Exercise training ameliorates adrenergic control in spontaneously hypertensive rats.

The goal of this study was to examine vascular control after sympathetic stimulation by tyramine infusion in hypertensive rats submitted to swimming training. To this end, male rats were assigned to the following groups: sedentary (SN) and trained normotensive (TN), sedentary (SH) and trained hypertensive (TH). Arterial pressure (AP), heart rate (HR), HR variability (HRV), AP variability (APV), and cardiac autonomic function were recorded. Following, infusion of tyramine was administrated. The TN and TH showed a lower resting HR compared with their respective sedentary groups (p < .05). Pressure levels were less in TH than SH (p < .05). The TH showed a higher HRV together with a lower APV in comparison to SH (p < .05). The sympathetic modulation of HRV and APV was lower in TH than in SH (p < .05). Both trained groups presented an increased parasympathetic modulation of HRV compared with their respective sedentary groups (p < .05). The TN and TH groups had a higher vagal effect in comparison with their respective sedentary groups (p < .001). The sympathetic effect was lower in TH than in SH (p < .001). Pressor and HR responses to tyramine in different doses were attenuated in TH (p < .001). Further analysis showed a significant association between infusion of tyramine and normalized LF component of HRV (r = 0.84, p < .001), systolic APV (r = 0.58, p < .001) and diastolic APV (r = 0.49, p < .001). In conclusion, exercise training provokes less pressor response variation by tyramine infusion in hypertensive animals suggesting sympathetic nerve endings adjustments and decrease of the vasoconstrictor effect attenuates injury caused by hypertension improving cardiovascular autonomic dysfunction, which can be associated with sympathetic attenuation.

Priming Mesenchymal Stem Cells with Endothelial Growth Medium Boosts Stem Cell Therapy for Systemic Arterial Hypertension.

Systemic arterial hypertension (SAH), a clinical syndrome characterized by persistent elevation of arterial pressure, is often associated with abnormalities such as microvascular rarefaction, defective angiogenesis, and endothelial dysfunction. Mesenchymal stem cells (MSCs), which normally induce angiogenesis and improve endothelial function, are defective in SAH. The central aim of this study was to evaluate whether priming of MSCs with endothelial growth medium (EGM-2) increases their therapeutic effects in spontaneously hypertensive rats (SHRs). Adult female SHRs were administered an intraperitoneal injection of vehicle solution (n = 10), MSCs cultured in conventional medium (DMEM plus 10% FBS, n = 11), or MSCs cultured in conventional medium followed by 72 hours in EGM-2 (pMSC, n = 10). Priming of the MSCs reduced the basal cell death rate in vitro. The administration of pMSCs significantly induced a prolonged reduction (10 days) in arterial pressure, a decrease in cardiac hypertrophy, an improvement in endothelium-dependent vasodilation response to acetylcholine, and an increase in skeletal muscle microvascular density compared to the vehicle and MSC groups. The transplanted cells were rarely found in the hearts and kidneys. Taken together, our findings indicate that priming of MSCs boosts stem cell therapy for the treatment of SAH.