Salt sensitivity in genetically hypertensive rats of the Lyon strain

Florin, Marine; Lo, Ming; Liu, Kiao Ling; Sassard, J

doi:10.1046/j.1523-1755.2001.0590051865.x

Cited by 28 publications

(19 citation statements)

References 24 publications

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“…The objective of this experiment was to determine whether the procedures employing very low doses of systemic ANG II or Aldo that induced the sensitization of slow pressor ANG II-induced hypertension (48,49) could be used to sensitize the hypertensive response to another hypertension-generating stimulus, i.e., 2% saline as the sole drinking fluid (38,10,27). Rats were randomly assigned to one of three groups (n ϭ 9 or 10/group): 1) Induction with subcutaneous vehicle (isotonic saline; control), 2) Induction with subcutaneous ANG II (10 ng·kg Ϫ1 ·min Ϫ1 ; Sigma, St. Louis, MO), or 3) Induction with subcutaneous Aldo (750 ng/h; Sigma).…”

Section: Experimental Protocol Imentioning

confidence: 99%

“…There are several genetic models of salt-sensitive hypertensive rats, including the Dahl salt-sensitive-(Dahl S) (8), borderline hypertensive (26), salt-sensitive spontaneous hypertensive (1), and Lyon genetically hypertensive (10). These strains were initially bred specifically for either a BP increase to high-salt intake or first selected for high BP and discovered later to be salt-sensitive.…”

Section: Salt Sensitivity and Hypertensionmentioning

confidence: 99%

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CNS neuroplasticity and salt-sensitive hypertension induced by prior treatment with subpressor doses of ANG II or aldosterone

Clayton

Zhang

Beltz

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Although sensitivity to high dietary NaCl is regarded to be a risk factor for cardiovascular disease, the causes of salt-sensitive hypertension remain elusive. Previously, we have shown that rats pretreated with subpressor doses of either ANG II or aldosterone (Aldo) show sensitized hypertensive responses to a mild pressor dose of ANG II when tested after an intervening delay. The current studies investigated whether such treatments will induce salt sensitivity. In studies employing an induction-delay-expression experimental design, male rats were instrumented for chronic mean arterial pressure (MAP) recording. In separate experiments, ANG II, Aldo, or vehicle was delivered either subcutaneously or intracerebroventricularly during the induction. There were no sustained differences in BP during the delay prior to being given 2% saline. While consuming 2% saline during the expression, both ANG II- and Aldo-pretreated rats showed significantly greater hypertension. When hexamethonium was used to assess autonomic control of MAP, no differences in the decrease of MAP in response to ganglionic blockade were detected during the induction. However, during the expression, the fall was greater in sensitized rats. In separate experiments, brain tissue that was collected at the end of delay showed increases in message or activation of putative markers of neuroplasticity (i.e., brain-derived neurotrophic factor, p38 mitogen-activated protein kinase, and cAMP response element-binding protein). These experiments demonstrate that prior administration of nonpressor doses of either ANG II or Aldo will induce salt sensitivity. Collectively, our findings indicate that treatment with subpressor doses of ANG II and Aldo initiate central neuroplastic changes that are involved in hypertension of different etiologies.

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Section: Experimental Protocol Imentioning

confidence: 99%

Section: Salt Sensitivity and Hypertensionmentioning

confidence: 99%

CNS neuroplasticity and salt-sensitive hypertension induced by prior treatment with subpressor doses of ANG II or aldosterone

Clayton

Zhang

Beltz

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Moreover, the hypertension of LH rats is a lowrenin and salt-sensitive form [6]. In addition, LH rats compared with normotensive (LL) controls exhibit a reduced renal blood flow (RBF) and glomerular filtration rate (GFR) as well as a blunted pressure-natriuresis curve [7,8].…”

Section: Introductionmentioning

confidence: 99%

Acute pressure–natriuresis function shows early impairment in Lyon hypertensive rats

Liu¹,

Benzoni²,

Sassard³

2005

Journal of Hypertension

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“…200 mmHg), whereas the hypertension development in NIDDM is modest and progressive. The LH rat develops a mild hypertension (SBP 160-170 mmHg at adult age) associated with numerous metabolic risk factors and renal dysfunctions such as obesity, spontaneous hyperlipidemia, elevated glucose/insulin ratio, blunted pressurenatriuresis function, glomerular lesions and exaggerated urinary protein excretion [19][20][21][22][23]. It could be the fact that the development of a moderate NIDDM in LH rats might better reconcile the BP and metabolic disorders.…”

Section: Discussionmentioning

confidence: 99%

“…The blood pressure (BP) of LH rats is progressively elevated to reach a mild hypertension in adults associated with altered renal function, glomerular lesions and exaggerated urinary protein excretion [20][21][22][23]. In the present study, we aimed to develop, in LH rats in which the metabolic syndrome is genetically predisposed [19,20,24], a model of NIDDM by neonatal administration of STZ.…”

Section: Introductionmentioning

confidence: 99%

Neonatal streptozotocin-induced glucose intolerance: different consequences in Lyon normotensive and hypertensive rats

Emonnot¹,

Cohen

2007

Journal of Hypertension

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Salt sensitivity in genetically hypertensive rats of the Lyon strain

Abstract: The present work demonstrates that LH rats are salt sensitive. This characteristic manifests despite the lack of an active renin-angiotensin system and is not explained by a hypersensitivity to aldosterone.

Cited by 28 publications

References 24 publications

CNS neuroplasticity and salt-sensitive hypertension induced by prior treatment with subpressor doses of ANG II or aldosterone

CNS neuroplasticity and salt-sensitive hypertension induced by prior treatment with subpressor doses of ANG II or aldosterone

Acute pressure–natriuresis function shows early impairment in Lyon hypertensive rats

Neonatal streptozotocin-induced glucose intolerance: different consequences in Lyon normotensive and hypertensive rats

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