ABSTRACT
<p><b>OBJECTIVE</b>To observe the effect of β₃adrenoceptors (β₃-AR) activation on rat thoracic aorta smooth muscle contractility and the possible related mechanism.</p><p><b>METHODS</b>The endothelium removed thoracic aorta was pre-contracted with 30 mmol/L KCl physiological saline solution (PSS). Then the tension of the thoracic aorta was recorded in presence of BRL37344 (BRL) to determine the action of β₃-AR. The tension of the thoracic aorta was also recorded in the presence of Propranolol (PRA), SR59230A (SR), L-NNA, H-89 and Iberiotoxin (IBTX) respectively to reveal the underling mechanism of β₃-AR activation on rat vascular smooth muscle. Immunohistochemistry was adopted to confirm the existence and the distribution of β₃-AR in rat thoracic aorta.</p><p><b>RESULTS</b>The results showed that: (1) The thoracic aorta was relaxed by β₃-AR activation, with a relaxation percentage of (10.59 ± 0.79). (2) β₃-AR was expressed in both endothelial and smooth muscle layer in thoracic aorta sections of rats. (3) PRA did not block the effect of BRL on the thoracic aorta. The relaxation actions of BRL could be antagonized by pre-incubating the thoracic aorta with SR. (4) L-NNA (a NOS inhibitor) and H-89 (a PKA inhibitor) reversed the relaxation effect of BRL on vascular smooth muscle. (5) The effect of BRL was decreased after application of Ibriotoxin (IBTX), a large conductance calcium dependent potassium channel blocker.</p><p><b>CONCLUSION</b>The results confirmed that activation of β₃-AR led to relaxation of thoracic aorta smooth muscle. The relaxation action of β₃-AR on smooth muscle of rat thoracic aorta was related to activation of NOS and PKA signaling pathway. Large conductance Ca²⁺-K⁺ channels were involved in the relaxation action of β₃-AR activation on rat thoracic aorta smooth muscle.</p>
Subject(s)
Animals , Rats , Aorta, Thoracic , Physiology , In Vitro Techniques , Isoquinolines , Large-Conductance Calcium-Activated Potassium Channels , Physiology , Muscle Contraction , Muscle Relaxation , Muscle, Smooth, Vascular , Physiology , Nitroarginine , Peptides , Propanolamines , Propranolol , Receptors, Adrenergic, beta-3 , Physiology , Signal Transduction , SulfonamidesABSTRACT
<p><b>OBJECTIVE</b>To investigate the therapeutic efficacy of intravenous implanted bone marrow-derived endothelial progenitor cells (BM-EPC) preconditioned with 17β-estradiol in ovariectomized mice model of acute myocardial infarction (AMI).</p><p><b>METHODS</b>BM-EPC were cultured and identified from ovariectomized BALB/C mice tibia and femur. The ovariectomized BALB/C mice models of acute myocardial infarction (AMI) were established, and randomly divided into 17β-estradiol + BM-EPC group (n = 6), BM-EPC group (n = 6) and control group (n = 6). Three days after AMI, BM-EPC pretreated with or without 17β-estradiol was infused via tail vein. The equal volume of saline was infused in control group. Twenty-five days after infusion, left ventricular (LV) function and dimensions, capillary density and ratio of fibrosis area to LV area were measured.</p><p><b>RESULTS</b>LV function and dimensions, capillary density and LV fibrosis were significantly improved in 17β-estradiol + BM-EPC group than in control group [(LVDs: (3.09 ± 0.05) mm vs. (3.27 ± 0.10)mm, P < 0.05; LVDd: (4.18 ± 0.07) mm vs. (4.31 ± 0.05) mm, P < 0.05; FS: (33.0 ± 3.8)% vs. (26.0 ± 3.2)%, P < 0.05; capillary density: (1428 ± 214)/mm² vs. (1070 ± 168)/mm², P < 0.05; ratio of fibrosis: (38.8 ± 4.9)% vs. (49.0 ± 4.6)%, P < 0.05]. However, Above mentioned parameters were similar between BM-EPC group and control group (P > 0.05).</p><p><b>CONCLUSIONS</b>BM-EPC preconditioned with 17β-estradiol can enhance capillary density, decrease LV fibrosis and improve cardiac function in this mice model of AMI.</p>