Intravenous administration of apeling-13 induces a depressor response by releasing an unidentified substance.

Apelin and APJ receptor play an important role in the regulating cardiovascular function; however, conflicting results have been reported regarding the effect of apelin on cardiovascular regulation. In this study, blood pressure and heart rate were measured by femoral arterial catheterization; and cardiac contractility was recorded by left ventricular catheterization through the right carotid artery in rats before and after intravenous administration of [pyr1]-apelin-13. The results show that intravenous administration of apelin-13 caused a dramatic reduction in BP but did not significantly alter heart rate and contractility.

Estrogen dampens central cannabinoid receptor 1-mediated neuroexcitation and pressor response in conscious female rats.

Activation of the rostral ventrolateral medulla (RVLM) cannabinoid receptor-1 (CBR) causes neuronal nitric oxide synthase (nNOS)-dependent increases in sympathetic activity, blood pressure (BP) and heart rate (HR) in male rats. However, it remains unknown if the CBR-mediated neurochemical and cardiovascular responses are influenced by the ovarian sex hormones, particularly estrogen (E). Therefore, we studied the effects of intra-RVLM CBR activation (WIN 55,212-2) on BP and HR in conscious female rats under the following hormonal states: (1) highest E level (proestrus sham-operated, SO); (2) E-deprivation (ovariectomized, OVX); (3) OVX with E replacement (OVXE2).

Tetrahydrobiopterin paradoxically mediates cardiac oxidative stress and mitigates ethanol-evoked cardiac dysfunction in conscious female rats.

Oxidation of tetrahydrobiopterin (BH4), a cofactor of nitric oxide synthase (NOS), by reactive oxidative species (ROS), leads to NOS uncoupling and superoxide production instead of NO. Further, oxidative stress plays a major role in ethanol-evoked cardiac dysfunction in proestrus female rats, and acute ethanol administration reduces brain BH4 level. Therefore, we discerned the unknown role of BH4 in ethanol-evoked cardiac dysfunction by pharmacologically increasing BH4 levels or inhibiting its effect in proestrus female rats.

Emergent Coordination of the CHKB and CPT1B Genes in Eutherian Mammals: Implications for the Origin of Brown Adipose Tissue.

Mitochondrial fatty acid oxidation (FAO) contributes to the proton motive force that drives ATP synthesis in many mammalian tissues. In eutherian (placental) mammals, brown adipose tissue (BAT) can also dissipate this proton gradient through uncoupling protein 1 (UCP1) to generate heat, but the evolutionary events underlying the emergence of BAT are unknown. An essential step in FAO is the transport of cytoplasmic long chain acyl-coenzyme A (acyl-CoA) into the mitochondrial matrix, which requires the action of carnitine palmitoyltransferase 1B (CPT1B) in striated muscle and BAT.

Aldehyde Dehydrogenase Inhibition Ameliorates Cardiac Dysfunction and Exacerbates Hypotension Caused by Alcohol in Female Rats.

Background: Aldehyde dehydrogenase 2 (ALDH2) protects against alcohol-evoked cardiac dysfunction in male rodents, but its role in the estrogen (E )-dependent hypersensitivity of female rats to alcohol-evoked myocardial oxidative stress and dysfunction is not known.

Methods: We addressed this question by studying the effect of cyanamide (ALDH2 inhibitor) on cardiac function, blood pressure, alcohol-metabolizing enzyme (alcohol dehydrogenase, cytochrome P450 2E1, catalase, and ALDH2) activities, and cardiac redox status (reactive oxygen species, ROS; malondialdehyde, MDA) in the absence or presence of ethanol (EtOH) in female sham-operated (SO) and ovariectomized (OVX) rats.

Results: Cyanamide attenuated the EtOH-evoked myocardial dysfunction (reduced dP/dt and LVDP) in SO rats.

Orexin Receptor-1 in the Rostral Ventrolateral Medulla Mediates the Antihypertensive Effects of Electroacupuncture.

Electroacupuncture (EA) has been used to treat numerous diseases, including hypertension. This study aimed to investigate the long-term effect and underlying mechanisms of EA stimulation at the LI11 point on the hypertension and sympathetic nerve activity in two-kidney, one-clip (2K1C) hypertensive rats. EA (0.

Electroacupuncture Improves Baroreflex and -Aminobutyric Acid Type B Receptor-Mediated Responses in the Nucleus Tractus Solitarii of Hypertensive Rats.

Electroacupuncture (EA) has been reported to benefit hypertension, but the underlying mechanisms are still unclear. We hypothesized that EA attenuates hypertension, in part, through modulation of -aminobutyric acid (GABA) receptor function in the nucleus tractus solitarii (NTS). In the present study, the long-term effect of EA on GABA receptor function and expression was examined in the NTS of two-kidney, one-clip (2K1C) renovascular hypertensive rats.

Combined Catalase and ADH Inhibition Ameliorates Ethanol-Induced Myocardial Dysfunction Despite Causing Oxidative Stress in Conscious Female Rats.

