Plasma Concentration of Atrial Natriuretic Peptide in Different Phases of Korean Hemorrhagic Fever

Cho, Kyung Woo; Kim, Suhn Hee; Koh, Gou Young; Seul, Kyung Hwan; Huh, Ki Suck; Chu, David; Rapp, Neville S.; Moon, Hyung Bae; Kim, Kyung Keun; Kook, Y.

doi:10.1159/000185288

Cited by 27 publications

(7 citation statements)

References 20 publications

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“…Plasma atrial natriuretic peptide (ANP) was extracted using a Sep-Pak C 18 cartridge and the ANP concentrations in plasma and ventricles were measured using specific radioimmunoassay (RIA), as described previously [ 12 ]. The plasma renin concentration (PRC) was also measured using RIA, as described previously [ 12 ]. Severity of lung injury was determined by the concentration of lactate dehydrogenase (LDH) using LDH ELISA kit (Takara Bio Inc., Japan) [ 13 14 ].…”

Section: Methodsmentioning

confidence: 99%

Angiotensin-(1-9) ameliorates pulmonary arterial hypertension via angiotensin type II receptor

Park

Kim

2018

Korean J Physiol Pharmacol

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Angiotensin-(1-9) [Ang-(1-9)], generated from Ang I by Ang II converting enzyme 2, has been reported to have protective effects on cardiac and vascular remodeling. However, there is no report about the effect of Ang-(1-9) on pulmonary hypertension. The aim of the present study is to investigate whether Ang-(1-9) improves pulmonary vascular remodeling in monocrotaline (MCT)-induced pulmonary hypertensive rats. Sprague-Dawley rats received Ang-(1-9) (576 µg/kg/day) or saline via osmotic mini-pumps for 3 weeks. Three days after implantation of osmotic mini-pumps, 50 mg/kg MCT or vehicle were subcutaneously injected. MCT caused increases in right ventricular weight and systolic pressure, which were reduced by co-administration of Ang-(1-9). Ang-(1-9) also attenuated endothelial damage and medial hypertrophy of pulmonary arterioles as well as pulmonary fibrosis induced by MCT. The protective effects of Ang-(1-9) against pulmonary hypertension were inhibited by Ang type 2 receptor (AT2R) blocker, but not by Mas receptor blocker. Additionally, the levels of LDH and inflammatory cytokines, such as TNF-α, MCP-1, IL-1β, and IL-6, in plasma were lower in Ang-(1-9) co-treated MCT group than in vehicle-treated MCT group. Changes in expressions of apoptosis-related proteins such as Bax, Bcl-2, Caspase-3 and -9 in the lung tissue of MCT rats were attenuated by the treatment with Ang-(1-9). These results indicate that Ang-(1-9) improves MCT-induced pulmonary hypertension by decreasing apoptosis and inflammatory reaction via AT2R.

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Section: Methodsmentioning

confidence: 99%

Angiotensin-(1-9) ameliorates pulmonary arterial hypertension via angiotensin type II receptor

Park

Kim

2018

Korean J Physiol Pharmacol

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“…The ANP in effluent was extracted using Sep‐Pak C 18 cartridges (Cho et al. ), dried, and measured using a specific radioimmunoassay, as described previously (Cho et al. ).…”

Section: Methodsmentioning

confidence: 99%

Cardioprotective effects of angiotensin III against ischemic injury via the AT₂ receptor and K_ATP channels

Park

Gao

et al. 2013

Physiol Rep

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Angiotensin III (Ang III) has similar effects on blood pressure and aldosterone secretion as Ang II, but cardioprotective effects are also proposed. In this study, we investigated whether Ang III protects the heart against ischemia/reperfusion (I/R) injury. After sacrificing Sprague-Dawley rats, the hearts were perfused with Krebs–Henseleit buffer for a 20 min preischemic period with and without Ang III followed by 20-min global ischemia and 50-min reperfusion. Pretreatment with Ang III (1 μmol/L) improved an increased postischemic left ventricular end-diastolic pressure (LVEDP) and a decreased postischemic left ventricular developed pressure (LVDP) induced by reperfusion compared to untreated hearts. Ang III markedly decreased infarct size and lactate dehydrogenase levels in effluent during reperfusion. Ang III increased coronary flow and the concentrations of atrial natriuretic peptide in coronary effluent during reperfusion. Pretreatment with Ang II type 2 receptor (AT2R) antagonist or ATP-sensitive K+ channel (KATP) blocker for 15 min before ischemia attenuated the improvement of LVEDP, LVDP, and ±dP/dt induced by Ang III. Ang III treatment increased Mn-superoxide dismutase, catalase, and heme oxygenase-1 protein levels, which was attenuated by pretreatment with AT2R antagonist or KATP blocker. Ang III treatment also decreased Bax, caspase-3, and caspase-9 protein levels, and increased Bcl-2 protein level, which were attenuated by pretreatment with AT2R antagonist or KATP blocker. These results suggest that the cardioprotective effects of Ang III against I/R injury may be partly related to activating antioxidant and antiapoptotic enzymes via AT2R and KATP channels.

