Angiotensin II type 1 receptor A1166C polymorphism in relation to incident cardiovascular events, hypertension, and blood pressure control in elderly Caucasians and African Americans

P17 Objective: The C allele of the angiotensin II type 1 receptor (AT1R) A1166C polymorphism has been associated in several studies with increased risks of hypertension (HTN) and myocardial infarction (MI), and with enhanced blood pressure (BP) response to ACE inhibitors but not calcium antagonists. Most of these studies were small, and none included large numbers of African Americans. We examined these associations in the Cardiovascular Health Study, an observational cohort study of risk factors for coronary disease and stroke in men and women ≥ 65 years of age. Methods: All 771 self-identified African Americans plus 1333 randomly-selected Caucasians were genotyped for the AT1R polymorphism. BP, medication use, and HTN were assessed annually. Incident MI/coronary death (CHD, n = 125 in whites; n = 60 in blacks), incident total cardiovascular events (CVD, n = 226 in whites; n = 101 in blacks), incident congestive heart failure (CHF, n = 146 in whites; n = 55 in blacks), and incident HTN (n = 184 in whites; n = 85 in blacks) were identified during up to 8 years of follow-up. Results: Genotype frequency distributions differed between whites (AA 49%, AC 41%, CC 10%) and blacks (85%, 15%, 1%, p < 0.0005). Age, gender or HTN at baseline did not differ by genotype in either group. In both whites and blacks, genotype was not associated with incident CHD (HR for AC/CC vs. AA, 95% CI in whites = 1.0, 0.7-1.5; blacks, HR = 0.7, 0.3-1.5), incident total CVD events (whites, HR = 1.0, 0.8-1.3; blacks, HR = 0.9, 0.5-1.6), incident CHF (whites, HR = 1.1, 0.8-1.5; blacks, 0.6, 0.3-1.4) or newly-identified HTN (whites, HR = 0.8, 0.6-1.1; blacks, HR = 1.1, 0.6-1.9). Among treated hypertensives, the association of genotype with controlled BP (<140/<90) did not differ between users of calcium channel blockers and users of ACE inhibitors in either race. Conclusion: In this large population-based elderly cohort, the AT1R A1166C polymorphism was not associated with prevalent or newly-identified HTN, incident CVD events, or BP response to antihypertensive agents in either Caucasians or African Americans.

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Angiotensin II type 1 receptor polymorphisms in the cardiovascular health study: relation to blood pressure, ethnicity, and cardiovascular events

American Journal of Hypertension ◽

10.1016/s0895-7061(02)03063-7 ◽

2002 ◽

Vol 15 (12) ◽

pp. 1050-1056 ◽

Cited By ~ 43

Author(s):

L Hindorff

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Cardiovascular Events ◽

Cardiovascular Health ◽

Health Study ◽

Cardiovascular Health Study

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A1166C polymorphism of angiotensin II type 1 receptor, blood pressure and arterial stiffness in hypertension

Journal of Hypertension ◽

10.1097/00004872-200411000-00016 ◽

2004 ◽

Vol 22 (11) ◽

pp. 2135-2142 ◽

Cited By ~ 21

Author(s):

St??phany Gardier ◽

Madeleine Vincent ◽

Pierre Lantelme ◽

Marie-Odile Rial ◽

Giampiero Bricca ◽

...

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Arterial Stiffness ◽

A1166c Polymorphism

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Brain Angiotensin II Type 1 Receptor Blockade Improves Dairy Blood Pressure Variability via Sympathoinhibition in Hypertensive Rats

International Journal of Hypertension ◽

10.1155/2015/759629 ◽

2015 ◽

Vol 2015 ◽

pp. 1-7

Author(s):

Takuya Kishi ◽

Yoshitaka Hirooka ◽

Kenji Sunagawa

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Cardiovascular Events ◽

Blood Pressure Variability ◽

Active Phase ◽

Early Morning ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Intracerebroventricular Infusion

