Reconstitution of autophagy ameliorates vascular function and arterial stiffening in spontaneously hypertensive rats.
Acid Phosphatase
/ metabolism
Animals
Antihypertensive Agents
/ pharmacology
Arterial Pressure
/ drug effects
Autophagy
/ drug effects
Autophagy-Related Proteins
/ metabolism
Disease Models, Animal
Hypertension
/ drug therapy
Male
Mesenteric Arteries
/ drug effects
Rats, Inbred SHR
Rats, Wistar
Reactive Oxygen Species
/ metabolism
Signal Transduction
Trehalose
/ pharmacology
Vascular Stiffness
/ drug effects
Vasodilation
/ drug effects
rho-Associated Kinases
/ metabolism
arterial stiffening
autophagy
hypertension
vascular aging
vascular function
Journal
American journal of physiology. Heart and circulatory physiology
ISSN: 1522-1539
Titre abrégé: Am J Physiol Heart Circ Physiol
Pays: United States
ID NLM: 100901228
Informations de publication
Date de publication:
01 11 2019
01 11 2019
Historique:
pubmed:
31
8
2019
medline:
9
4
2020
entrez:
31
8
2019
Statut:
ppublish
Résumé
Insufficient autophagy has been proposed as a mechanism of cellular aging, as this leads to the accumulation of dysfunctional macromolecules and organelles. Premature vascular aging occurs in hypertension. In fact, many factors that contribute to the deterioration of vascular function as we age are accelerated in clinical and experimental hypertension. Previously, we have reported decreased autophagy in arteries from spontaneously hypertensive rats (SHRs); however, the effects of restoring autophagic activity on blood pressure and vascular function are currently unknown. We hypothesized that reconstitution of arterial autophagy in SHRs would decrease blood pressure and improve endothelium-dependent relaxation. We treated 14- to 18-wk-old Wistar rats (
Identifiants
pubmed: 31469290
doi: 10.1152/ajpheart.00227.2019
pmc: PMC6879927
doi:
Substances chimiques
Antihypertensive Agents
0
Autophagy-Related Proteins
0
Reactive Oxygen Species
0
Trehalose
B8WCK70T7I
rho-Associated Kinases
EC 2.7.11.1
Acid Phosphatase
EC 3.1.3.2
Acp2 protein, rat
EC 3.1.3.2
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Webcast
Langues
eng
Sous-ensembles de citation
IM
Pagination
H1013-H1027Subventions
Organisme : NHLBI NIH HHS
ID : P01 HL134604
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL143082
Pays : United States
Organisme : NIGMS NIH HHS
ID : K99 GM118885
Pays : United States
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