Comparing the Apelin Level in Hypertensive Patients Who Received Hypertension Drugs

Background: Apelin, an adipokine secreted from adipose tissue, plays an important role in regulating blood pressure and hypertension. Objectives: The current study aimed to compare the plasma Apelin level in hypertensive patients under treatment with amlodipine, losartan, and amlodipine + losartan. Methods: In this case-control study, the serum level of Apelin was compared in four groups of (A) Healthy subjects (n = 31); (B) Hypertensive patients, received amlodipine (n = 31); Hypertensive patients, received losartan (n = 45); and patients (n = 33) that received amlodipine and losartan. Apelin level in serum samples was measured using Human Apelin ELISA Kit according to the manufacturers’ instructions. Data were analyzed using SPSS version 19 (Chicago: SPSS Inc.), at the significant level of α = 0.05. Results: The mean blood level of Apelin in the control group and groups receiving amlodipine, losartan, and amlodipine + losartan was 366.16 ± 36.04, 247.19 ± 27.77, 282.93 ± 47.08, and 289.84 ± 32.20 g/dl, respectively. Losartan + amlodipine group had a higher level of Apelin compared with amlodipine alone (P < 0.05). Conclusions: This study demonstrated that Apelin has a definite protective effect in preventing hypertension. Also, according to the results, the renin-angiotensin-aldosterone system inhibitors, such as losartan, caused a higher increase in the Apelin, resulting in better blood pressure control.

Plasma apelin level in acute myocardial infarction and its relation with prognosis: A prospective study

Objective Apelin is a novel adipocytokine with a significant role in ischemia/reperfusion injury that is synthesized and secreted in myocardial cells and coronary endothelium. There is debate on its value for the diagnosis and prognosis of myocardial infarction. We aimed to investigate plasma apelin level in patients with acute ST segment elevation (STEMI) and non-ST segment elevation (NSTEMI) myocardial infarction and its relationship with left ventricular function and prognostic parameters. Methods Forty-one patients with STEMI, 21 patients with NSTEMI and 10 patients as control group with normal coronary angiograms were included. Plasma apelin level at presentation was investigated regarding its relationship with other diagnostic and prognostic parameters. Results Apelin level was significantly higher in acute myocardial infarction (0.31 ± 0.56 ng/mL) compared to control group (0.08 ± 0.05 ng/mL) (p < 0.01). Likewise, it was found to be significantly higher in STEMI group (0.45 ± 0.73 ng/mL) compared to control group (0.08 ± 0.05 ng/mL) (p < 0.01). Although apelin was higher in NSTEMI group (0.13 ± 0.10 ng/mL) compared to control group (0.08 ± 0.05 ng/mL), this difference was not statistically significant (p > 0.05). No correlation was found between apelin and NT-proBNP, hsCRP, troponin, ejection fraction (EF) and Killip score (p > 0.05). A positive correlation was found between apelin and TIMI, GRACE and Gensini scores (p < 0.05). Only GRACE score was found to be correlated with apelin in MI groups. Conclusion Apelin level was found to be high in acute myocardial infarction. With its inotropic and vasodilator effects, apelin was thought to have a protective role against severe ischemia.

Interaction between the apelinergic system and ACE2 in the cardiovascular system: therapeutic implications

The apelinergic system is widely expressed and acts through autocrine and paracrine signaling to exert protective effects, including vasodilatory, metabolic, and inotropic effects on the cardiovascular (CV) system. The apelin pathway’s dominant physiological role has delineated therapeutic implications for coronary artery disease, heart failure (HF), aortic aneurysm, pulmonary arterial hypertension (PAH), and transplant vasculopathy. Apelin peptides interact with the renin–angiotensin system (RAS) by promoting angiotensin converting enzyme 2 (ACE2) transcription leading to increased ACE2 protein and activity while also antagonizing the effects of angiotensin II (Ang II). Apelin modulation of the RAS by increasing ACE2 action is limited due to its rapid degradation by proteases, including ACE2, neprilysin (NEP), and kallikrein. Apelin peptides are hence tightly regulated in a negative feedback manner by ACE2. Plasma apelin levels are suppressed in pathological conditions, but its diagnostic and prognostic utility requires further clinical exploration. Enhancing the beneficial actions of apelin peptides and ACE2 axes while complementing existing pharmacological blockade of detrimental pathways is an exciting pathway for developing new therapies. In this review, we highlight the interaction between the apelin and ACE2 systems, discuss their pathophysiological roles and potential for treating a wide array of CV diseases (CVDs).

Resistance Exercise-Induced Apelin Is Not Modulated by Higher Dietary Protein Density in Overweight Adults

Objectives Apelin is a putative exercise-sensitive myokine that has been shown to be associated with physical independence during aging. Physical performance is highly dependent on muscle strength, with a clear role of dietary protein (i.e., &gt; Recommended Dietary Allowance) for the maintenance of age-related muscle strength. However, the influence of dietary protein density on exercise-induced apelin remains unknown. Therefore, our aim was to evaluate plasma apelin concentrations and its relationship with muscle strength in middle-aged adults consuming differential amounts of animal-based protein during progressive resistance training. Methods 41 overweight middle-aged adults (50 ± 2 y, BMI 28 ± 1 kg · m−2, M = 19, F = 22) were stratified and randomized to consume either high protein (1.68 ± 0.06 g · kg−1·d−1) or moderate amounts of animal-based protein (1.16 ± 0.04 g · kg−1·d−1) during a 10-week weight-maintenance nutrition counseling-controlled resistance training program. Body composition was assessed by dual-energy x-ray absorptiometry. Muscle strength was assessed by one-repetition maximum (1RM) and isometric maximal voluntary contraction (MVC) at 60° knee angle. Oral glucose tolerance tests were performed at baseline and post-intervention. Results Main effects of time were observed for increases in lean body mass (P = 0.003), upper and lower body 1RM (all P ≤ 0.001), isometric MVC (P = 0.013), and plasma apelin concentrations (P = 0.007). There were no changes in body adiposity or glucose-insulin regulation (e.g., HOMA-IR, Matsuda) with the intervention (all P ≥ 0.152). Apelin was positively and significantly associated with isometric MVC (extension: r = 0.233, P = 0.047; flexion: r = 0.308, P = 0.008), but not 1RM. Conclusions Our results show that resistance training increases circulating apelin concentrations which is related to isometric strength gain. However, higher consumption of animal-based protein foods does not potentiate these resistance-exercise induced adaptations in overweight middle-aged adults. Funding Sources Funded in part by the Beef Checkoff. CFM funded by JBT Fellowship, UIUC.