Abnormal blood pressure (BP) elevation in early morning is known to cause cardiovascular events. Previous studies have suggested that one of the reasons in abnormal dairy BP variability is sympathoexcitation. We have demonstrated that brain angiotensin II type 1 receptor (AT1R) causes sympathoexcitation. The aim of the present study was to investigate whether central AT1R blockade attenuates the excess BP elevation in rest-to-active phase in hypertensive rats or not. Stroke-prone spontaneously hypertensive rats (SHRSP) were treated with intracerebroventricular infusion (ICV) of AT1R receptor blocker (ARB), oral administration of hydralazine (HYD), or ICV of vehicle (VEH). Telemetric averaged mean BP (MBP) was measured at early morning (EM), after morning (AM), and night (NT). At EM, MBP was significantly lower in ARB to a greater extent than in HYD compared to VEH, though MBP at AM was the same in ARB and HYD. At NT, MBP was also significantly lower in ARB than in HYD. These results in MBP were compatible to those in sympathoexcitation and suggest that central AT1R blockade attenuates excess BP elevation in early active phase and continuous BP elevation during rest phase independent of depressor response in hypertensive rats.

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Antihypertensive Agents and Cardiovascular Events in Patients With Coronary Disease and Normal Blood Pressure

JAMA ◽

10.1001/jama.293.10.1188-a ◽

2005 ◽

Vol 293 (10) ◽

pp. 1187

Keyword(s):

Blood Pressure ◽

Coronary Disease ◽

Cardiovascular Events ◽

Antihypertensive Agents ◽

Normal Blood ◽

Normal Blood Pressure

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C allele of angiotensin II type 1 receptor gene A1166C polymorphism affects plasma adiponectin concentrations in healthy young Japanese women

Hypertension Research ◽

10.1038/hr.2009.111 ◽

2009 ◽

Vol 32 (10) ◽

pp. 901-905 ◽

Cited By ~ 4

Author(s):

Katsuko Miyanaga ◽

Keisuke Fukuo ◽

Hiroshi Akasaka ◽

Tomohiro Katsuya ◽

Rumi Fukada ◽

...

Keyword(s):

Angiotensin Ii ◽

Receptor Gene ◽

Japanese Women ◽

Plasma Adiponectin ◽

A1166c Polymorphism ◽

Young Japanese Women

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Optimal blood pressure for patients with chronic kidney disease: a nationwide population-based cohort study

Scientific Reports ◽

10.1038/s41598-021-81328-y ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

You-Bin Lee ◽

Ji Sung Lee ◽

So-hyeon Hong ◽

Jung A. Kim ◽

Eun Roh ◽

...

Keyword(s):

Blood Pressure ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Cardiovascular Events ◽

Antihypertensive Treatment ◽

Antihypertensive Agents ◽

Population Based ◽

Adverse Outcomes ◽

Optimal Blood Pressure ◽

Stage Renal Disease

AbstractThe effect of blood pressure (BP) on the incident cardiovascular events, progression to end-stage renal disease (ESRD) and mortality were evaluated among chronic kidney disease (CKD) patients with and without antihypertensive treatment. This nationwide study used the Korean National Health Insurance Service-Health Screening Cohort data. The hazards of outcomes were analysed according to the systolic BP (SBP) or diastolic BP (DBP) among adults (aged ≥ 40 years) with CKD and without previous cardiovascular disease or ESRD (n = 22,278). The SBP and DBP were ≥ 130 mmHg and ≥ 80 mmHg in 10,809 (48.52%) and 11,583 (51.99%) participants, respectively. During a median 6.2 years, 1271 cardiovascular events, 201 ESRD incidents, and 1061 deaths were noted. Individuals with SBP ≥ 130 mmHg and DBP ≥ 80 mmHg had higher hazards of hypertension-related adverse outcomes compared to the references (SBP 120–129 mmHg and DBP 70–79 mmHg). SBP < 100 mmHg was associated with hazards of all-cause death, and composite of ESRD and all-cause death during follow-up only among the antihypertensive medication users suggesting that the BP should be < 130/80 mmHg and the SBP should not be < 100 mmHg with antihypertensive agents to prevent the adverse outcome risk of insufficient and excessive antihypertensive treatment in CKD patients.

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Angiotensin II Type 1 Receptor Gene A1166C Polymorphism Was Not Associated With Acute Coronary Syndrome in an Iranian Population

Iranian Red Crescent Medical Journal ◽

10.5812/ircmj.23942 ◽

2016 ◽

Vol 18 (11) ◽

Cited By ~ 1

Author(s):

Navid Delshad ◽

Majid Ghayour-Mobarhan ◽

Hamed Mirzaei ◽

Kamal Razavi-Azarkhiavi ◽

Mohsen Moohebati ◽

...

