Do incremental increases in blood pressure elicit neointimal plaques through endothelial injury?

2004 ◽  
Vol 287 (6) ◽  
pp. R1486-R1493
Author(s):  
Ciro A. Ruiz-Feria ◽  
Yimu Yang ◽  
Hiroko Nishimura
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Pulse Wave ◽  
Balloon Catheter ◽  
Endothelial Injury ◽  
Lower Segment ◽  
Hemodynamic Forces ◽  
Prone Area ◽  
Propranolol Treatment ◽  
Balloon Catheter Injury

Fowl (males more than females) show maturation-dependent rises in blood pressure (BP) and formation of neointimal plaques (NPs), resembling balloon catheter injury-induced neointima, in the abdominal aorta (AbA) just above the bifurcation. The plaque comprises neointimal cells containing abundant endoplasmic reticulum and extracellular matrix. Hence, we investigated whether rapid incremental BP increases in male chicks trigger NP formation, possibly via endothelial injury in hemodynamically selective areas. In 6-wk-old chicks ( n = 8) treated 4 wk with solvent (Sv; minipump) or arginine supplement (Arg; 0.3% in drinking water), BP increased from 140 ± 5 to 159 ± 4 (Sv) and from 138 ± 4 to 157 ± 3 (Arg) mmHg, whereas propranolol treatment (Prop, 8 mg·kg−1·day−1; minipump) prevented the rise. Arg and Prop groups had, respectively, 73% and 77% smaller ( P < 0.05) NP areas and 19% and 25% less ( P < 0.01) AbA medial thickness than Sv controls. In 16-wk-old cockerels, established BP remained high after Sv and Arg treatments. In the Prop group, BP decreased, but neither NP area nor medial thickness was lower than in the Sv group, whereas the Arg group showed greater NP area and medial thickness. Pulse pressure, determined by intravascular transducer, increased as the pulse wave descended the aorta. The results suggest that maturation-dependent rises in BP in chicks may trigger NP formation in the lower segment of the AbA, which was prevented by inhibition of BP increase, or via a possible increase in nitric oxide availability. BP reduction exerts no effect once BP reaches a plateau. Involvement of endothelial injury leading to NP formation and hemodynamic forces selective for the lesion-prone area remain to be determined.

Secondhand tobacco smoke, arterial stiffness, and altered circadian blood pressure patterns are associated with lung inflammation and oxidative stress in rats

2012 ◽  
Vol 302 (3) ◽  
pp. H818-H825 ◽  
Author(s):  
Nicole J. Gentner ◽  
Lynn P. Weber
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Stiffness ◽  
Tobacco Smoke ◽  
Pulse Wave ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Secondhand Tobacco Smoke ◽  
Blood Pressure Patterns

Chronic smoking and secondhand tobacco smoke exposure are major risk factors for cardiovascular disease that are known to adversely alter the structural and mechanical properties of arteries. The objective of this study was to determine the effects of subchronic secondhand tobacco smoke exposure on circadian blood pressure patterns, arterial stiffness, and possible sources of oxidative stress in conscious, unsedated radiotelemetry-implanted rats. Pulse wave change in pressure over time (dP/d t) was used an indicator of arterial stiffness and was compared with both structural (wall thickness) and functional (nitric oxide production and bioactivity and endothelin-1 levels) features of the arterial wall. In addition, histology of lung, heart, and liver was examined as well as pulmonary and hepatic detoxifying enzyme activity (cytochrome P450, specifically CYP1A1). Subchronic secondhand tobacco smoke exposure altered the circadian pattern of heart rate and blood pressure, with a loss in the normal dipping pattern of blood pressure during sleep. Secondhand tobacco smoke exposure also increased pulse wave dP/d t in the absence of any structural modifications in the arterial wall. Furthermore, although nitric oxide production and endothelin-1 levels were not altered by secondhand tobacco smoke, there was increased inactivation of nitric oxide as indicated by peroxynitrite production. Increased lung neutrophils or pulmonary CYP1A1 may be responsible for the increase in oxidative stress in rats exposed to secondhand tobacco smoke. In turn, this may be related to the observed failure of blood pressure to dip during periods of sleep and a possible increase in arterial stiffness.

