• Journal of Chest Surgery
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• v.28 no.12
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• pp.1079-1095
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• 1995

Recently endogenous digitalis-like substances were found in the blood of various cardiovascular diseases and they have been considered one of the causes of evoking hypertension. However, the mechanism of endogenous digitalis-like substances-induced hypertension is not clarified yet. Therefore, the effects of Na-K pump inhibition on the contractility of vascular smooth muscle[conduit and resistant artery were investigated, using organ bath and bioassay experiment. Aortic and carotid arterial rings[conduit artery and the branches of brachial and superior mesenteric artery[resistant artery were used to find the effect of Na-K pump inhibition. The results obtained were as followes;The magnitudes of contractions induced by norepinephrine, serotonin, or acetylcholine in all these arteries were significantly increased by the inhibition of Na-K pump. The increased contractile responses to these agonists, especially to serotonin, were much more prominant in resistant arteries. Nitroprusside-induced relaxations were attenuated by Na-K pump inhibition and there were no significant differences in the effects of Na-K pump inhibition on nitroprusside-induced relaxations of these blood vessels. Endothelium-dependent relaxation was suppressed by the inhibition of Na-K pump, especially by the administration of ouabain, and this inhibitory effect was much more prominent in the branches of superior mesenteric artery, compared with other arteries. In the branches of superior mesenteric arteries, endothelium-dependent relaxation was completely blocked by ouabain. The release of EDRF was partially suppressed by Na-K pump inhibition.From the above results, it is suggested that the hypertension due to the increase in vascular resistance can be evoked by the inhibition of Na-K pump and endogenous digitalis-like substances induce hypertension through this mechanism.

• Journal of Korean Physical Therapy Science
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• v.9 no.4
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• pp.45-52
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• 2002

Rats that are fed a fructose-rich diet develop hypertension, insulin resistance, and hypertriglyceridemia. To elucidate whether altered expression levels of endothelin-1 and nitric oxide synthase are related to the development of insulin-resistant hypertension, we examined the present study. Male Sprague-Dawley rats were fed a fructose-rich diet for 5 weeks. Systolic blood pressure significantly increased in fructose-fed rats. While serum free fatty acid and plasma nitrite/nitrate levels did not significantly differ between the fructose-fed and control groups, plasma insulin and serum triglyceride concentrations significantly increased in the former. Endothelin-1 mRNA expression in the aorta increased in fructose-fed rats. Neither the protein expression of constitutive nitric oxide synthase nor that of inducible nitric oxide synthase were significantly affected by fructose feeding. However, nitrite/nitrate levels in the aorta were significantly increased. These results suggest that an increase in vascular endothelin-1 is an important contributing factor to the development of hypertension in fructose-fed rats. However, the vascular nitric oxide pathway may not be causally related to the development of fructose-induced hypertension.

• The Korean Journal of Food And Nutrition
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• v.36 no.6
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• pp.452-461
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• 2023

Hypertension caused by high-fat and high-salt diets is is a well-known significant risk factor for cardiovascular and cerebrovascular diseases. In this study, to confirm the relationship between hypertension and immune cells, angiotensin (Ang) II was administered to Dahl salt-sensitive (SS) rats and Dahl salt-resistant (SR) rats. Then the expression of immune cells and the proinflammatory cytokines were compared between the SS and SR rats. It was observed that after administration of Ang II (50ng/kg/min) for three weeks, blood pressure was increased in the SS rats, but there was no significant change in the SR rats. In addition, the expression of T helper (Th) cells and Th 17 cells in the spleen and the expression of Th cell Rorγt and regulatory T regulatory (Treg) cells in the peripheral blood mononuclear cells did not show a significant difference between the two experimental groups even after the administration of Ang II.IL-1β expression was significantly increased in the kidney tissue of the SS rats, while there was no significant difference in the IL-6 expression in all the experimental groups. The results of this study suggest that Ang II induces hypertension by stimulating IL-1β secretion from renal macrophage in SS rats.