Keyword(s):

Acute Coronary Syndrome ◽

Angiotensin Ii ◽

Receptor Gene ◽

Iranian Population ◽

Coronary Syndrome ◽

A1166c Polymorphism

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Effects of a domain-selective ACE inhibitor in a mouse model of chronic angiotensin II-dependent hypertension

Clinical Science ◽

10.1042/cs20130808 ◽

2014 ◽

Vol 127 (1) ◽

pp. 57-63 ◽

Cited By ~ 15

Author(s):

Dylan Burger ◽

Timothy L. Reudelhuber ◽

Aman Mahajan ◽

Kelly Chibale ◽

Edward D. Sturrock ◽

...

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Mouse Model ◽

Ace Inhibitors ◽

Ace Inhibitor

The C-domain selective ACE inhibitor lisW-S reduced blood pressure and AngII levels in hypertensive TtRhRen mice similarly to classical ACE inhibitors and has the potential to avoid undesirable effects on the bradykinin system common to classic ACE inhibitors.

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PERAN KOMPLEKS JUKSTAGLOMERULUS TERHADAP RESISTENSI PEMBULUH DARAH

JURNAL BIOMEDIK (JBM) ◽

10.35790/jbm.4.3.2012.1213 ◽

2013 ◽

Vol 4 (3) ◽

Author(s):

Renny M. Toreh ◽

Sonny J.R. Kalangi ◽

Sunny Wangko

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Vascular Resistance ◽

Sodium Intake ◽

Angiotensin Receptor Blockers ◽

Antihypertensive Agents ◽

Angiotensin I ◽

Renin Angiotensin ◽

Renin Synthesis ◽

Receptor Blockers

Abstract: As the main structural component of the renin-angiotensin-aldosterone system (RAAS), the juxtaglomerular complex plays a very important role in the regulation of vascular resistance. The synthesis and release of renin into the circulation occurs due to the decrease of blood pressure, loss of body fluid, and a decrease of sodium intake. Renin converts angiotensinogen into angiotensin I, which is further converted by the angiotensin converting enzyme (ACE) into angiotensin II. This angiotensin II causes vasoconstriction of blood vessels, resulting in an increase of vascular resistance and blood pressure. The ACE inhibitors and the angiotensin receptor blockers (ARBs) do not inhibit the RAAS completely since they cause an increase of renin activity. The renin blockers are more effective in inhibiting RAAS activity; therefore, these renin blockers can be applied as antihypertensive agents with fewer side effects. The RAAS activity can be inhibited by a decrease of renin synthesis in the juxtaglomerular complex by blocking the signals in the juxtaglomerular complex that stimulate renin synthesis, and by blocking the gap junctions in the juxtaglomerular complex. Keywords: juxtaglomerular complex, vascular resistance, RAAS. Abstrak: Kompleks jukstaglomerulus sebagai komponen struktural utama sistem renin angiotensin berperan penting dalam pengaturan resistensi pembuluh darah. Sintesis dan pelepasan renin ke sirkulasi terjadi karena tekanan darah yang rendah, kehilangan cairan tubuh, dan kurangnya intake natrium. Renin akan memecah angiotensinogen menjadi angiotesin I yang kemudian secara cepat dikonversi oleh enzim pengonversi angiotensin menjadi angiotensin II. Angiotensin II menyebabkan vasokontriksi pembuluh darah sehingga meningkatkan resistensi pembuluh darah yang pada akhirnya akan meningkatkan tekanan darah. ACEinhibitor dan ARB kurang sempurna dalam menghambat kerja SRAA oleh karena keduanya memutuskan rantai mekanisme timbal balik sehingga meningkatkan aktifitas renin. Penghambat renin lebih efektif digunakan untuk menghambat aktifitas SRAA sehingga penghambat renin dapat digunakan sebagai obat anti-hipertensi dan memiliki efek samping yang rendah. Metode penghambatan SRAA yang juga dapat dikembangkan ialah penghambatan sintesis renin dalam kompleks jukstaglomerulus dengan cara menekan sinyal-sinyal dalam kompleks jukstaglomerulus yang merangsang sintesis renin dan menghambat fungsi taut kedap yang terdapat dalam kompleks jukstaglomerulus. Kata kunci: kompleks juksta glomerulus, resistensi vaskular, SRAA.

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