scholarly journals Acute inhibition of PMCA4, but not global ablation, reduces blood pressure and arterial contractility via a nNOS-dependent mechanism

2017 ◽  
Author(s):  
Sophronia Lewis ◽  
Robert Little ◽  
Florence Baudoin ◽  
Sukhpal Prehar ◽  
Ludwig Neyses ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Contractility ◽  
Dependent Mechanism

scholarly journals Blood pressure response to angiotensin II is enhanced in obese Zucker rats and is attributed to an aldosterone-dependent mechanism

2012 ◽  
Vol 166 (8) ◽  
pp. 2417-2429 ◽  
Author(s):  
Helge Müller-Fielitz ◽  
Margot Lau ◽  
Olaf Jöhren ◽  
Florian Stellmacher ◽  
Markus Schwaninger ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Pressure Response ◽  
Pressure Response ◽  
Zucker Rats ◽  
Obese Zucker Rats ◽  
Dependent Mechanism

scholarly journals Intermittent Hypoxia Increases Arterial Blood Pressure in Humans Through a Renin-Angiotensin System-Dependent Mechanism

Hypertension ◽  
2010 ◽  
Vol 56 (3) ◽  
pp. 369-377 ◽  
Author(s):  
Glen E. Foster ◽  
Patrick J. Hanly ◽  
Sofia B. Ahmed ◽  
Andrew E. Beaudin ◽  
Vincent Pialoux ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Intermittent Hypoxia ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Dependent Mechanism

Arginase inhibition slows the progression of renal failure in rats with renal ablation

2003 ◽  
Vol 284 (4) ◽  
pp. F680-F687 ◽  
Author(s):  
Massimo Sabbatini ◽  
Antonio Pisani ◽  
Francesco Uccello ◽  
Giorgio Fuiano ◽  
Raffaele Alfieri ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Renal Failure ◽  
Filtration Rate ◽  
Arginase Activity ◽  
Glomerular Sclerosis ◽  
Renal Ablation ◽  
Progression Of Renal Failure ◽  
Metabolic Data ◽  
Dependent Mechanism

Exogenous arginine slows the progression of chronic renal failure (CRF) in remnant rats through a nitric oxide (NO)-dependent mechanism. We tested whether the inhibition of arginase could induce similar results through the increased availability of endogenous arginine. Three groups of remnant rats were studied for 8 wk: 1) untreated rats (REM); 2) remnant rats treated with 1% l-arginine (ARG); and 3) remnant rats administered a Mn2+-free diet to inhibit arginase (MNF). Normal rats (NOR) were used as controls. Liver arginase activity was depressed in MNF rats (−35% vs. REM, P < 0.01). No difference in metabolic data was detected among the groups throughout the study; blood pressure was significantly lower in MNF vs. ARG and REM rats after 6 wk ( P < 0.001). The glomerular filtration rate (GFR) was greatly depressed in REM rats (−47% vs. NOR, P < 0.03) but was higher in ARG and MNF rats (+40 and +43% vs. REM, respectively, P < 0.05), with comparable changes in renal hemodynamics. Despite the better GFR, proteinuria was decreased in both ARG and MNF rats (−42%, P < 0.05, and −57%, P < 0.01, respectively, vs. REM rats). Arginine plasma levels, significantly reduced in REM rats (−41% vs. NOR, P < 0.01), were partially restored in MNF rats (+38% vs. REM), and urinary nitrite excretion, greatly depressed in REM rats (−76% vs. NOR, P < 0.01), was significantly increased in MNF rats (+209% vs. REM, P < 0.05). At the renal level, arginase activity was only slightly depressed in MNF rats (−18% vs. REM), but intrarenal concentrations of arginine were lower in this latter group ( P < 0.05 vs. other groups). Beyond the hemodynamic modifications, MNF rats showed a lower glomerular sclerosis index ( P < 0.05 vs. REM and ARG). Inhibition of arginase slows the progression of CRF in remnant rats similarly to arginine-treated rats; the better histological protection in MNF rats, however, suggests that additional factors are involved in these modifications.

scholarly journals Sympathetic baroreflex gain in normotensive pregnant women

2015 ◽  
Vol 119 (5) ◽  
pp. 468-474 ◽  
Author(s):  
Charlotte W. Usselman ◽  
Rachel J. Skow ◽  
Brittany A. Matenchuk ◽  
Radha S. Chari ◽  
Colleen G. Julian ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Pregnant Women ◽  
Sympathetic Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Sequence Method ◽  
Normotensive Pregnancy ◽  
Dependent Mechanism

