The Role of Matrix Structure in Pressure Regulation of Enzymes Encapsulated in Ternary Surfactant-Water-Organic Solvent Systems

2003 ◽  
pp. 235-239
Author(s):  
N. L. Klyachko ◽  
R. Köhling ◽  
J. Woenckhaus ◽  
A. K. Kazarov ◽  
S. A. Smirnov ◽  
...  
Keyword(s):  
Organic Solvent ◽  
Matrix Structure ◽  
Pressure Regulation ◽  
Solvent Systems

Anti-Hypertensive Potential and Epigenetics of Angiotensin II type 2 Receptor (AT2R)

2020 ◽  
Vol 16 ◽  
Author(s):  
Mayank Chaudhary
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Blood Pressure Regulation ◽  
Biologically Active ◽  
Pressure Regulation ◽  
Tissue Remodelling ◽  
Critical Pathway

Background:: Renin angiotensin system (RAS) is a critical pathway involved in blood pressure regulation. Octapeptide, angiotensin II (Ang aII), is biologically active compound of RAS pathway which mediates its action by binding to either angiotensin II type 1 receptor (AT1R) or angiotensin II type 2 receptor (AT2R). Binding of Ang II to AT1R facilitates blood pressure regulation whereas AT2R is primarily involved in wound healing and tissue remodelling. Objective:: Recent studies have highlighted additional role of AT2R to counter balance detrimental effects of AT1R. Activation of angiotensin II type 2 receptor using AT2R agonist has shown effect on natriuresis and release of nitric oxide. Additionally, AT2R activation has been found to inhibit angiotensin converting enzyme (ACE) and enhance angiotensin receptor blocker (ARB) activity. These findings highlight the potential of AT2R as novel therapeutic target against hypertension. Conclusion:: The potential role of AT2R highlights the importance of exploring additional mechanisms that might be crucial for AT2R expression. Epigenetic mechanisms including DNA methylation and histone modification have been explored vastly with relation to cancer but role of such mechanisms on expression of AT2R has recently gained interest.

scholarly journals Sex- and age-based differences in the effect of central serotonin on arterial blood pressure regulation

2020 ◽  
Vol 129 (6) ◽  
pp. 1310-1323
Author(s):  
Jennifer L. Magnusson ◽  
Craig A. Emter ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Nrem Sleep ◽  
Blood Pressure Regulation ◽  
Pressure Regulation ◽  
Adult Rats ◽  
Arterial Blood ◽  
Serotonin Neurons ◽  
Older Males

The role of serotonin in arterial blood pressure (ABP) regulation across states of vigilance is unknown. We hypothesized that adult rats devoid of CNS serotonin (TPH2−/−) have low ABP in wakefulness and NREM sleep, when serotonin neurons are active. However, TPH2−/− rats experience higher ABP than TPH2+/+ rats in wakefulness and REM only, a phenotype present only in older males and not females. CNS serotonin may be critical for preventing high ABP in males with aging.

Hydrogen sulfide-mediated cardioprotection: mechanisms and therapeutic potential

2010 ◽  
Vol 120 (6) ◽  
pp. 219-229 ◽  
Author(s):  
Madhav Lavu ◽  
Shashi Bhushan ◽  
David J. Lefer
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Hydrogen Sulfide ◽  
Therapeutic Potential ◽  
Blood Pressure Regulation ◽  
Pressure Regulation ◽  
Signalling Molecule ◽  
Anti Inflammatory ◽  
Antioxidant Effects

H2S (hydrogen sulfide), viewed with dread for more than 300 years, is rapidly becoming a ubiquitously present and physiologically relevant signalling molecule. Knowledge of the production and metabolism of H2S has spurred interest in delineating its functions both in physiology and pathophysiology of disease. Although its role in blood pressure regulation and interaction with NO is controversial, H2S, through its anti-apoptotic, anti-inflammatory and antioxidant effects, has demonstrated significant cardioprotection. As a result, a number of sulfide-donor drugs, including garlic-derived polysulfides, are currently being designed and investigated for the treatment of cardiovascular conditions, specifically myocardial ischaemic disease. However, huge gaps remain in our knowledge about this gasotransmitter. Only by additional studies will we understand more about the role of this intriguing molecule in the treatment of cardiovascular disease.

scholarly journals Nitric oxide synthase-mediated blood pressure regulation in obese melanocortin-4 receptor-deficient pregnant rats

2016 ◽  
Vol 311 (5) ◽  
pp. R851-R857 ◽  
Author(s):  
Frank T. Spradley ◽  
Jennifer M. Sasser ◽  
Jacqueline B. Musall ◽  
Jennifer C. Sullivan ◽  
Joey P. Granger
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Mesenteric Arteries ◽  
Elevated Blood Pressure ◽  
Pressure Regulation ◽  
Elevated Blood ◽  
Pregnant Rats ◽  
Melanocortin 4 Receptor ◽  
Regulation Of Blood Pressure