Using blood pressure telemetry to assess acute changes in arterial stiffness in rats after nitric oxide synthase inhibition or environmental tobacco smoke exposure

2010 ◽  
Vol 88 (9) ◽  
pp. 918-928 ◽  
Author(s):  
Nicole J. Gentner ◽  
Lynn P. Weber
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Stiffness ◽  
Environmental Tobacco Smoke ◽  
Tobacco Smoke ◽  
Pulse Wave ◽  
No Production ◽  
Arterial Pulse ◽  
Arterial Pulse Wave ◽  
Acute Changes

Although environmental tobacco smoke (ETS) exposure has been reported to acutely increase arterial stiffness in humans, understanding of the underlying mechanisms is unclear and few studies have measured these effects in experimental animals. One potential mechanism for the increased arterial stiffness is reduced nitric oxide (NO) bioactivity as a result of oxidative stress. Thus, the objective of this study was to determine whether acute changes in arterial stiffness could be detected using arterial pulse wave dP/dt in blood pressure telemetry implanted rats and to investigate the role of NO in regulating dP/dt. Intravenous injection of acetylcholine (0.91 ng/kg) decreased and norepinephrine (0.02 mg/kg) increased dP/dt compared to saline vehicle (0.5 mL/kg). Injection of the NO synthase inhibitor, NG-nitro-l-arginine methyl ester (L-NAME; 30 mg/kg) decreased plasma nitrate/nitrite (NOx), but transiently increased dP/dt. ETS at low and high doses had no effect on dP/dt, but increased plasma NOx levels at high ETS exposure and increased plasma nitrotyrosine levels in both ETS groups. In conclusion, acute changes in NO production via acetylcholine or L-NAME alter the arterial pulse wave dP/dt consistently with the predicted changes in arterial stiffness. Although acute ETS appears to biologically inactivate NO, a concomitant increase in NO production at high ETS exposure may explain why dP/dt was not acutely altered by ETS in the current study.

scholarly journals Blue light exposure decreases systolic blood pressure, arterial stiffness, and improves endothelial function in humans

2018 ◽  
Vol 25 (17) ◽  
pp. 1875-1883 ◽  
Author(s):  
Manuel Stern ◽  
Melanie Broja ◽  
Roberto Sansone ◽  
Michael Gröne ◽  
Simon S Skene ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Endothelial Function ◽  
Blue Light ◽  
Pulse Wave ◽  
Light Exposure ◽  
Nitroso Compounds ◽  
Whole Body ◽  
Flow Mediated Dilation ◽  
Forearm Vascular Resistance

Aims Previous studies have shown that ultraviolet light can lead to the release of nitric oxide from the skin and decrease blood pressure. In contrast to visible light the local application of ultraviolet light bears a cancerogenic risk. Here, we investigated whether whole body exposure to visible blue light can also decrease blood pressure and increase endothelial function in healthy subjects. Methods In a randomised crossover study, 14 healthy male subjects were exposed on 2 days to monochromatic blue light or blue light with a filter foil (control light) over 30 minutes. We measured blood pressure (primary endpoint), heart rate, forearm vascular resistance, forearm blood flow, endothelial function (flow-mediated dilation), pulse wave velocity and plasma nitric oxide species, nitrite and nitroso compounds (secondary endpoints) during and up to 2 hours after exposure. Results Blue light exposure significantly decreased systolic blood pressure and increased heart rate as compared to control. In parallel, blue light significantly increased forearm blood flow, flow-mediated dilation, circulating nitric oxide species and nitroso compounds while it decreased forearm vascular resistance and pulse wave velocity. Conclusion Whole body irradiation with visible blue light at real world doses improves blood pressure, endothelial function and arterial stiffness by nitric oxide released from photolabile intracutanous nitric oxide metabolites into circulating blood.

scholarly journals Tetrahydrobiopterin lowers muscle sympathetic nerve activity and improves augmentation index in patients with chronic kidney disease

2015 ◽  
Vol 308 (3) ◽  
pp. R208-R218 ◽  
Author(s):  
Jeanie Park ◽  
Peizhou Liao ◽  
Salman Sher ◽  
Robert H. Lyles ◽  
Don D. Deveaux ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Folic Acid ◽  
Sympathetic Nerve Activity ◽  
Pulse Wave ◽  
Augmentation Index ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
No Bioavailability

