Multiple Interactions Between the Renin-Angiotensin and the Kallikrein-Kinin Systems: Role of ACE Inhibition and AT1 Receptor Blockade

2002 ◽  
Vol 39 (4) ◽  
pp. 478-487 ◽  
Author(s):  
Carsten Tschöpe ◽  
Heinz-Peter Schultheiss ◽  
Thomas Walther
Keyword(s):  
Ace Inhibition ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Renin Angiotensin ◽  
Multiple Interactions

scholarly journals Renin–angiotensin–aldosterone system blockade with telmisartan prevents the decline in cardiac contractility orchiectomy-dependent in SHR: role of PPAR-γ activation

2021 ◽  
Author(s):  
Marito Afonso Sousa Costa Silva ◽  
Camila Almenara ◽  
Antonio Marcos Birocale ◽  
Renata Andrade Ávila ◽  
Ivanita Stefanon ◽  
...  
Keyword(s):  
Cardiac Contractility ◽  
Renin Angiotensin System ◽  
At1 Receptor ◽  
Control Group ◽  
Receptor Blockade ◽  
Testosterone Deficiency ◽  
Renin Angiotensin ◽  
Ppar Γ ◽  
Cardiac Contractile

Abstract The present study aimed to investigate the beneficial role of AT1 receptor blockade and PPAR-γ activation in preventing cardiac contractile changes in hypertensive animals (SHR) with testosterone deficiency. Rats were divided into a control group (sham), orchiectomized (OCT), orchiectomized that received telmisartan (OCT + Tel) or telmisartan plus PPAR-γ antagonist (OCT + Tel + BADGE). After 8 weeks, contractility of isolated papillary muscles was evaluated. The OCT group showed a reduction in the contraction force, avoided in the OCT + Tel and Tel + BADGE groups. Post-pause potentiation (PPP) was similar in the Sham, OCT and OCT + Tel group, suggesting prevention of sarcoplasmic reticulum activity. In contrast, PPP in the OCT + Tel + BADGE group decreased. The reduction in response to calcium or isoproterenol in the OCT group was prevented in the OCT + Tel and Tel + BADGE group. The influx of calcium, assessed indirectly, although it was similar in the OCT and Sham groups, increased both in the OCT + Tel groups and in the OCT + Tel + BADGE groups. SERCA2a protein expression was increased in the OCT group, which was avoided in the OCT + Tel and Tel + BADGE group. NCX expression was increased in the Tel + BADGE group compared to OCT + Tel and sham. Our results suggest that AT1 receptor blockade with telmisartan prevents compromised papillary muscle contractility in SHR. Moreover, it has been shown that the activation of PPAR-γ adds benefits to the inhibition of renin-angiotensin system with telmisartan in preventing harmful effects on the contractility of hypertensive rats with testosterone deficiency.

scholarly journals Prevention of atherosclerosis by specific AT1-receptor blockade with candesartan cilexetil

2001 ◽  
Vol 2 (1_suppl) ◽  
pp. S77-S80
Author(s):  
Vasilios Papademetriou ◽  
Philippe Mammillot ◽  
Robert Redman ◽  
Aldo Notargiacomo ◽  
Puneet Narayan ◽  
...  
Keyword(s):  
At1 Receptor ◽  
Receptor Blockade ◽  
Dependent Manner ◽  
Vascular Events ◽  
Oxidised Ldl ◽  
Atherosclerotic Plaque Formation ◽  
Maximum Inhibition ◽  
Prevention Of Atherosclerosis ◽  
Dose Dependent

Several studies indicate that blockade of the renin-angiotensin-aldosterone system (RAAS) can prevent atherosclerosis and vascular events, but the precise mechanisms involved are still unclear. In this study, we investigated the effect of the AT 1-receptor blocker, candesartan, in the prevention of atherosclerosis in Watanabe heritable hyperlipidaemic (WHHL) rabbits and also the effect of AT1-receptor blockade in the uptake of oxidised LDL by macrophage cell cultures. In the first set of experiments, 12 WHHL rabbits were randomly assigned to three groups: placebo, atenolol 5 mg/kg daily or candesartan 2 mg/kg daily for six months. Compared with controls and atenolol-treated rabbits, candesartan treatment resulted in a significant 50—60% reduction of atherosclerotic plaque formation and a 66% reduction in cholesterol accumulation in the thoracic aorta. Studies in macrophage cultures indicated that candesartan prevented uptake of oxidised LDL-(oxLDL)-cholesterol by cultured macrophages. Candesartan inhibited the uptake of oxLDL in a dose-dependent manner, reaching a maximum inhibition of 70% at concentrations of 5.6 µg/ml. Further studies in other animal models and well-designed trials in humans are warranted to further explore the role of AT1-receptor blockade in the prevention of atherosclerosis.