Muscle sympathetic nerve activity is increased during normotensive pregnancy while mean arterial pressure is maintained or reduced, suggesting baroreflex resetting. We hypothesized spontaneous sympathetic baroreflex gain would be reduced in normotensive pregnant women relative to nonpregnant matched controls. Integrated muscle sympathetic burst incidence and total sympathetic activity (microneurography), blood pressure (Finometer), and R-R interval (ECG) were assessed at rest in 11 pregnant women (33 ± 1 wk gestation, 31 ± 1 yr, prepregnancy BMI: 23.5 ± 0.9 kg/m2) and 11 nonpregnant controls (29 ± 1 yr; BMI: 25.2 ± 1.7 kg/m2). Pregnant women had elevated baseline sympathetic burst incidence (43 ± 2 vs. 33 ± 2 bursts/100 heart beats, P = 0.01) and total sympathetic activity (1,811 ± 148 vs. 1,140 ± 55 au, P < 0.01) relative to controls. Both mean (88 ± 3 vs. 91 ± 2 mmHg, P = 0.4) and diastolic (DBP) (72 ± 3 vs. 73 ± 2 mmHg, P = 0.7) pressures were similar between pregnant and nonpregnant women, respectively, indicating an upward resetting of the baroreflex set point with pregnancy. Baroreflex gain, calculated as the linear relationship between sympathetic burst incidence and DBP, was reduced in pregnant women relative to controls (−3.7 ± 0.5 vs. −5.4 ± 0.5 bursts·100 heart beats−1·mmHg−1, P = 0.03), as was baroreflex gain calculated with total sympathetic activity (−294 ± 24 vs. −210 ± 24 au·100 heart beats−1·mmHg−1; P = 0.03). Cardiovagal baroreflex gain (sequence method) was not different between nonpregnant controls and pregnant women (49 ± 8 vs. 36 ± 8 ms/mmHg; P = 0.2). However, sympathetic (burst incidence) and cardiovagal gains were negatively correlated in pregnant women ( R = −0.7; P = 0.02). Together, these data indicate that the influence of the sympathetic nervous system over arterial blood pressure is reduced in normotensive pregnancy, in terms of both long-term and beat-to-beat regulation of arterial pressure, likely through a baroreceptor-dependent mechanism.

C5a-induced myocardial ischemia: role for CD18-dependent PMN localization and PMN-platelet interactions

1993 ◽  
Vol 265 (5) ◽  
pp. H1750-H1761 ◽  
Author(s):  
M. P. Fletcher ◽  
G. L. Stahl ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Myocardial Ischemia ◽  
Myocardial Segment ◽  
Artery Blood Flow ◽  
Arterial Blood ◽  
Pmn Functions ◽  
Dependent Mechanism

Intracoronary C5a in swine decreases coronary blood flow and regional myocardial segment shortening, responses mediated by thromboxane (Tx) A2-induced coronary vasoconstriction and intramyocardial trapping of granulocytes (PMNs). We sought to determine the origin of TxA2 and to investigate the role of CD18-dependent PMN function by utilizing an anti-CD18 monoclonal antibody, IB4. Isolated C5a-stimulated PMNs or platelets did not produce TxB2. However, together, C5a-stimulated PMNs and platelets produced TxB2. IB4 bound porcine PMN surface CD18 and blocked C5a-induced PMN functions. In vivo, IB4 loading (2 mg/kg) transiently decreased arterial blood pressure and circulating platelet counts in six of nine animals (390 +/- 31 vs. 176 +/- 41 X 10(6)/ml, control vs. IB4; P < 0.002) and significantly ameliorated C5a-induced decreases in coronary venous PMN count (-4.1 +/- 0.6 vs. -1.4 +/- 0.8 X 10(6) cells/ml), coronary artery blood flow (-10 +/- 1 vs. -4 +/- 1 ml/min), and segment shortening (-15 +/- 2 vs. -8 +/- 2%, C5a vs. C5a + IB4). We conclude that 1) production of TxB2 in response to C5a is mediated by a PMN-platelet interaction, 2) IB4 functionally blocks CD18 on porcine PMNs, and 3) C5a-induced myocardial PMN extraction is mediated, in part, by a CD18-dependent mechanism. These results suggest that PMN-platelet interactions and CD18-dependent PMN extraction are important in C5a-induced myocardial ischemia.

Abstract 203: Angiotensin II Induced ER Stress in the Heart is Attenuated by Exercise

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Gustavo S Masson ◽  
Anand R. Nair ◽  
Mary E White ◽  
Deepmala Agarwal ◽  
Lisete C Michelini ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Er Stress ◽  
Male Rats ◽  
Rt Pcr ◽  
Protein Expression Pattern ◽  
Baseline Blood Pressure ◽  
Cardiac Functions ◽  
Pathophysiological Role ◽  
Dependent Mechanism

Recent evidence indicates that endoplasmic reticulum (ER) stress plays an important pathophysiological role in a number of chronic diseases including cardiovascular disease. In this study, we demonstrate that ANGII-induced ER stress in the heart is attenuated by exercise. Methods: Male rats were implanted with telemetry probes and trained to do exercise. After collecting baseline blood pressure, hypertension was induced by implanting osmotic minipumps containing ANGII 200ng/kg/min for 42 days or saline. Rats were randomized into sedentary (SED) or exercise trained (ExT). BP and cardiac functions were measured by radiotelemetry and echocardiography. At the end of the study, heart tissues were analyzed for ER stress and hypertrophy markers by real time RT-PCR and Western blotting. Results: are tabulated. The protein expression pattern for Grp78 and CHOP were similar to mRNA. Conclusions: 1. ANGII infusion induces ER stress in the heart and contributes to cardiac hypertrophy. 2. EXT attenuates hypertensive response, cardiac hypertrophy and ER stress. 3. ER stress and ROS dependent mechanism contribute to ANGII induced cardiac hypertrophy and contribute to the development of hypertension.

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