• Toxicological Research
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• v.17
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• pp.289-292
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• 2001

Gene targeting allows precise, predetermined changes to be made in a chosen gene in the mouse genome. To date, targeting has been used most often for generation of animals completely lacking the product of a gene of interest. Models of essential hypertension have been produced by mutated genes relating renin angiotensin system. The most significant contribution to understanding the genetic etiology of essential hypertension is probably the demonstration that discrete alterations in the expression of a variety of different genes can individually cause changes in the blood pressures of mice, even when the mice have all their compensatory mechanisms intact. These effects are readily detected in animals having moderate decreases in gene function due to heterozygosity for gene disruptions or modest increases due to gene duplication. As a species the mouse is highly resistant to atherosclerosis. However. through induced mutations it has been possible to develop lines oj mice that are deficient in apolipoprotein E, a ligand important in lipoprotein clearance, develop atherosclerotic lesions resembling those observed in humans. The atherosclerotic lesions in apoE-deficient mice have been well characterized, and they resemble human lesions in their sites of predilection and progression to the fibroproliferative stage. Other promising models are mice that are deficient in the low-density lipoprotein receptor. Considerable work still remains to be done in dissecting out in a rigorous manner the effects of alterations in single genes on the induction or progression of atherosclerosis and on the control of blood pressures. Perhaps even more exciting is the opportunity now becoming available to breed animals in which the effects oj precise differences in more than one gene can be studied in combination.

• Childhood Kidney Diseases
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• v.16 no.1
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• pp.46-50
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• 2012

C1q nephropathy is a distinct clinicopathologic entity, characterized by mesangial immunoglobulin and complement deposits, predominantly C1q, with no evidence for systemic lupus erythematosus. Clinically it may present as nephrotic syndrome and non-nephrotic proteinuria per se or associated with microscopic hematuria, gross hematuria, hypertension, or renal insufficiency. So far there is only one report about a familial case of C1q nephropathy (in two sisters). We present two cases of familial C1q nephropathy with nephrotic syndrome which was steroid resistant, but partially remitted with cyclosporine.

• Childhood Kidney Diseases
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• v.11 no.1
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• pp.92-99
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• 2007

The posterior reversible encephalopathy syndrome(PRES) is characterized clinically by a combination of acute or subacute confusion, lethargy, visual disturbance, and seizures. PRES has been described in various clinical settings, including severe hypertension, chemotherapy, eclampsia, and seizure. We report a case of a 7-year-old girl who had taken cyclosporine for steroid resistant nephrotic syndrome. Twenty one days after the cyclosporine therapy, she was admitted due to generalized tonic clonic seizure and headache. Her blood pressure was 170/90 mmHg. Magnetic resonance(MR) imaging showed necrotic/cystic lesions involving the bilateral parieto-occipital region. After discontinuation of cyclosporine, and control of blood pressure, she had no more seizure and headache. The follow-up MR examination which was performed 6 months later showed the decreased extent of the lesion.

• Clinical and Experimental Pediatrics
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• v.52 no.3
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• pp.370-375
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• 2009

Purpose : The risk of metabolic syndrome (MS) and cardiovascular disease in Turner syndrome (TS) patients is high. We analyzed metabolic factors in adults with TS and evaluated the metabolic risk of insulin resistance. Methods : Forty-three adults with TS were enrolled. The frequency of MS and the values of the metabolic factors were analyzed. Patients were divided into insulin resistant and non-resistant groups according to values of homeostasis model assessment of insulin resistance (HOMA-IR). The correlations of HOMA-IR with metabolic parameters were analyzed. Results : The frequency of MS was 7% and those of each metabolic parameter were as follows: insulin resistance, 16.3%; central obesity, 15.4%; hypertriglyceridemia, 2.3%; low HDL cholesterol, 9.3%; hypertension, 36.8%. The insulin-resistant group had significantly higher values of body mass index (BMI), waist circumference (WC), fasting plasma glucose (FPG), HOMA-IR, and systolic blood pressure (SBP) than the non-resistant group (P<0.05). HOMA-IR showed a significantly positive correlation with BMI, WC, FPG, and SBP and showed a negative correlation with HDL cholesterol. Conclusion : This study suggests that adults with TS have a high risk of metabolic syndrome, and insulin resistance is correlated with metabolic factors. Therefore, TS patients should have their metabolic parameters monitored regularly to minimize metabolic complications and prevent cardiovascular diseases.

• Advances in Traditional Medicine
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• v.10 no.4
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• pp.304-309
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• 2010

