Studies of salt and stress sensitivity on arterial pressure in renin-b deficient mice.

Excessive sodium intake is known to increase the risk for hypertension, heart disease, and stroke. Individuals who are more susceptible to the effects of high salt are at higher risk for cardiovascular diseases even independent of their blood pressure status. Local activation of the renin-angiotensi...

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Autores principales:	Pablo Nakagawa, Javier Gomez, Ko-Ting Lu, Justin L Grobe, Curt D Sigmund
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/264e6700e71a4992ac880d793ce758f1
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spelling	oai:doaj.org-article:264e6700e71a4992ac880d793ce758f12021-12-02T20:04:48ZStudies of salt and stress sensitivity on arterial pressure in renin-b deficient mice.1932-620310.1371/journal.pone.0250807https://doaj.org/article/264e6700e71a4992ac880d793ce758f12021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0250807https://doaj.org/toc/1932-6203Excessive sodium intake is known to increase the risk for hypertension, heart disease, and stroke. Individuals who are more susceptible to the effects of high salt are at higher risk for cardiovascular diseases even independent of their blood pressure status. Local activation of the renin-angiotensin system (RAS) in the brain, among other mechanisms, has been hypothesized to play a key role in contributing to salt balance. We have previously shown that deletion of the alternative renin isoform termed renin-b disinhibits the classical renin-a encoding preprorenin in the brain resulting in elevated brain RAS activity. Thus, we hypothesized that renin-b deficiency results in higher susceptibility to salt-induced elevation in blood pressure. Telemetry implanted Ren-bNull and wildtype littermate mice were first offered a low salt diet for a week and subsequently a high salt diet for another week. A high salt diet induced a mild blood pressure elevation in both Ren-bNull and wildtype mice, but mice lacking renin-b did not exhibit an exaggerated pressor response. When renin-b deficient mice were exposed to a high salt diet for a longer duration (4 weeks), there was a trend for increased myocardial enlargement in Ren-bNull mice when compared with control mice, but this did not reach statistical significance. Multiple studies have also demonstrated the association of environmental stress with hypertension. Activation of the RAS in the rostral ventrolateral medulla and the hypothalamus is required for stress-induced hypertension. Thus, we next questioned whether the lack of renin-b would result in exacerbated response to an acute restraint-stress. Wildtype and Ren-bNull mice equally exhibited elevated blood pressure in response to restraint-stress, which was similar in mice fed either a low or high salt diet. These studies suggest that mechanisms unrelated to salt and acute stress alter the cardiovascular phenotype in mice lacking renin-b.Pablo NakagawaJavier GomezKo-Ting LuJustin L GrobeCurt D SigmundPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 7, p e0250807 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Pablo Nakagawa Javier Gomez Ko-Ting Lu Justin L Grobe Curt D Sigmund Studies of salt and stress sensitivity on arterial pressure in renin-b deficient mice.
description	Excessive sodium intake is known to increase the risk for hypertension, heart disease, and stroke. Individuals who are more susceptible to the effects of high salt are at higher risk for cardiovascular diseases even independent of their blood pressure status. Local activation of the renin-angiotensin system (RAS) in the brain, among other mechanisms, has been hypothesized to play a key role in contributing to salt balance. We have previously shown that deletion of the alternative renin isoform termed renin-b disinhibits the classical renin-a encoding preprorenin in the brain resulting in elevated brain RAS activity. Thus, we hypothesized that renin-b deficiency results in higher susceptibility to salt-induced elevation in blood pressure. Telemetry implanted Ren-bNull and wildtype littermate mice were first offered a low salt diet for a week and subsequently a high salt diet for another week. A high salt diet induced a mild blood pressure elevation in both Ren-bNull and wildtype mice, but mice lacking renin-b did not exhibit an exaggerated pressor response. When renin-b deficient mice were exposed to a high salt diet for a longer duration (4 weeks), there was a trend for increased myocardial enlargement in Ren-bNull mice when compared with control mice, but this did not reach statistical significance. Multiple studies have also demonstrated the association of environmental stress with hypertension. Activation of the RAS in the rostral ventrolateral medulla and the hypothalamus is required for stress-induced hypertension. Thus, we next questioned whether the lack of renin-b would result in exacerbated response to an acute restraint-stress. Wildtype and Ren-bNull mice equally exhibited elevated blood pressure in response to restraint-stress, which was similar in mice fed either a low or high salt diet. These studies suggest that mechanisms unrelated to salt and acute stress alter the cardiovascular phenotype in mice lacking renin-b.
format	article
author	Pablo Nakagawa Javier Gomez Ko-Ting Lu Justin L Grobe Curt D Sigmund
author_facet	Pablo Nakagawa Javier Gomez Ko-Ting Lu Justin L Grobe Curt D Sigmund
author_sort	Pablo Nakagawa
title	Studies of salt and stress sensitivity on arterial pressure in renin-b deficient mice.
title_short	Studies of salt and stress sensitivity on arterial pressure in renin-b deficient mice.
title_full	Studies of salt and stress sensitivity on arterial pressure in renin-b deficient mice.
title_fullStr	Studies of salt and stress sensitivity on arterial pressure in renin-b deficient mice.
title_full_unstemmed	Studies of salt and stress sensitivity on arterial pressure in renin-b deficient mice.
title_sort	studies of salt and stress sensitivity on arterial pressure in renin-b deficient mice.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/264e6700e71a4992ac880d793ce758f1
work_keys_str_mv	AT pablonakagawa studiesofsaltandstresssensitivityonarterialpressureinreninbdeficientmice AT javiergomez studiesofsaltandstresssensitivityonarterialpressureinreninbdeficientmice AT kotinglu studiesofsaltandstresssensitivityonarterialpressureinreninbdeficientmice AT justinlgrobe studiesofsaltandstresssensitivityonarterialpressureinreninbdeficientmice AT curtdsigmund studiesofsaltandstresssensitivityonarterialpressureinreninbdeficientmice
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Studies of salt and stress sensitivity on arterial pressure in renin-b deficient mice.

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