Chronic kidney disease (CKD) is characterized by overactivation of the sympathetic nervous system (SNS) that contributes to cardiovascular risk. Decreased nitric oxide (NO) bioavailability is a major factor contributing to SNS overactivity in CKD, since reduced neuronal NO leads to increased central SNS activity. Tetrahydrobiopterin (BH4) is an essential cofactor for nitric oxide synthase that increases NO bioavailability in experimental models of CKD. We conducted a randomized, double-blinded, placebo-controlled trial testing the benefits of oral sapropterin dihydrochloride (6R-BH4, a synthetic form of BH4) in CKD. 36 patients with CKD and hypertension were randomized to 12 wk of 1) 200 mg 6R-BH4 twice daily + 1 mg folic acid once daily; vs. 2) placebo + folic acid. The primary endpoint was a change in resting muscle sympathetic nerve activity (MSNA). Secondary endpoints included arterial stiffness using pulse wave velocity (PWV) and augmentation index (AIx), endothelial function using brachial artery flow-mediated dilation and endothelial progenitor cells, endothelium-independent vasodilatation (EID), microalbuminuria, and blood pressure. We observed a significant reduction in MSNA after 12 wk of 6R-BH4 (−7.5 ± 2.1 bursts/min vs. +3.2 ± 1.3 bursts/min; P = 0.003). We also observed a significant improvement in AIx (by −5.8 ± 2.0% vs. +1.8 ± 1.7 in the placebo group, P = 0.007). EID increased significantly (by +2.0 ± 0.59%; P = 0.004) in the 6R-BH4 group, but there was no change in endothelial function. There was a trend toward a reduction in diastolic blood pressure by −4 ± 3 mmHg at 12 wk with 6R-BH4 ( P = 0.055). 6R-BH4 treatment may have beneficial effects on SNS activity and central pulse wave reflections in hypertensive patients with CKD.

Effects of Neuroactive Amino Acids Derivatives on Cardiac and Cerebral Mitochondria and Endothelial functions in Animals Exposed to Stress

2017 ◽  
Vol 2 (2) ◽  
pp. 34
Author(s):  
TA Popova ◽  
II Prokofiev ◽  
IS Mokrousov ◽  
Valentina Perfilova ◽  
AV Borisov ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Platelet Aggregation ◽  
Atp Synthesis ◽  
Elevated Concentration ◽  
Blood Pressure Monitor ◽  
Pressure Monitor ◽  
Griess Reagent ◽  
Arterial Blood ◽  
Endothelial Functions

Introduction: To study the effects of glufimet, a new derivative of glutamic acid, and phenibut, a derivative of γ-aminobutyric acid (GABA), on cardiac and cerebral mitochondria and endothelial functions in animals following exposure to stress and inducible nitric oxide synthase (iNOS) inhibition. Methods: Rats suspended by their dorsal cervical skin fold for 24 hours served as the immobilization and pain stress model. Arterial blood pressure was determined using a non-invasive blood pressure monitor. Mitochondrial fraction of heart and brain homogenates were isolated by differential centrifugation and analysed for mitochondrial respiration intensity, lipid peroxidation (LPO) and antioxidant enzyme activity using polarographic method. The concentrations of nitric oxide (NO) terminal metabolites were measured using Griess reagent. Hemostasis indices were evaluated. Platelet aggregation was estimated using modified version of the Born method described by Gabbasov et al., 1989. Results: The present study demonstrated that stress leads to an elevated concentration of NO terminal metabolites and LPO products, decreased activity of antioxidant enzymes, reduced mitochondrial respiratory function, and endothelial dysfunction. Inhibition of iNOS by aminoguanidine had a protective effect. Phenibut and glufimet inhibited a rise in stress-induced nitric oxide production. This resulted in enhanced coupling of substrate peroxidation and ATP synthesis. The reduced LPO processes caused by glufimet and phenibut normalized the endothelial function which was proved by the absence of average daily blood pressure (BP) elevation episodes and a significant increase in platelet aggregation level. Conclusion: Glufimet and phenibut restrict the harmful effects of stress on the heart and brain possibly by modulating iNOS activity.

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