Scutellaria pinnatifida A. Hamilt. (Lamiaceae) is an endemic Turkish herb. This plant is also endemic to Iran, and grows abundantly in other central and western Asian countries. Several species of the Scutellaria are known for their traditional uses in the treatment of hypertension, arteriosclerosis, inflammatory diseases, hepatitis, allergy, cancer and diarrhoea. Free-radical-scavenging property, antibacterial activity and brine shrimp toxicity of the n-hexane, dichloromethane (DCM) and methanol (MeOH) extracts of S. pinnatifida were assessed using the 2,2-diphenyl-1-picryl-hydrazyl (DPPH) assay, the resazurin microtitre plate based assay, and the brine shrimp lethality assay, respectively. The DCM and MeOH extracts exhibited free-radical-scavenging property, with the $RC_{50}$ values of 0.362 and 0.127 mg/ml, respectively. Among the solid-phase extraction fractions of the MeOH extract, the 50% aqueous-MeOH fraction showed the highest level of free-radicalscavenging activity ($RC_{50}$ = 0.039 mg/ml). While the DCM extract showed low level of antibacterial activity against Bacillus subtilis and ampicillin-resistant Escherichia coli, the MeOH extract was active against B. cereus, B. subtilis, E. coli and ampicillin-resistant E. coli. However, the minimum inhibitory concentrations (MIC) of the MeOH extract against these bacterial strains were >10 mg/ml. None of the extracts showed any significant toxicity towards brine shrimps ($LD_{50}$ = > 1.00 mg/ml).

• Journal of Nutrition and Health
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• v.50 no.3
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• pp.217-224
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• 2017

Purpose: Although it is well known thatmortality and morbidity due to cardiovascular diseases are higher in salt-sensitive subjects than in salt-resistant subjects, their underlying mechanisms related to obesity remain unclear. Here, we focused on salt-sensitive gene variants unrelated to monogenic obesity that interacted with sodium intake in humans. Methods: This review was written based on the modified $3^rd$ step of Khans' systematic review. Instead of the literature, subject genes were based on candidate genes screened from our preliminary Genome-Wide Association Study (GWAS). Finally, literature related to five genes strongly associated with salt sensitivity were analyzed to elucidate the mechanism of obesity. Results: Salt sensitivity is a measure of how blood pressure responds to salt intake, and people are either salt-sensitive or salt-resistant. Otherwise, dietary sodium restriction may not be beneficial for everyone since salt sensitivity may be associated with inherited susceptibility. According to our previous GWAS studies, 10 candidate genes and 11 single nucleotide polymorphisms (SNPs) associated with salt sensitivity were suggested, including angiotensin converting enzyme (ACE), ${\alpha}$-adducin1 (ADD1), angiotensinogen (AGT), cytochrome P450 family 11-subfamily ${\beta}$-2 ($CYP11{\beta}$-2), epithelial sodium channel (ENaC), G-protein b3 subunit (GNB3), G protein-coupled receptor kinases type 4 (GRK4 A142V, GRK4 A486V), $11{\beta}$-hydroxysteroid dehydrogenase type-2 (HSD $11{\beta}$-2), neural precursor cell-expressed developmentally down regulated 4 like (NEDD4L),and solute carrier family 12(sodium/chloride transporters)-member 3 (SLC 12A3). We found that polymorphisms of salt-sensitive genes such as ACE, $CYP11{\beta}$-2, GRK4, SLC12A3, and GNB3 may be positively associated with human obesity. Conclusion: Despite gender, ethnic, and age differences in genetics studies, hypertensive obese children and adults who are carriers of specific salt-sensitive genes are recommended to reduce their sodium intake. We believe that our findings can contribute to the prevention of early-onset of chronic diseases in obese children by facilitating personalized diet-management of obesity from childhood to adulthood.

• IMMUNE NETWORK
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• v.19 no.1
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• pp.5.1-5.12
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• 2019

Autophagy is a homeostatic mechanism that discards not only invading pathogens but also damaged organelles and denatured proteins via lysosomal degradation. Increasing evidence suggests a role for autophagy in inflammatory diseases, including infectious diseases, Crohn's disease, cystic fibrosis, and pulmonary hypertension. These studies suggest that modulating autophagy could be a novel therapeutic option for inflammatory diseases. Eosinophils are a major type of inflammatory cell that aggravates airway inflammatory diseases, particularly corticosteroid-resistant inflammation. The eosinophil count is a useful tool for assessing which patients may benefit from inhaled corticosteroid therapy. Recent studies demonstrate that autophagy plays a role in eosinophilic airway inflammatory diseases by promoting airway remodeling and loss of function. Genetic variant in the autophagy gene ATG5 is associated with asthma pathogenesis, and autophagy regulates apoptotic pathways in epithelial cells in individuals with chronic obstructive pulmonary disease. Moreover, autophagy dysfunction leads to severe inflammation, especially eosinophilic inflammation, in chronic rhinosinusitis. However, the mechanism underlying autophagy-mediated regulation of eosinophilic airway inflammation remains unclear. The aim of this review is to provide a general overview of the role of autophagy in eosinophilic airway inflammation. We also suggest that autophagy may be a new therapeutic target for airway inflammation, including that mediated by eosinophils.