scholarly journals SP082THE ROLE OF SODIUM HYDROSULFIDE ON HYDROGEN SULFIDE GENERATING PATHWAY, NITRIC OXIDE PATHWAY, AND RENIN ANGIOTENSIN SYSTEM IN SPONTANEOUSLY HYPERTENSIVE RATS

2016 ◽  
Vol 31 (suppl_1) ◽  
pp. i113-i113
Author(s):  
You-Lin Tain ◽  
Chien-Ning Hsu
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Hypertensive Rats ◽  
Sodium Hydrosulfide ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Nitric Oxide Pathway

Role of renin–angiotensin system and oxidative status on the maternal cardiovascular regulation in spontaneously hypertensive rats

2012 ◽  
Vol 25 (4) ◽  
pp. 498-504 ◽  
Author(s):  
Dayane T. Ognibene ◽  
Lenize C.R.M. Carvalho ◽  
Cristiane A. Costa ◽  
Ana Paula M. Rocha ◽  
Roberto S. de Moura ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Cardiovascular Regulation ◽  
Oxidative Status ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin

scholarly journals The Impact of Four Different Classes of Anesthetics on the Mechanisms of Blood Pressure Regulation in Normotensive and Spontaneously Hypertensive Rats

2013 ◽  
pp. 471-478 ◽  
Author(s):  
M. BENCZE ◽  
M. BEHULIAK ◽  
J. ZICHA
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
No Synthase ◽  
Hypertensive Rats ◽  
Major Drawback ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
The Impact

Most anesthetics induce characteristic hemodynamic changes leading to blood pressure (BP) reduction but the role of renin-angiotensin system (RAS), sympathetic nervous system (SNS) and nitric oxide (NO) synthesis in this BP reduction is unknown. We therefore studied the influence of four widely used anesthetics – pentobarbital (P), isoflurane (ISO), ketamine-xylazine (KX) and chloralose-urethane (CU) – on the participation of these vasoactive systems in BP maintenance. BP effects elicited by the acute sequential blockade of RAS (captopril), SNS (pentolinium) and NO synthase (L-NAME) were compared in conscious and anesthetized Wistar or spontaneously hypertensive rats (SHR). Except for pentobarbital all studied anesthetics evidenced by diminished BP responses to pentolinium. The absolute pentolinium-induced BP changes were always greater in SHR than Wistar rats. KX anesthesia eliminated BP response to pentolinium and considerably enhanced BP response to NO synthase inhibition in SHR. In both rat strains the anesthesia with ISO or CU augmented BP response to captopril, decreased BP response to pentolinium and attenuated BP response to NO synthase inhibition. In conclusion, pentobarbital anesthesia had a modest influence on BP level and its maintenance by the above vasoactive systems. Isoflurane and chloralose-urethane anesthesia may be used in cardiovascular experiments if substantial BP decrease due to altered contribution of RAS, SNS and NO to BP regulation does not interfere with the respective research aim. Major BP reduction (namely in SHR) due to a complete SNS absence is a major drawback of ketamine-xylazine anesthesia.

AHU377+Valsartan (LCZ696) Modulates Renin–Angiotensin System (RAS) in the Cardiac of Female Spontaneously Hypertensive Rats Compared With Valsartan

2019 ◽  
Vol 24 (5) ◽  
pp. 450-459 ◽  
Author(s):  
Yang Zhao ◽  
Ruixin Ma ◽  
Xiaorong Yu ◽  
Ningyin Li ◽  
Xu Zhao ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Mrna Expression ◽  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Oxide Synthase

Background: Hypertension is a major cause of death and morbidity worldwide and is increasing in prevalence. The Renin–angiotensin system (RAS) is the most common mechanism involved in the pathophysiology of hypertension. Understanding the mechanism of the pathophysiologic processes will help direct potential therapeutic strategies to treat hypertension and improve cardiac function. Recently, a novel drug LCZ696 containing both an angiotensin receptor blocker valsartan and a neprilysin inhibitor (AHU377) has shown a promising effect on the treatment of hypertension. However, the effects of LCZ696 on the expression of main components of RAS, namely, angiotensin-converting enzyme (ACE), angiotensin-converting enzyme 2 (ACE2), angiotensin II type 1 receptor (AT1 R), angiotensin II type 2 receptor (AT2 R), and angiotensin (1-7) receptor/Mas receptor (MasR) remain unclear. The aim of the present study was to evaluate the effects of LCZ696 on the protective arms of RAS in the cardiac tissue when compared with valsartan under the equal inhibition of AT1 R. We hypothesized that the superior effects of LCZ696 may contribute to its greater effect on the RAS than valsartan. Materials and Methods: Sixteen-week-old female spontaneously hypertensive rats (SHRs) were used in this study. Wistar-Kyoto (WKY) rats were used as controls. All rats were randomly divided into LCZ696 (n = 10), valsartan (n = 10), SHR (n = 10), and WKY (n = 10) groups under a 12-hour dark and 12-hour light cycle and provided with regular chow diet and water. The tail-cuff method was performed to measure blood pressure. Cardiac function was assessed by echocardiography. Results: The blood pressure value was lower in LCZ696 than valsartan in SHR after 12 weeks of treatment. Further, LCZ696 inhibits the ACE and AT1 R protein expression in the cardiac of SHR and significantly upregulate the protective axis of RAS components, including ACE2, MasR, and AT2 R. Left ventricular AT2 R messenger RNA (mRNA) expression was higher in the LCZ696+SHR group compared with valsartan. In addition, real-time polymerase chain reaction analysis revealed that LCZ696 enhanced the mRNA expression of antihypertensive components AT2 R, ACE2, and MasR and decreased the expression of AT1 R. However, only AT2 R and ACE2 mRNA expressions have a statistical difference between the LCZ696 and valsartan groups. No difference was observed in the mRNA expression of ACE and MasR. The stronger positive signal of transforming growth factor β in the left ventricle was inhibited in each administrated group compared with SHR groups. Conclusions: LCZ696 ameliorates the vasoconstrictor axis of the RAS AT1 R and stimulate the protective arm effectors, ACE2 and AT2 R, as well as reverses the compensatory upregulation of neuronal nitric oxide synthase and endothelial nitric oxide synthase in SHR. These findings suggest the mechanistic insight of the cardiac-protective and greater hypotensive effects of LCZ696.