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“…Plasma ANP was extracted using a Sep-Pak C18 cartridge and then dried using a Speed-Vac concentrator (Savant, Farmingdale, NY) (9). Concentrations of ANP in tissue, plasma, and perfusate were measured using a specific RIA, as described previously (9).…”

Section: (Da)mentioning

confidence: 99%

Leptin reduces plasma ANP level via nitric oxide-dependent mechanism

Yuan¹,

Shah³

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Leptin is a circulating adipocyte-derived hormone that influences blood pressure (BP) and metabolism. This study was designed to define the possible role of leptin in regulation of the atrial natriuretic peptide (ANP) system using acute and chronic experiments. Intravenous infusion of rat leptin (250 g/kg injection plus 2 g·kg Ϫ1 ·min Ϫ1 for 20 min) into Sprague-Dawley rats increased BP by 25 mmHg and decreased plasma level of ANP from 80.3 Ϯ 3.45 to 51.8 Ϯ 3.3 pg/ml. Reserpinization attenuated the rise in BP, but not the reduction of plasma ANP during leptin infusion. N -nitro-L-arginine methyl ester prevented the effects of leptin on the reduction of ANP level. In hyperleptinemic rats that received adenovirus containing rat leptin cDNA (AdCMV-leptin), BP increased during first 2 days and then recovered to control value. Plasma concentration of ANP and expression of ANP mRNA, but not of atrial ANP, in hyperleptinemic rats were lower than in the control groups on the first and second week after administration of AdCMV-leptin. These effects were not observed by the pretreatment with N -nitro-L-arginine methyl ester. No differences in renal function and ANP receptor density in the kidney were found between hyperleptinemic and control rats. Basal ANP secretion and isoproterenol-induced suppression of ANP secretion from isolated, perfused atria of hyperleptinemic rats were not different from those of other control groups. These data suggest that leptin inhibits ANP secretion indirectly through nitric oxide without changing basal or isoproterenolinduced ANP secretion. sympathetic nervous system; atrial natriuretic peptide; adenosine 3=,5=-cyclic monophosphate; hypertension; receptor LEPTIN IS A CIRCULATING adipocyte-derived hormone that regulates energy balance through binding to leptin receptors (Ob-R) at the hypothalamus (37). Leptin decreases appetite and increases body temperature and energy consumption, thereby decreasing adipose tissue mass and body weight (BW) (11,28,32). The Ob-R is a member of the extended class I cytokine receptor family, with at least six splice variants, Ob-R (a-f) (27), and is distributed in various tissues, such as lung, kidney, heart, vascular endothelium, and brain (23, 31). Wide distributions of the Ob-R and leptin mRNA suggest a diversity of its functions. In addition to the well-known metabolic functions of leptin, it also regulates autonomic, cardiovascular, endocrine, and renal functions. However, these functions are still controversial and are under investigation (22). Recent studies have focused on the potential effects of leptin on blood pressure (BP) and renal function through activation of the sympathetic nervous system (SNS). Dose-dependent increases in sympathetic discharge from the kidney and brown adipose tissue by murine leptin have been reported (15). Acute intravenous infusion of leptin showed no effect on BP (15, 16), whereas chronic infusion of murine leptin caused an increase in BP and heart rate (HR), as well as renal vascular resistance (6). Hypertension was deve...

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Plasma Concentration of Atrial Natriuretic Peptide in Different Phases of Korean Hemorrhagic Fever

Cited by 27 publications

References 20 publications

Angiotensin-(1-9) ameliorates pulmonary arterial hypertension via angiotensin type II receptor

Angiotensin-(1-9) ameliorates pulmonary arterial hypertension via angiotensin type II receptor

Cardioprotective effects of angiotensin III against ischemic injury via the AT₂ receptor and K_ATP channels

Leptin reduces plasma ANP level via nitric oxide-dependent mechanism

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Plasma Concentration of Atrial Natriuretic Peptide in Different Phases of Korean Hemorrhagic Fever

Cited by 27 publications

References 20 publications

Angiotensin-(1-9) ameliorates pulmonary arterial hypertension via angiotensin type II receptor

Angiotensin-(1-9) ameliorates pulmonary arterial hypertension via angiotensin type II receptor

Cardioprotective effects of angiotensin III against ischemic injury via the AT2 receptor and KATP channels

Leptin reduces plasma ANP level via nitric oxide-dependent mechanism

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Product

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Cardioprotective effects of angiotensin III against ischemic injury via the AT₂ receptor and K_ATP channels