472 healthy, normotensive subjects [normotension (NT) group], 454 prehypertensive subjects [prehypertension (PH) group] and 978 hypertensive patients [essential hypertension (EH) group] were screened for an association study between 5'-UCR -1248 A>G of Mfn2/HSG and hypertension by polymerase chain reaction and DNA sequencing after venous blood was drawn and DNA was extracted.
The common AGTR1A1166C (rs5186) polymorphism in the 3'-UTR region, particularly the presence of the 1166C allele, which fails to downregulate gene expression, predicted greater likelihood of being in the prehypertension group and higher SBP.
These findings indicate that at the stage of pre-hypertension a disturbance in the ANF-c-GMP regulatory pathway may occur, which is expressed primarily at the circulatory rather than the renal excretory level.
We determined whether nod-like receptor with pyrin domain containing 3 (NLRP3) involved in the process of prehypertension, central blockade of NLRP3 decreased inflammation reaction, regulated neurohormonal excitation, and delayed the progression of prehypertension.
Losartan administered at the onset of prehypertension is more effective than amlodipine in ameliorating hypertension and improving vascular remodeling and function, which is likely mediated by the renin-angiotensin-aldosterone system.
Although a familial occurrence of subtle disturbances in AngII-dependent control of aldosterone and renal hemodynamics appears possible, BP regulation by the renin-angiotensin system is probably often intact at the stage of prehypertension.
This study tested whether prehypertension ExT protects against hypertension and cardiac remodeling in spontaneously hypertensive rats (SHR) and explored the underlying mechanisms by examining the cardiac angiotensin-converting enzyme (ACE) and ACE2 signaling axes.
Risk of total CVDs, MI, and stroke was increased with low-range prehypertension (low-range: SBP 120-129 mmHg and/or DBP 80-84 mmHg) versus normal BP - RR 1.42 (95% CI 1.29-1.55), 1.43 (1.10-1.86), and 1.52 (1.27-1.81), respectively - and risk of total CVDs, CHD, MI, and stroke was increased with high-range prehypertension (high-range: SBP 130-139 mmHg and/or DBP 85-89 mmHg) - RR 1.81 (95% CI 1.56-2.10), 1.65 (1.13-2.39), 1.99 (1.59-2.50), and 1.99 (1.68-2.36), respectively.
Risk of total CVDs, MI, and stroke was increased with low-range prehypertension (low-range: SBP 120-129 mmHg and/or DBP 80-84 mmHg) versus normal BP - RR 1.42 (95% CI 1.29-1.55), 1.43 (1.10-1.86), and 1.52 (1.27-1.81), respectively - and risk of total CVDs, CHD, MI, and stroke was increased with high-range prehypertension (high-range: SBP 130-139 mmHg and/or DBP 85-89 mmHg) - RR 1.81 (95% CI 1.56-2.10), 1.65 (1.13-2.39), 1.99 (1.59-2.50), and 1.99 (1.68-2.36), respectively.
Risk of total CVDs, MI, and stroke was increased with low-range prehypertension (low-range: SBP 120-129 mmHg and/or DBP 80-84 mmHg) versus normal BP - RR 1.42 (95% CI 1.29-1.55), 1.43 (1.10-1.86), and 1.52 (1.27-1.81), respectively - and risk of total CVDs, CHD, MI, and stroke was increased with high-range prehypertension (high-range: SBP 130-139 mmHg and/or DBP 85-89 mmHg) - RR 1.81 (95% CI 1.56-2.10), 1.65 (1.13-2.39), 1.99 (1.59-2.50), and 1.99 (1.68-2.36), respectively.
Risk of total CVDs, MI, and stroke was increased with low-range prehypertension (low-range: SBP 120-129 mmHg and/or DBP 80-84 mmHg) versus normal BP - RR 1.42 (95% CI 1.29-1.55), 1.43 (1.10-1.86), and 1.52 (1.27-1.81), respectively - and risk of total CVDs, CHD, MI, and stroke was increased with high-range prehypertension (high-range: SBP 130-139 mmHg and/or DBP 85-89 mmHg) - RR 1.81 (95% CI 1.56-2.10), 1.65 (1.13-2.39), 1.99 (1.59-2.50), and 1.99 (1.68-2.36), respectively.