Oryeongsan (Wulingsan) Ameliorates Impaired ANP Secretion of Atria from Spontaneously Hypertensive Rats

2021 ◽  
Author(s):  
Hye Yoom Kim ◽  
You Mee Ahn ◽  
Se Won Na ◽  
Youn Jae Jang ◽  
Dae Gill Kang ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renin Angiotensin System ◽  
Positive Control ◽  
Receptor Expression ◽  
Hypertensive Rats ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Mas Receptor ◽  
Channel Expression

Abstract Background: Oryeongsan (ORS), a herbal medicine formula, has long been used for the treatment of impaired body water balance in Asian countries. Recently, it was shown that ORS modulates the renin-angiotensin system (RAS). Purpose of the present study was to determine characteristics of atrial ANP secretion and effects of ORS on the secretion in the atria from spontaneously hypertensive rats (SHR). Methods: WKY-V treated with vehicle, SHR groups treated with vehicle (SHR-V), ORS (SHR-ORS), and losartan as a positive control (SHR-LOS). Experiments were performed in perfused beating atria (1.3 Hz) allowing atrial distension, acetylcholine (ACh) stimulation, and serial collection of atrial perfusates. The secreted ANP concentration was measured using radioimmunoassay. Interstitial fluid (ISF) translocation was measured using [3H]inulin clearance. Results: Stepwise increase in atrial distension by 1.1, 2.0, and 2.7 cmH2O above basal distension further increased ANP secretion proportionally in the atria from WKY-V, but the response was significantly suppressed in the atria from SHR-V. Cardiomyocyte ANP release, the first step of atrial ANP secretion, was suppressed in the atria from SHR-V compared to those from WKY-V (-8.02 ± 2.86, -15.86 ± 2.27, and -20.09 ± 3.62%; n = 8, vs. 8.59 ± 2.81, 15.65 ± 7.14, and 38.12 ± 8.28%; n = 8; p < 0.001 for all stepwise distension, respectively). Subacute treatment with ORS reversed the suppressed ANP release in atria from SHR-ORS (6.76 ± 3.92, 9.12 ± 2.85, and 28.79 ± 1.79% for SHR-ORS; n = 5 vs. SHR-V; n = 8; p = 0.01, p < 0.001, p < 0.001, respectively). The effects of ORS were comparable to those of losartan. ISF translocation was not significantly different between groups except SHR-V. ACh-induced ANP secretion and cardiomyocyte ANP release were also suppressed in the atria from SHR-V and ORS reversed the suppression. These findings were accompanied with accentuation of the AT1 receptor expression and suppression of the AT2/Mas receptor, M2 mACh receptor and GIRK4 expression in the atria from SHR-V. Further, treatment with ORS or losartan reversed the expressions. Conclusions: These results show that ANP secretion is suppressed in the atria from SHR in association with accentuation of AT1 receptor and suppression of AT2/Mas receptor and KACh channel expression. ORS ameliorates impaired ANP secretion through improving cardiomyocyte ANP release with modulation of the cardiac RAS and muscarinic signaling. These findings provide experimental evidence which supports the role of ORS in the regulation of atrial ANP secretion in the atria from SHR.

Upregulation of platelet L-arginine – nitric oxide pathway after exercise training in hypertension

2012 ◽  
Vol 90 (4) ◽  
pp. 501-505 ◽  
Author(s):  
Cristiane Matsuura ◽  
Tatiana M.C. Brunini ◽  
Wanda V. Mury ◽  
Angelica B. Garcia-Pinto ◽  
Jorge J. Carvalho ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Protein Levels ◽  
Wistar Kyoto ◽  
Oxide Synthase ◽  
Enos Protein ◽  
Nitric Oxide Pathway

We investigated whether physical exercise can affect platelet L-arginine – nitric oxide pathway in spontaneously hypertensive rats (SHR). Sixteen male SHR and 16 Wistar Kyoto rats (WKY) were divided among exercise (EX) and sedentary (SED) groups. After 20 weeks of treadmill training, systolic blood pressure (mm Hg) was significantly lower in exercised spontaneously hypertensive rats (SHR/EX; 138 ± 8) than in sedentary spontaneously hypertensive rats (SHR/SED; 214 ± 9). Exercise significantly increased platelet L-arginine transport (pmol L-arginine·(109 cells)–1·min–1), assessed by incubation with L-[3H]-arginine, in both WKY (SED, 0.196 ± 0.054 compared with EX, 0.531 ± 0.052) and SHR (SED, 0.346 ± 0.076 compared with EX, 0.600 ± 0.049). Nitric oxide synthase (NOS) activity (pmol L-citrulline·(108 cells)–1), measured by the conversion of L-[3H]-arginine to L-[3H]-citrulline, was significantly increased in SHR/EX (0.072 ± 0.007) compared with SHR/SED (0.038 ± 0.007), but no changes were observed in WKY. The iNOS and eNOS protein levels assessed by Western blot were not affected by exercise. This upregulation of the platelet L-arginine–NO pathway may attenuate the risk of thromboembolic events, supporting the role of exercise in hypertension management.

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