scholarly journals Secondary rise of albuminuria under AT1-receptor blockade--what is the potential role of aldosterone escape?

2006 ◽  
Vol 22 (1) ◽  
pp. 5-8 ◽  
Author(s):  
L. C. Rump
Keyword(s):  
Potential Role ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Secondary Rise

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.

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.

Angiotensin II regulates V2 receptor and pAQP2 during ureteral obstruction

2009 ◽  
Vol 296 (1) ◽  
pp. F127-F134 ◽  
Author(s):  
Anja M. Jensen ◽  
Eun Hui Bae ◽  
Robert A. Fenton ◽  
Rikke Nørregaard ◽  
Søren Nielsen ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sodium Fluoride ◽  
Ureteral Obstruction ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Receptor Complex ◽  
Camp Generation ◽  
Outer Stripe ◽  
V2 Receptor

Release of bilateral ureteral obstruction (BUO) is associated with nephrogenic diabetes insipidus (NDI) and a reduced abundance of the vasopressin-regulated aquaporins. To evaluate the role of the vasopressin type 2 receptor (V2R), we determined V2R abundance in kidneys from rats subjected to 24-h BUO or 24-h unilateral ureteral obstruction (UUO) followed by 48-h release. Because angiotensin II type 1 (AT1) receptor blockade attenuates postobstructive polyuria and aquaporin-2 (AQP2) downregulation, we examined the effect of AT1 receptor blockade on AQP2 phosphorylated at serine 256 (pS256-AQP2) and V2 receptor complex abundance in kidney inner medulla (IM). Furthermore, cAMP generation in sodium fluoride- and forskolin-stimulated inner medullary membrane fractions was studied after release of BUO. V2R was significantly reduced to 12% of sham levels in IM and to 52% of sham levels in cortex and outer stripe of outer medulla (OSOM) from BUO rats. In UUO rats, V2R abundance in the obstructed kidney IM decreased to 35% of sham levels, whereas it was comparable to sham levels in the nonobstructed kidney IM. No significant change was observed in cortex and OSOM. AT1 receptor blockade attenuated V2R, pS256-AQP2, and Gsα protein downregulation in IM and partially reversed the obstruction-induced inhibition of sodium fluoride- and forskolin-stimulated cAMP generation in inner medullary membrane fractions from BUO rats. In conclusion, V2R downregulation plays a pivotal role in development of NDI after release of BUO. In addition, we have shown that angiotensin II regulates the V2 receptor complex and pS256-AQP2 in postobstructive kidney IM, probably by stimulating cAMP generation.

AT1-RECEPTOR BLOCKADE AND INSULIN SENSITIVITY IN HYPERTENSIVE SUBJECTS: THE ROLE OF CAPILLARY RECRUITMENT: PP.11.435

2010 ◽  
Vol 28 ◽  
pp. e181
Author(s):  
AM Jonk ◽  
AJHM Houben ◽  
NC Schaper ◽  
PW de Leeuw ◽  
EH Serné ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
At1 Receptor ◽  
Receptor Blockade ◽  
Capillary Recruitment
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