Background: Ethanol (EtOH)-evoked oxidative stress, which contributes to myocardial dysfunction in proestrus rats, is mediated by increases in NADPH oxidase (Nox) activity, malondialdehyde (MDA), and ERK1/2 phosphorylation. Whether these biochemical responses, which are triggered by alcohol-derived acetaldehyde in noncardiac tissues, occur in proestrus rats' hearts remains unknown. Therefore, we elucidated the roles of alcohol dehydrogenase (ADH), cytochrome P4502E1 (CYP2E1), and catalase, which catalyze alcohol oxidation to acetaldehyde, in these alcohol-evoked biochemical and hemodynamic responses in proestrus rats.

Estrogen receptor α activation enhances its cell surface localization and improves myocardial redox status in ovariectomized rats.

Aims: Little is known about the role of subcellular trafficking of estrogen receptor (ER) subtypes in the acute estrogen (E)-mediated alleviation of oxidative stress. We tested the hypothesis that ERα migration to the cardiac myocyte membrane mediates the acute E-dependent improvement of cellular redox status.

Main Methods: Myocardial distribution of subcellular ERα, ERβ and G-protein coupled estrogen receptor (GPER) was determined in proestrus sham-operated (SO) and in ovariectomized (OVX) rats, acutely treated with E (1μg/kg) or a selective ERα (PPT), ERβ (DPN) or GPER (G1) agonist (10μg/kg), by immunofluorescence and Western blot.

Estrogen Receptors α and β Play Major Roles in Ethanol-Evoked Myocardial Oxidative Stress and Dysfunction in Conscious Ovariectomized Rats.

Background: We documented the dependence of ethanol (EtOH)-evoked myocardial dysfunction on estrogen (E ), and our recent estrogen receptor (ER) blockade study, in proestrus rats, implicated ERα signaling in this phenomenon. However, a limitation of selective pharmacological loss-of-function approach is the potential contribution of the other 2 ERs to the observed effects because crosstalk exists between the 3 ERs. Here, we adopted a "regain"-of-function approach (using selective ER subtype agonists) to identify the ER subtype(s) required for unraveling the E -dependent myocardial oxidative stress/dysfunction caused by EtOH in conscious ovariectomized (OVX) rats.

Estrogen receptor ERα plays a major role in ethanol-evoked myocardial oxidative stress and dysfunction in conscious female rats.

Our previous studies showed that ethanol elicited estrogen (E2)-dependent myocardial oxidative stress and dysfunction. In the present study we tested the hypothesis that E2 signaling via the estrogen receptor (ER), ERα, mediates this myocardial detrimental effect of alcohol. To achieve this goal, conscious female rats in proestrus phase (highest endogenous E2 level) received a selective ER antagonist (200 μg/kg; intra-venous [i.

Electrical signal propagated across acupoints along Foot Taiyang Bladder Meridian in rats.

Objective: To investigate the electrical signals propagated along Foot Taiyang Bladder Meridian (BL) in a rat model.

Methods: The experiments were performed on Dark-Agouti (DA), DA.1U and Sprague Dawley (SD) rats.

The local effect of octreotide on mechanical pain sensitivity is more sensitive in DA rats than DA.1U rats.

A recent study by the authors indicated that major histocompatibility complex (MHC) genes are associated with the differences in basal pain sensitivity and in formalin model between Dark-Agouti (DA) and novel congenic DA.1U rats, which have the same genetic background as DA rats except for the u alleles of MHC. The objective of the present study is to investigate whether there is a difference in the pristane-induced arthritis (PIA) model and local analgesic effect of octreotide (OCT) between DA and DA.

20-Hydroxyeicosatetraenoic Acid Is a Key Mediator of Angiotensin II-induced Apoptosis in Cardiac Myocytes.

Cardiomyocyte apoptosis is involved in a variety of cardiac stresses, including ischemia-reperfusion injury, heart failure, and cardiomyopathy. Both Angiotensin II (Ang II) and 20-hydroxyeicosatetraenoic acid (20-HETE) induce apoptosis in cardiomyocytes. Here, we examined the relationship between 20-HETE and Ang II in cardiomyocyte apoptosis.

The major histocompatibility complex genes impact pain response in DA and DA.1U rats.

Our recent studies have shown that the difference in basal pain sensitivity to mechanical and thermal stimulation between Dark-Agouti (DA) rats and a novel congenic DA.1U rats is major histocompatibility complex (MHC) genes dependent. In the present study, we further used DA and DA.

Polydatin prevents angiotensin II-induced cardiac hypertrophy and myocardial superoxide generation.

Our studies and others recently demonstrate that polydatin, a resveratrol glucoside, has antioxidative and cardioprotective effects. This study aims to investigate the direct effects of polydatin on Ang II-induced cardiac hypertrophy to explore the potential role of polydatin in cardioprotection. Our results showed that in primary cultured cardiomyocytes, polydatin blocked Ang II-induced cardiac hypertrophy in a dose-dependent manner, which were associated with reduction in the cell surface area and [(3)H]leucine incorporation, as well as attenuation of the mRNA expressions of atrial natriuretic factor and β-myosin heavy chain.

