ACE inhibitory peptides derived from food protein sources are regarded as safer alternatives to synthetic antihypertensive drugs for treating hypertension.
Patients with bradykinin-mediated angiœdema were more frequently women [33 (62%) vs. 44 (42%); P = 0.01], had higher frequency of prior ischemic stroke [12 (23%) vs. 9 (8%); P = 0.01], hypertension [46 (87%) vs. 70 (66%); P = 0.005], were more frequently treated with angiotensin-converting enzyme inhibitor [37 (70%) vs. 28 (26%); P < 0.001] and were more frequently hospitalized in intensive care medicine [ICU; 11 (21%) vs. 5 (5%); P = 0.004].
We assessed the following quality indicators: (<i>1</i>) BP measurement, (<i>2</i>) uncontrolled hypertension, (<i>3</i>) uncontrolled diabetes, (<i>4</i>) angiotensin-converting enzyme inhibitor or angiotensin receptor blocker use among patients with hypertension, (<i>5</i>) statin use if age ≥50 years old, and (6) nonsteroidal anti-inflammatory drug use.
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.
ACE inhibitors, fibrates and AGIs were associated with increased prevalence of cortical cataract in this Asian population, independent of the presence of hypertension, hyperlipidaemia and diabetes, respectively.
Because hCE1 is critical for the activation of imidapril, an angiotensin-converting enzyme (ACE)-inhibitor prodrug prescribed to treat hypertension, the most potent inhibitors, TPHP and 4tBPDPP, and an environmentally relevant mixture (house dust) were further evaluated for their effect on imidapril bioactivation in vitro.
Logistic regression analysis showed that the independent risk factors for AKI in patients with AMI included: age (>60 years old) (odds ratio [OR] 1.04, 95% confidence interval [CI] 1.02-1.05, P = 0.000), hypertension (OR 2.51, 95% CI 1.62-3.87, P = 0.000), chronic kidney disease (OR 3.52, 95% CI 2.01-6.16, P = 0.000), Killip class ≥3 (OR 5.22, 95% CI 3.07-8.87, P = 0.000), extensive anterior myocardial infarction (OR 3.02, 95% CI 1.85-4.93, P = 0.000), use of furosemide (OR 1.02, 95% CI 1.02-1.03, P = 0.000), non-use of angiotensin-converting enzyme inhibitors/angiotensin receptor blocker (OR 1.58, 95% CI 1.04-2.40, P = 0.032).
However, in patients with PFO, this was predicted by TAPSE, lack of arterial hypertension and usage of angiotensin-converting enzyme inhibitors, R2 = 0.30; p < 0.001.
Since renin-angiotensin-aldosterone system activation is the most important mechanism of hypertension in these children, the first-line therapy involves the use of inhibitors of this axis, including angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers type I, which also promote an anti-fibrotic effect.
These include drugs used to treat lipid disorders (HMG-CoA reductase inhibitors), hypertension (ACE inhibitors), osteoporosis (bisphosphonates), cancer (proteasome inhibitors) and others.
Patients with hypertension plus nonuse of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers potentiated kidney damage by metformin.
Due to prevalent comorbidities, such as hypertension and albuminuria, patients often receive other agents that alter intrarenal hemodynamics, including angiotensin converting enzyme inhibitors/angiotensin receptor blockers (ACEi/ARBs), calcium channel blockers (CCBs) and diuretics.
These findings suggest that PASE has the antihypertensive effect that may involve a mechanism of ACE inhibition and simultaneously protect organ damage against hypertension.
Whether ACE inhibition enhances Aβ42 aggregation or impairs human cognitive ability are very important issues for preventing AD onset and for optimal hypertension management.
Deletion Polymorphism of Angiotensin Converting Enzyme Gene is Associated with Left Ventricular Hypertrophy in Uighur Hypertension-Obstructive Sleep Apnea Hypopnea Syndrome (OSAHS) Patients.
The present study investigated whether angiotensin (Ang) II-elicited hypertensive response is sensitized in a model of PTSD and whether inhibition of angiotensin-converting enzyme (ACE) or tumor necrosis factor (TNF)-α prior to PTSD blocks this sensitization of Ang II hypertension.
Considering that hypertension and poor placental perfusion are important features in PE, polymorphisms in the angiotensin-converting enzyme (ACE) and estrogen nuclear receptor 1 (ESR1) genes could be involved in the predisposition and/or development of the disease.
Consensus recommendations were that (i) there is evidence of harm associated with postoperative systolic arterial pressure <90 mm Hg; (ii) for patients with preoperative hypertension, the threshold at which harm occurs may be higher than a systolic arterial pressure of 90 mm Hg; (iii) there is insufficient evidence to precisely define the level of postoperative hypertension above which harm will occur; (iv) a greater frequency of postoperative blood pressure measurement is likely to identify risk of harm and clinical deterioration earlier; and (v) there is evidence of harm from withholding beta-blockers, angiotensin receptor blockers, and angiotensin-converting enzyme inhibitors in the postoperative period.
The main approaches to the management of hypertension in CKD include dietary salt restriction, initiation of treatment with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, and diuretic therapy.
Therefore, ACE could be a potential therapeutic target in regulating the conversion of angiotensin I to angiotensin II and eventually controlling hypertension.