Pivotal role of the renin-angiotensin system in Lyon hypertensive rats

1997 ◽  
Vol 273 (5) ◽  
pp. R1793-R1799 ◽  
Author(s):  
Pierre Lantelme ◽  
Ming Lo ◽  
Laurent Luttenauer ◽  
Jean Sassard
Keyword(s):  
Renin Angiotensin System ◽  
Ace Inhibition ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Adult Age ◽  
Enhanced Sensitivity ◽  
Regional Hemodynamics ◽  
Renal Vascular

We assessed the role of the renin-angiotensin system (RAS) in Lyon genetically hypertensive (LH) and normotensive (LN) rats by measuring 1) kidney renin and prorenin contents; 2) effects of early, prolonged angiotensin-converting enzyme (ACE) inhibition on blood pressure (BP) and regional hemodynamics; and 3) acute and chronic responses to angiotensin II (ANG II) and norepinephrine (NE). At the adult age, LH rats differed from LN rats by elevated BP, left ventricle weight, and vascular resistances, especially in the kidneys, associated with lower kidney renin and prorenin contents. ACE inhibition (perindopril, 3 mg ⋅ kg−1 ⋅ 24 h−1 orally from 3 to 15 wk of age) suppressed the development of hypertension, cardiac hypertrophy, and the increase in renal vascular resistances. No specific hypersensitivity to ANG II could be disclosed in acute conditions. In perindopril-treated LH rats, a 4-wk infusion of ANG II (200 ng ⋅ kg−1 ⋅ min−1) but not of NE (1,000 ng ⋅ kg−1 ⋅ min−1) restored hypertension, mimicked the hemodynamic alterations seen in untreated LH rats, and produced a brief sodium retention. It is concluded that in LH rats, despite a low basal renin secretion, hypertension and hemodynamic abnormalities 1) are fully dependent on an active RAS and 2) may involve an enhanced sensitivity to the chronic effects of ANG II.

Role of the renin-angiotensin system in the systemic microvascular inflammation of alveolar hypoxia

2007 ◽  
Vol 292 (5) ◽  
pp. H2285-H2294 ◽  
Author(s):  
Norberto C. Gonzalez ◽  
Julie Allen ◽  
Eric J. Schmidt ◽  
Alfred J. Casillan ◽  
Teresa Orth ◽  
...  
Keyword(s):  
Ace Inhibitor ◽  
Renin Angiotensin System ◽  
Ace Inhibition ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Alveolar Hypoxia ◽  
Microvascular Inflammation

Alveolar hypoxia (AH) induces widespread systemic inflammation. Previous studies have shown dissociation between microvascular Po2 and inflammation. Furthermore, plasma from AH rats (PAHR) induces mast cell (MC) activation, inflammation, and vasoconstriction in normoxic cremasters, while plasma from normoxic rats does not produce these responses. These results suggest that inflammation of AH is triggered by a blood-carried agent. This study investigated the involvement of the renin-angiotensin system (RAS) in the inflammation of AH. Both an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin II (ANG II) receptor blocker (ANG II RB) inhibited the leukocyte-endothelial adherence produced by AH, as well as the inflammation produced by PAHR in normoxic rat cremasters. MC stabilization with cromolyn blocked the effects of PAHR but not those of topical ANG II on normoxic cremasters, suggesting ANG II generation via MC activation by PAHR. This was supported by the observation that ACE inhibition and ANG II RB blocked the leukocyte-endothelial adherence produced by the MC secretagogue compound 48/80. These results suggest that the intermediary agent contained in PAHR activates MC and stimulates the RAS, leading to inflammation, and imply an RAS role in AH-induced inflammation.

The role of angiotensin AT1 receptor-associated protein in renin-angiotensin system regulation and function

2007 ◽  
Vol 9 (2) ◽  
pp. 121-127 ◽  
Author(s):  
Kouichi Tamura ◽  
Yutaka Tanaka ◽  
Yuko Tsurumi ◽  
Koichi Azuma ◽  
Atsu-Ichiro Shigenaga ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
At1 Receptor ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Receptor Associated Protein ◽  
And Function
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