Blockade of the renin-angiotensin system in small arteries and anticontractile function of perivascular adipose tissue. 2015

Claudia Agabiti Rosei, and Sarah B Withers, and Laila Belcaid, and Carolina De Ciuceis, and Damiano Rizzoni, and Anthony M Heagerty
aInstitute of Cardiovascular Sciences, Faculty of Medical and Human Sciences, University of Manchester, UK bClinica Medica, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.

OBJECTIVE In patients with obesity, there is increased inflammation with attendant oxidative stress in perivascular adipose tissue. This has functional consequences with loss of vasodilator adipokine bioavailability. Part of the inflammatory response is mediated by increased activation of the renin-angiotensin-aldosterone axis. Therefore, this study was designed to investigate whether angiotensin-converting enzyme inhibitors or angiotensin receptor blockers can improve the anticontractile function of perivascular adipose tissue. METHODS Segments of rat mesenteric small artery were dissected and mounted in a wire myograph and contracted to incremental doses of norepinephrine in the presence and absence of perivascular adipose tissue and in conditions of normal oxygenation or after hypoxia and incubated with captopril or telmisartan. RESULTS Vessels with perivascular adipose tissue contracted significantly less than arteries with perivascular adipose tissue removed under normal oxygenation conditions, indicating that perivascular adipose tissue exerts an anticontractile effect. Hypoxia induced a loss of this anticontractile effect which could be completely prevented with captopril or telmisartan. CONCLUSIONS The in-vitro creation of a hypoxic environment can simulate the loss of anticontractile perivascular adipose tissue function seen in vivo in obese patients, and this can be prevented using inhibitors of the renin-angiotensin cascade.

UI MeSH Term Description Entries
D007249 Inflammation A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. Innate Inflammatory Response,Inflammations,Inflammatory Response, Innate,Innate Inflammatory Responses
D008297 Male Males
D008638 Mesenteric Arteries Arteries which arise from the abdominal aorta and distribute to most of the intestines. Arteries, Mesenteric,Artery, Mesenteric,Mesenteric Artery
D009638 Norepinephrine Precursor of epinephrine that is secreted by the ADRENAL MEDULLA and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers, and of the diffuse projection system in the brain that arises from the LOCUS CERULEUS. It is also found in plants and is used pharmacologically as a sympathomimetic. Levarterenol,Levonorepinephrine,Noradrenaline,Arterenol,Levonor,Levophed,Levophed Bitartrate,Noradrenaline Bitartrate,Noradrénaline tartrate renaudin,Norepinephrin d-Tartrate (1:1),Norepinephrine Bitartrate,Norepinephrine Hydrochloride,Norepinephrine Hydrochloride, (+)-Isomer,Norepinephrine Hydrochloride, (+,-)-Isomer,Norepinephrine d-Tartrate (1:1),Norepinephrine l-Tartrate (1:1),Norepinephrine l-Tartrate (1:1), (+,-)-Isomer,Norepinephrine l-Tartrate (1:1), Monohydrate,Norepinephrine l-Tartrate (1:1), Monohydrate, (+)-Isomer,Norepinephrine l-Tartrate (1:2),Norepinephrine l-Tartrate, (+)-Isomer,Norepinephrine, (+)-Isomer,Norepinephrine, (+,-)-Isomer
D009765 Obesity A status with BODY WEIGHT that is grossly above the recommended standards, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).
D011921 Rats, Inbred WKY A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR). Rats, Wistar Kyoto,Wistar Kyoto Rat,Rats, WKY,Inbred WKY Rat,Inbred WKY Rats,Kyoto Rat, Wistar,Rat, Inbred WKY,Rat, WKY,Rat, Wistar Kyoto,WKY Rat,WKY Rat, Inbred,WKY Rats,WKY Rats, Inbred,Wistar Kyoto Rats
D012084 Renin-Angiotensin System A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM. Renin-Angiotensin-Aldosterone System,Renin Angiotensin Aldosterone System,Renin Angiotensin System,System, Renin-Angiotensin,System, Renin-Angiotensin-Aldosterone
D004195 Disease Models, Animal Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases. Animal Disease Model,Animal Disease Models,Disease Model, Animal
D004353 Drug Evaluation, Preclinical Preclinical testing of drugs in experimental animals or in vitro for their biological and toxic effects and potential clinical applications. Drug Screening,Evaluation Studies, Drug, Pre-Clinical,Drug Evaluation Studies, Preclinical,Drug Evaluations, Preclinical,Evaluation Studies, Drug, Preclinical,Evaluation, Preclinical Drug,Evaluations, Preclinical Drug,Medicinal Plants Testing, Preclinical,Preclinical Drug Evaluation,Preclinical Drug Evaluations,Drug Screenings,Screening, Drug,Screenings, Drug
D005260 Female Females

Related Publications

Claudia Agabiti Rosei, and Sarah B Withers, and Laila Belcaid, and Carolina De Ciuceis, and Damiano Rizzoni, and Anthony M Heagerty
January 2020, Frontiers in physiology,
Claudia Agabiti Rosei, and Sarah B Withers, and Laila Belcaid, and Carolina De Ciuceis, and Damiano Rizzoni, and Anthony M Heagerty
March 2019, Nitric oxide : biology and chemistry,
Claudia Agabiti Rosei, and Sarah B Withers, and Laila Belcaid, and Carolina De Ciuceis, and Damiano Rizzoni, and Anthony M Heagerty
December 2020, American journal of physiology. Heart and circulatory physiology,
Claudia Agabiti Rosei, and Sarah B Withers, and Laila Belcaid, and Carolina De Ciuceis, and Damiano Rizzoni, and Anthony M Heagerty
January 2021, Frontiers in cardiovascular medicine,
Claudia Agabiti Rosei, and Sarah B Withers, and Laila Belcaid, and Carolina De Ciuceis, and Damiano Rizzoni, and Anthony M Heagerty
April 2008, Current hypertension reports,
Claudia Agabiti Rosei, and Sarah B Withers, and Laila Belcaid, and Carolina De Ciuceis, and Damiano Rizzoni, and Anthony M Heagerty
September 2012, Nihon rinsho. Japanese journal of clinical medicine,
Claudia Agabiti Rosei, and Sarah B Withers, and Laila Belcaid, and Carolina De Ciuceis, and Damiano Rizzoni, and Anthony M Heagerty
April 2008, The Journal of endocrinology,
Claudia Agabiti Rosei, and Sarah B Withers, and Laila Belcaid, and Carolina De Ciuceis, and Damiano Rizzoni, and Anthony M Heagerty
January 2012, Frontiers in pharmacology,
Claudia Agabiti Rosei, and Sarah B Withers, and Laila Belcaid, and Carolina De Ciuceis, and Damiano Rizzoni, and Anthony M Heagerty
December 2020, Clinical science (London, England : 1979),
Claudia Agabiti Rosei, and Sarah B Withers, and Laila Belcaid, and Carolina De Ciuceis, and Damiano Rizzoni, and Anthony M Heagerty
January 2022, Journal of vascular research,
Copied contents to your clipboard!