Protocatechuic acid (PCA), a strong antioxidant, has been reported for its cardiovascular-protective effects. This study aimed to investigate the effects of PCA administration on vascular endothelial function, mediated by insulin and insulin-like growth factor-1 (IGF-1), and antioxidant activities in aging hypertension. Thirty-six-week-old male aging spontaneously hypertensive rats were randomly divided into vehicle control (SHR) and PCA (SHR+PCA) groups, while age-matched Wistar–Kyoto rats (WKY) served as the normotensive vehicle control group. The oral PCA (200 mg/kg/day) was administered daily for a total of 12 weeks. When the rats reached the age of 48 weeks, the rat aortas were isolated for the evaluation of vascular reactivity and Western blotting. Also, nitric oxide (NO) production and antioxidant activities were examined among the three groups. The results showed that, when compared with the SHR group, the insulin-induced and IGF-1-induced vasorelaxation were significantly improved in the SHR+PCA group. There was no significant difference in the endothelium-denuded vessels among the three groups. After the pre-incubation of phosphatidylinositol 3-kinase (PI3K) or NO synthase (NOS) inhibitors, the vasorelaxation was abolished and comparable among the three groups. The protein levels of insulin receptors, IGF-1 receptors, phospho-protein kinase B (p-Akt)/Akt, and phospho-endothelial NOS (p-eNOS)/eNOS in aortic tissues were significantly enhanced in the SHR+PCA group when compared with the SHR group. Moreover, significant improvements of nitrate/nitrite concentration and antioxidant activities, including superoxide dismutase, catalase, and total antioxidants, were also found in the SHR+PCA group. In conclusion, the 12 weeks of PCA administration remarkably improved the endothelium-dependent vasorelaxation induced by insulin and IGF-1 in aging hypertension through enhancing the PI3K–NOS–NO pathway. Furthermore, the enhanced antioxidant activities partly contributed to the improved vasorelaxation.

The purpose of this study was to evaluate the effects of exercise training on renal fibrosis in hypertensive rats. Masson’s trichrome staining and Western blotting were performed on the excised renal cortex from sixteen male spontaneously hypertensive rats (SHR), which were randomly divided into either a sedentary hypertensive group (SHR) or exercise hypertensive group (SHR-EX, running on an exercise treadmill for 60 min/day, 5 sessions/week, for 12 weeks), and from eight male Wistar-Kyoto rats which served as a sedentary normotensive group (WKY). The systolic blood pressure (SBP) and renal fibrosis in hypertensive rats improved after exercise training. The inflammatory-related protein levels of interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2), as well as the fibrotic-related protein levels of transforming growth factor-beta (TGF-β), phospho-Smad2/3 (p-Smad2/3), connective tissue growth factor (CTGF), matrix metalloproteinase-9 (MMP-9), and matrix metalloproteinase-2 (MMP-2) were decreased in the SHR-EX group when compared with the SHR group. Exercise training suppressed the hypertension-induced renal cortical inflammatory and fibrotic pathways in hypertensive rat models. These findings might indicate a new therapeutic effect for exercise training to prevent renal fibrosis in hypertensive nephropathy.

Cardiovascular health and aerobic capacity play crucial roles in determining the performance of athletes in the highly competitive sport of badminton. Few studies have directly compared heart rate variability (HRV), arterial stiffness, and aerobic capacity between male and female athletes, especially among badminton athletes. This study investigated sex differences in HRV, arterial stiffness, and aerobic capacity in badminton athletes. Elite badminton athletes were recruited and divided into male (n = 20, 21.0 ± 1.8 years old) and female (n = 16, 21.2 ± 2.3 years old) groups. Both groups performed an incremental treadmill running test for the evaluation of maximal oxygen consumption ($\stackrel{.}{\mathrm{V}}$O₂max), anaerobic threshold, and time to exhaustion. They started exercising at a treadmill speed of 2.7 km/h and an inclination of 10% gradient for 3 min, and the speed and inclination were gradually increased every 3 min until they were exhausted or fatigued volitionally. HRV was examined using the Polar heart rate monitor over a period of 5 min at rest in the supine position. Subsequently, the index of arterial stiffness was examined under the same condition. Our results revealed significant differences between the male and female athletes in $\stackrel{.}{\mathrm{V}}$O₂max (men: 60.38 ± 8.98 mL/kg/min, women: 48.13 ± 7.72 mL/kg/min, p < 0.05), anaerobic threshold (men: 41.50 ± 7.26 mL/kg/min, women: 32.51 ± 6.19 mL/kg/min, p < 0.05), time to exhaustion (men: 902.15 ± 120.15 s, women: 780.56 ± 67.63 s, p < 0.05), systolic blood pressure (men: 125.27 ± 7.76 mmHg, women: 107.16 ± 11.09 mmHg, p < 0.05), and arterial stiffness index (men: 63.56 ± 12.55, women: 53.83 ± 8.03, p < 0.05). However, no significant differences in HRV measures were observed between the two groups. These findings suggested that the male badminton athletes demonstrated significantly higher aerobic capacity than did the female athletes, but there were no significant differences in HRV measures. The female athletes exhibited superior arterial function, compared with their male counterparts.