In the Dallas Heart Study, 2001 untreated participants 18 to 64 years of age (mean age: 42.3 years; 44% black race) were divided into the following groups based on office blood pressure (BP) measurements: (1) optimal BP (systolic BP [SBP] <120 mm Hg and diastolic BP [DBP] <80 mm Hg; n=837); (2) prehypertension (SBP 120-139 mm Hg and DBP 80-89 mm Hg; n=821); (3) ISH (SBP ≥140 mm Hg and DBP <90 mm Hg; n=121); (4) isolated diastolic hypertension (SBP <140 mm Hg and DBP ≥90 mm Hg; n=44); and (5) systolic-diastolic hypertension (SBP ≥140 mm Hg and DBP ≥90 mm Hg; n=178).
In the Dallas Heart Study, 2001 untreated participants 18 to 64 years of age (mean age: 42.3 years; 44% black race) were divided into the following groups based on office blood pressure (BP) measurements: (1) optimal BP (systolic BP [SBP] <120 mm Hg and diastolic BP [DBP] <80 mm Hg; n=837); (2) prehypertension (SBP 120-139 mm Hg and DBP 80-89 mm Hg; n=821); (3) ISH (SBP ≥140 mm Hg and DBP <90 mm Hg; n=121); (4) isolated diastolic hypertension (SBP <140 mm Hg and DBP ≥90 mm Hg; n=44); and (5) systolic-diastolic hypertension (SBP ≥140 mm Hg and DBP ≥90 mm Hg; n=178).
In the Dallas Heart Study, 2001 untreated participants 18 to 64 years of age (mean age: 42.3 years; 44% black race) were divided into the following groups based on office blood pressure (BP) measurements: (1) optimal BP (systolic BP [SBP] <120 mm Hg and diastolic BP [DBP] <80 mm Hg; n=837); (2) prehypertension (SBP 120-139 mm Hg and DBP 80-89 mm Hg; n=821); (3) ISH (SBP ≥140 mm Hg and DBP <90 mm Hg; n=121); (4) isolated diastolic hypertension (SBP <140 mm Hg and DBP ≥90 mm Hg; n=44); and (5) systolic-diastolic hypertension (SBP ≥140 mm Hg and DBP ≥90 mm Hg; n=178).
Those who converted to normotension were younger, less obese, and had significantly lower baseline SBP, fasting glucose, cholesterol levels, and homeostasis model assessment insulin resistance compared with study participants who continued to have prehypertension or progressed to hypertension.
Those who converted to normotension were younger, less obese, and had significantly lower baseline SBP, fasting glucose, cholesterol levels, and homeostasis model assessment insulin resistance compared with study participants who continued to have prehypertension or progressed to hypertension.
In the Dallas Heart Study, 2001 untreated participants 18 to 64 years of age (mean age: 42.3 years; 44% black race) were divided into the following groups based on office blood pressure (BP) measurements: (1) optimal BP (systolic BP [SBP] <120 mm Hg and diastolic BP [DBP] <80 mm Hg; n=837); (2) prehypertension (SBP 120-139 mm Hg and DBP 80-89 mm Hg; n=821); (3) ISH (SBP ≥140 mm Hg and DBP <90 mm Hg; n=121); (4) isolated diastolic hypertension (SBP <140 mm Hg and DBP ≥90 mm Hg; n=44); and (5) systolic-diastolic hypertension (SBP ≥140 mm Hg and DBP ≥90 mm Hg; n=178).
Those who converted to normotension were younger, less obese, and had significantly lower baseline SBP, fasting glucose, cholesterol levels, and homeostasis model assessment insulin resistance compared with study participants who continued to have prehypertension or progressed to hypertension.
Already at very young ages (6-8 years), with a high proportion of prehypertension, black boys in our study have increased arterial stiffness in all sections of the arterial tree, along with higher DBP, carotid intima-media thickness and AGEs.
The chicken- or fish-derived tripeptide, leucine-lysine-proline (LKP), inhibits the angiotensin converting enzyme and may be used as an alternative treatment for prehypertension.
The purpose of this study is to determine the effect of 10 weeks of moderate-intensity aerobic exercise training (MIET) on blood pressure (BP), angiotensin-converting enzyme (ACE) and β2-adrenergic receptor (ADRB2) gene expression in leukocytes, plasma angiotensin II (Ang II), and flow-mediated dilation (FMD) in obese postmenopausal women (PMW) with prehypertension.
Prehypertension exercise training attenuates hypertension and cardiac hypertrophy accompanied by temporal changes in the levels of angiotensin II and angiotensin (1-7).
The purpose of this study is to determine the effect of 10 weeks of moderate-intensity aerobic exercise training (MIET) on blood pressure (BP), angiotensin-converting enzyme (ACE) and β2-adrenergic receptor (ADRB2) gene expression in leukocytes, plasma angiotensin II (Ang II), and flow-mediated dilation (FMD) in obese postmenopausal women (PMW) with prehypertension.