: 2023 ( Subtotal = $69,500 )
2023	2023	UNIVERSITY OF DELAWARE	220 HULLIHEN HALL	NEWARK	DE	19716	NEW CASTLE	USA	Cardiovascular Diseases Research	000	2	11/18/2022	NON-COMPETING CONTINUATION	$67,582
2023	2023	UNIVERSITY OF DELAWARE	220 HULLIHEN HALL	NEWARK	DE	19716	NEW CASTLE	USA	Cardiovascular Diseases Research	001	2	4/3/2023	NON-COMPETING CONTINUATION	$1,918
														Subtotal = $69,500

Issue Date FY: 2022 ( Subtotal = $67,174 )
2022	2022	UNIVERSITY OF DELAWARE	220 HULLIHEN HALL	NEWARK	DE	19716	NEW CASTLE	USA	Cardiovascular Diseases Research	002	1	7/1/2022	NEW	$1,180
2022	2022	UNIVERSITY OF DELAWARE	220 HULLIHEN HALL	NEWARK	DE	19716	NEW CASTLE	USA	Cardiovascular Diseases Research	001	1	12/20/2021	NEW	$0
2022	2022	UNIVERSITY OF DELAWARE	220 HULLIHEN HALL	NEWARK	DE	19716	NEW CASTLE	USA	Cardiovascular Diseases Research	000	1	12/20/2021	NEW	$65,994
														Subtotal = $67,174

Grand Total All Awards = $169,746

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Mechanisms of Central Sodium Sensing and Salt-Sensitive Hypertension

Award Number: F32HL158149

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 01/03/2022

PERIOD OF PERFORMANCE END DATE: 08/11/2024

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