Although obesity increases the risk for hypertension in pregnancy, the mechanisms responsible are unknown. Increased nitric oxide (NO) production results in vasodilation and reduced blood pressure during normal pregnancy in lean rats; however, the role of NO is less clear during obese pregnancies. We examined the impact of obesity on NO synthase (NOS)-mediated regulation of blood pressure during pregnancy by testing the hypothesis that NOS activity, expression, and regulation of vascular tone and blood pressure are reduced in obese pregnant rats. At gestational day 19, melanocortin-4 receptor (MC4R)-deficient obese rats (MC4R) had greater body weight and fat mass with elevated blood pressure and circulating sFlt-1 levels compared with MC4R pregnant rats. MC4R pregnant rats also had less circulating cGMP levels and reduced total NOS enzymatic activity and expression in mesenteric arteries. Despite decreased biochemical measures of NO/NOS in MC4R rats, NOS inhibition enhanced vasoconstriction only in mesenteric arteries from MC4R rats, suggesting greater NOS-mediated tone. To examine the role of NOS on blood pressure regulation in obese pregnant rats, MC4R and MC4R pregnant rats were administered the nonselective NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME, 100 mg/l) from gestational day 14 to 19 in drinking water. The degree by which l-NAME raised blood pressure was similar between obese and lean pregnant rats. Although MC4R obese pregnant rats had elevated blood pressure associated with reduced total NOS activity and expression, they had enhanced NOS-mediated attenuation of vasoconstriction, with no evidence of alterations in NOS-mediated regulation of blood pressure.

Blood pressure regulation by ETA and ETB receptors in conscious, telemetry-instrumented mice and role of ETA in hypertension produced by selective ETB blockade

2006 ◽  
Vol 290 (6) ◽  
pp. H2554-H2559 ◽  
Author(s):  
Ryan M. Fryer ◽  
Pamela A. Rakestraw ◽  
Patricia N. Banfor ◽  
Bryan F. Cox ◽  
Terry J. Opgenorth ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Pressure Regulation ◽  
Pressure Regulation ◽  
Type B ◽  
Selective Antagonist ◽  
Relevant Role ◽  
Basal Blood Pressure ◽  
Baseline Values

The net contribution of endothelin type A (ETA) and type B (ETB) receptors in blood pressure regulation in humans and experimental animals, including the conscious mouse, remains undefined. Thus we assessed the role of ETA and ETB receptors in the control of basal blood pressure and also the role of ETA receptors in maintaining the hypertensive effects of systemic ETB blockade in telemetry-instrumented mice. Mean arterial pressure (MAP) and heart rate were recorded continuously from the carotid artery and daily (24 h) values determined. At baseline, MAP ranged from 99 ± 1 to 101 ± 1 mmHg and heart rate ranged between 547 ± 15 and 567 ± 19 beats/min ( n = 6). Daily oral administration of the ETB selective antagonist A-192621 [10 mg/kg twice daily] increased MAP to 108 ± 1 and 112 ± 2 mmHg on days 1 and 5, respectively. Subsequent coadministration of the ETA selective antagonist atrasentan (5 mg/kg twice daily) in conjunction with A-192621 (10 mg/kg twice daily) decreased MAP to baseline values on day 6 (99 ± 2 mmHg) and to below baseline on day 8 (89 ± 3 mmHg). In a separate group of mice ( n = 6) in which the treatment was reversed, systemic blockade of ETB receptors produced no hypertension in animals pretreated with atrasentan, underscoring the importance of ETA receptors to maintain the hypertension produced by ETB blockade. In a third group of mice ( n = 10), ETA blockade alone (atrasentan; 5 mg/kg twice daily) produced an immediate and sustained decrease in MAP to values below baseline (baseline values = 101 ± 2 to 103 ± 2 mmHg; atrasentan decreased pressure to 95 ± 2 mmHg). Thus these data suggest that ETA and ETB receptors play a physiologically relevant role in the regulation of basal blood pressure in normal, conscious mice. Furthermore, systemic ETB receptor blockade produces sustained hypertension in conscious telemetry-instrumented mice that is absent in mice pretreated with an ETA antagonist, suggesting that ETA receptors maintain the hypertension produced by ETB blockade.

scholarly journals SPIKE PROTEIN AND ITS PROTEASES ROLE IN SARS-COV-2 PATHOGENICITY AND TREATMENT; A REVIEW

2021 ◽  
Vol 64 (1) ◽  
Author(s):  
Fateme Tavakoli Far ◽  
◽  
Ehsan Amiri-Ardekani ◽  
Keyword(s):  
Blood Pressure ◽  
Severe Acute Respiratory Syndrome ◽  
Small Molecules ◽  
Cathepsin B ◽  
Host Cells ◽  
Spike Protein ◽  
Pressure Regulation ◽  
Common Receptor ◽  
The World

Since December 2019, a novel beta coronavirus has spread around the world. This virus can cause severe acute respiratory syndrome (SARS). In this study, we reviewed proteases of SARS-CoV-2 based on related articles published in journals indexed by Scopus, PubMed, and Google Scholar from December 2019 to April 2020. Based on this study, we can claim that this coronavirus has about 76% genotype similarity to SARS coronavirus (SARS-CoV). Also, similarities between these two viruses have been found in the mechanism of entry into host cells and pathogenicity. ACE 2, the angiotensin convertase enzyme 2, plays a role in the Renin-Angiotensin-Aldosterone system (RAAS) and blood pressure regulation. Some mechanisms have been reported for the role of ACE 2 in the pathogenicity of SARS-CoV-2. For example, the interaction between the ACE 2 receptor and spike protein mediated by TMPRSS2, Cathepsin B/L, and other enzymes is responsible for the entry of the virus into human cells and pathogenicity. Some host cell endosomal enzymes are necessary to cleavage coronavirus spike protein and cause binding to their common receptor. So, we conclude that molecules like antibodies or small molecules like ACE 2 antagonists and soluble ACE 2 can be used as a good therapeutic candidate to prevent SARS-CoV-2.

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