Polydatin supplementation ameliorates diet-induced development of insulin resistance and hepatic steatosis in rats.

The pathophysiology of non-alcoholic fatty liver disease remains to be elucidated, and the currently available treatments are not entirely effective. Polydatin, a stilbenoid compound derived from the rhizome of Polygonum cuspidatum, has previously been demonstrated to possess hepatoprotective effects. The present study aimed to determine the effects of polydatin supplementation on hepatic fat accumulation and injury in rats fed a high-fat diet.

The inhibitory effect of somatostatin receptor activation on bee venom-evoked nociceptive behavior and pCREB expression in rats.

The present study examined nociceptive behaviors and the expression of phosphorylated cAMP response element-binding protein (pCREB) in the dorsal horn of the lumbar spinal cord and the dorsal root ganglion (DRG) evoked by bee venom (BV). The effect of intraplantar preapplication of the somatostatin analog octreotide on nociceptive behaviors and pCREB expression was also examined. Subcutaneous injection of BV into the rat unilateral hindpaw pad induced significant spontaneous nociceptive behaviors, primary mechanical allodynia, primary thermal hyperalgesia, and mirror-thermal hyperalgesia, as well as an increase in pCREB expression in the lumbar spinal dorsal horn and DRG.

Polydatin alleviates non-alcoholic fatty liver disease in rats by inhibiting the expression of TNF-α and SREBP-1c.

The pathophysiology of non-alcoholic fatty liver disease remains incompletely elucidated, and available treatments are not entirely satisfactory. Polydatin, a stilbenoid compound derived from the rhizome of Polygonum cuspidatum, has been recognised to possess hepatoprotective and anti-inflammatory activities. The purpose of the present study was to determine whether polydatin has a protective effect against hepatic steatosis induced by a high-fat diet (HFD) and to elucidate its underlying molecular mechanisms in rats.

Angiotensin-(1-7) attenuates the chronotropic response to angiotensin II via stimulation of PTEN in the spontaneously hypertensive rat neurons.

Several studies have focused on the beneficial effects of peripheral angiotensin-(1-7) [Ang-(1-7)] in the regulation of cardiovascular function, showing its counterregulatory effect against the actions of angiotensin II (ANG II). However, its actions in the central nervous system are not completely understood. In the present study, we investigated the intracellular mechanisms underlying the action of ANG-(1-7) using the patch-clamp technique in neurons cultured from the hypothalamus of neonatal spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats.

Lentil polyphenol extract prevents angiotensin II-induced hypertension, vascular remodelling and perivascular fibrosis.

The objective of the study was to investigate whether chronic administration of the Morton lentil polyphenol extract (MLPE), which possesses rich phenolic compounds and a high antioxidant activity, had any protective effects on angiotensin II-induced hypertension. After four weeks of subcutaneous infusion of angiotensin II (200 ng kg(-1) min(-1)) in male SD rats, the water intake and mean artery pressure was significantly increased by 39.8% and 48.

Pressor effect of apelin-13 in the rostral ventrolateral medulla: role of NAD(P)H oxidase-derived superoxide.

Microinjection of apelin-13 into the rostral ventrolateral medulla (RVLM) in the brainstem increases blood pressure in rats. In the present study, we tested the hypotheses that apelin-13 directly stimulates neuronal activity in neurons cultured from the brainstem and that NAD(P)H oxidase-derived reactive oxygen species are involved in this action of apelin-13. Microinjection of apelin-13 into the RVLM resulted in increases in arterial pressure and in renal sympathetic nerve activity in Sprague-Dawley rats.

Morton lentil extract attenuated angiotensin II-induced cardiomyocyte hypertrophy via inhibition of intracellular reactive oxygen species levels in vitro.

The objective was to investigate whether a lentil (Morton) extract had any protective effect on cardiac hypertrophy, which is one of the most significant sequelae of cardiovascular diseases. High phenolic compounds (43.4 mg of GAE/g), including thirteen phenolic acid and two flavonoids, were detected in the acetone/water/acetic acid lentil extract.

20-HETE increases NADPH oxidase-derived ROS production and stimulates the L-type Ca2+ channel via a PKC-dependent mechanism in cardiomyocytes.

The production of 20-hydroxyeicosatetraenoic acid (20-HETE) is increased during ischemia-reperfusion, and inhibition of 20-HETE production has been shown to reduce infarct size caused by ischemia. This study was aimed to discover the molecular mechanism underlying the action of 20-HETE in cardiac myocytes. The effect of 20-HETE on L-type Ca(2+) currents (I(Ca,L)) was examined in rat isolated cardiomyocytes by patch-clamp recording in the whole cell mode.