Low albumin was associated with increasing age, higher urea and C-reactive protein, lower sodium, hemoglobin, iron, less treatment with angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, reduced right ventricular function, and pulmonary hypertension.
Under the dominant model, the ACE 2350A allele conferred a reduced hypertension risk and such associations were divergent between Han Chinese and Muslims from the Arab Gulf and Pakistan.
Calcium antagonists can be used as alternatives to ACE inhibitors in patients with hypertension and concomitant diabetes mellitus and/or renal disease.
Angiotensin converting enzyme (ACE) is a well-known enzyme, largely studied for its action on hypertension, as it produces angiotensin II from angiotensin I.
Epidemiologic data suggest that inactivation of the peptidase angiotensin-converting enzyme in patients treated for hypertension increases the odds to develop CRPS.
Our data suggests that the ACE I/D polymorphism is not associated with hypertension but the G2350A polymorphism is associated with hypertension in the Punjabi population.
Specifically, we conducted a retrospective cohort analysis using health insurance claims data for enrollees who were diagnosed with a serious mental illness, initiated an atypical antipsychotic, as well as an SSRI (to treat serious mental illness), biguanides (to treat type 2 diabetes), or an ACE inhibitor (to treat hypertension).
Evidence was obtained that the AT 1 (-535)*T allele showed a synergistic effect on risk of hypertension with angiotensin I converting enzyme D allele (ACE*D).
We have previously shown that angiotensin converting enzyme (ACE) DD genotype is associated with exaggerated pulmonary hypertension and disturbance of tissue oxygenation during exercise in patients with chronic obstructive pulmonary disease (COPD).
Of 41 SNPs genotyped, rs3789678 and rs2493132 within AGT, rs4305 within ACE, rs275645 within AGTR1, rs3802230 and rs10086846 within CYP11B2 were shown to associate with hypertension.
There is clear evidence that polymorphisms at the renin, angiotensinogen, and angiotensin-converting enzyme loci influence both blood pressure and hypertension.
Angiotensin converting enzyme (ACE) polymorphism has been shown to be important in hypertension progression and also in diabetes complications, especially associated with heart disease.
The results suggest that the I/D polymorphism of the ACE gene is associated with interindividual differences in the blood pressure response to a low dose of a diuretic in a gender-specific manner in the Han Chinese population with hypertension.
Influence of angiotensin-converting enzyme inhibition on reversibility of alterations in arterial wall and cognitive performance associated with early hypertension: A follow-up study.
Articles evaluating race-specific outcomes in hypertension were gathered using a MEDLINE search with keywords black, African American, ACE inhibitor, angiotensin receptor blocker, angiotensin system, and hypertension.
Current guidelines on hypertension treatment in chronic kidney disease (CKD) patients discourage combined angiotensin-converting enzyme inhibitor (ACEi) and angiotensin II receptor blocker (ARB) use due to the risk of an increased kidney function decline.
Because hypertension is the most frequent comorbidity affecting cancer patients, treatment of hypertension with ACE inhibitors in patients undergoing paclitaxel chemotherapy should be reviewed, since this could enhance the P-APS and P-CPN.
In conclusion, no association was found between M235T polymorphism and insulin resistance or PAI-1 levels, but results indicate relationship between I/D polymorphism of the ACE gene and plasma PAI-1 levels in the early stage of hypertension.
Though, ACE inhibition is adequate to reduce SBP, targeting NEP and APN along with ACE is beneficial in tackling hypertension and associated fibrosis of heart.
The aim of this study was to identify and characterize the bioactive compounds of <i>Coriandrum sativum</i> responsible for the treatment of hypertension and to explore their mechanism of action as angiotensin-converting enzyme (ACE) inhibitors.