To investigate whether the coexistence of hypertension and ovariectomy will increase cardiac Fas receptor and mitochondrial-dependent apoptotic pathways, histopathological analysis, the TUNEL assay and Western blotting were performed on the excised hearts from three groups of female spontaneously hypertensive rats (SHR), which were divided into a sham-operated group (SHR-Sham), bilaterally ovariectomized group (SHR-OVX) and normotensive Wistar Kyoto rats (WKY). Compared with the WKY group, the SHR-Sham group exhibited decreased protein levels of ERα, ERβ, p-Akt/Akt, Bcl-2, Bcl-xL and p-Bad and decreased further in the SHR-OVX group, as well as protein levels of t-Bid, Bak, Bad, Bax, cytochrome c, activated caspase-9 and activated caspase-3 (mitochondria-dependent apoptosis) increased in the SHR-Sham group and increased further in the SHR-OVX group. Compared with the WKY group, protein levels of Fas ligand, TNF-α, Fas death receptors, TNFR1, FADD and activated caspase-8 (Fas receptor-dependent apoptosis) increased in the SHR-Sham group, but did not increase in the SHR-OVX group, except Fas ligand and TNF-α. The coexistence of hypertension and ovariectomy attenuated the estrogen receptor survival pathway and appeared to additively increase the cardiac mitochondria-dependent, but not the Fas receptor-dependent apoptosis pathway, which might provide one possible mechanism for the development of cardiac abnormalities in hypertensive postmenopausal women.

Dysfunction of insulin and insulin-like growth factor-1 (IGF-1) is associated with the pathophysiology of hypertension. The influence of long-term exercise on vascular dysfunction caused by hypertension remains unclear. We investigated whether long-term treadmill training improved insulin- and IGF-1-mediated vasorelaxation in hypertensive rats. Eight-week-old male spontaneously hypertensive rats (SHR) were randomly divided into sedentary and exercise (SHR-EX) groups. The SHR-EX group was trained on a treadmill for 60 min/day, 5 days/wk, for 8 wk. Wistar-Kyoto rats (WKY) were used as the normal control group. After training, aortic insulin- and IGF-1-mediated vasorelaxation was evaluated in organ baths. Additionally, the roles of phosphatidylinositol 3-kinase (PI3K), nitric oxide synthase (NOS), and aortic protein expression were examined in the three groups. Compared with sedentary SHR and WKY groups, insulin- and IGF-1-mediated vasorelaxation was significantly enhanced to a nearly normal level in the SHR-EX group. After endothelial denudation, blunted and comparable vasorelaxation was found among the three groups. Pretreatment with selective PI3K and NOS inhibitors attenuated insulin- and IGF-1-mediated vasorelaxation, and no significant difference was found among the three groups after the pretreatment. The aortic protein levels of the insulin receptor (IR), IGF-1 receptor (IGF-1R), insulin receptor substrate-1 (IRS-1), and endothelial NOS (eNOS) were also significantly increased in the SHR-EX group compared with the other two groups. These results suggested that treadmill training elicited the amelioration of endothelium-dependent insulin/IGF-1-mediated vasorelaxation partly via the increased activation of PI3K and NOS, as well as the enhancement of protein levels of IR, IGF-1R, IRS-1, and eNOS, in hypertension.

The prevalence of autism spectrum disorder (ASD) among children has been recently increasing. The severity of symptoms greatly varies between individuals with ASD, ranging from relatively mild to extremely severe. It is important to have a clearer understanding of the possible adverse consequences resulting from this disorder, such as delayed motor development, autonomic dysregulation, and arterial stiffness. Thus, the objective of this study was to investigate differences in motor skills, heart rate variability (HRV), and arterial stiffness between children with ASD and typically developing children. In this study, the school-aged children with mild symptoms of ASD (n = 17, 11.1 ± 1.0 years old) and typically developing peers (n = 15, 11.0 ± 0.5 years old) were recruited. Motor skills, HRV, and arterial stiffness were measured in these two groups. Motor skills were evaluated by the Bruininks–Oseretsky Test of Motor Proficiency-Second Edition. Moreover, HRV was measured through a short-term recording using the Polar heart rate monitor, and arterial stiffness was assessed by non-invasive computerized oscillometry. Compared with the typically developing group, children with ASD displayed significant deficits in some areas of motor skills, including manual coordination, strength and agility, and total motor composite. Moreover, children with ASD exhibited significantly reduced HRV, including time- and frequency-domain measures. However, the results did not demonstrate any statistically significant differences in arterial stiffness between the groups. Our findings demonstrated the presence of motor skill deficits and autonomic dysregulation in children with ASD.