---

Background and objectives: Hypertension is associated with vascular remodeling, which is supported by the protein disulfide isomerase A1 (PDIA1). Exercise training has beneficial effects on vascular function in subjects with hypertension. Alpha lipoic acid (ALA) is a powerful biological antioxidant. However, the role of exercise training and ALA on PDIA1 are not well understood. The aim of the present study was to investigate effects of training with different intensities and ALA supplementation on PDIA1 expression in cardiomyocytes of hypertensive rats.
Methods: In this experimental study, 35 male Wistar rats (age: eight weeks, weight: 190-220 g) were randomly divided into seven groups: control, hypertensive, hypertensive+ALA, hypertensive+high intensity interval training (HIIT), hypertensive+moderate-intensity training (MIT), hypertensive+HIIT+ALA, and hypertensive+MIT+ALA. Hypertension was induced by three weeks of L-NAME administration (40 mg/kg/day). The HIIT and MIT protocols was performed five days a week for six weeks. The HIIT protocol consisted of 10 bouts of four minute-running at 80–85% of Vmax, and the MIT protocol consisted of 13 bouts of four minute-running at 55–60% of Vmax. In the supplementation groups, 20 mg/kg of ALA was administered orally once a day. Immunohistochemistry staining was used to study protein expression.
 Results: Induction of hypertension significantly decreased PDIA1 expression compared to the control group (p=0.001). Moreover, PDIA1 expression increased significantly in the hypertensive+ALA (p=0.023), HIIT (p=0.001), MIT (p=0.007), MIT+ hypertensive+ALA (p=0.0001) and HIIT+ hypertensive+ALA (p=0.0001) group compared to the control group.
Conclusion: Hypertension is associated with decreased cardiac PDIA1 level, and both HIIT and MIT along with ALA supplementation are effective in increasing cardiac PDIA1 expression in hypertension.

---

Pregnancy-induced hypertension is a spectrum of multi-systemic dysfunction in pregnancy, usually seen in the third trimester in approximately 6–8% of pregnancies in the United States, according to the National High Blood Pressure Education Program (NHBPEP). The World Health Organization reported that this multisystem disorder accounts for 16% of maternal deaths in developed countries and 1.8%-16.7% in most developing countries.
The spectrum can progress from Preeclampsia to Eclampsia with short- and long-term complications that may impact significantly on the quality of life of both the fetus and the mother. Though the pathogenetic mechanisms remain unclear, evidence supporting the roles of genetic, immunologic, and environmental factors is rapidly evolving. Preeclampsia, an initial spectrum of the disorder, begins with abnormal placentation with failure of adaption, inflammatory changes, permanent vascular and metabolic damages, and increasing risk of cardiovascular, renal, endocrine, neurological, hematological, and socioeconomic complications. Regardless of the postulation, oxidative stress, placenta ischemia hypoxia with release of toxic substances, and endothelial dysfunction are essentially pivotal to multiple organ damage. American College of Obstetrics and Gynecology (ACOG) recommends starting treatment for Preeclampsia when the diastolic blood pressure (DBP) is above 105–110 mm Hg. This article describes the proposed pathophysiological mechanism associated with the spectrum of maternal complications in Pregnancy-induced hypertension.