scholarly journals β1-Adrenoceptor stimulation suppresses endothelial IKCa-channel hyperpolarization and associated dilatation in resistance arteries

2013 ◽  
Vol 169 (4) ◽  
pp. 875-886 ◽  
Author(s):  
PL Yarova ◽  
SV Smirnov ◽  
KA Dora ◽  
CJ Garland
Keyword(s):  
Resistance Arteries ◽  
Ikca Channel

Targeting the Endothelial Ca2+ Toolkit to Rescue Endothelial Dysfunction in Obesity Associated-Hypertension

2020 ◽  
Vol 27 (2) ◽  
pp. 240-257 ◽  
Author(s):  
Francesco Moccia ◽  
Sharon Negri ◽  
Pawan Faris ◽  
Roberto Berra-Romani
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Endothelial Damage ◽  
Vascular Damage ◽  
Zucker Rats ◽  
Bibliographic Databases ◽  
Resistance Arteries ◽  
Small Resistance ◽  
Obese Zucker Rats ◽  
Transient Receptor

Background: Obesity is a major cardiovascular risk factor which dramatically impairs endothelium- dependent vasodilation and leads to hypertension and vascular damage. The impairment of the vasomotor response to extracellular autacoids, e.g., acetylcholine, mainly depends on the reduced Nitric Oxide (NO) bioavailability, which hampers vasorelaxation in large conduit arteries. In addition, obesity may affect Endothelium-Dependent Hyperpolarization (EDH), which drives vasorelaxation in small resistance arteries and arterioles. Of note, endothelial Ca2+ signals drive NO release and trigger EDH. Methods: A structured search of bibliographic databases was carried out to retrieve the most influential, recent articles on the impairment of vasorelaxation in animal models of obesity, including obese Zucker rats, and on the remodeling of the endothelial Ca2+ toolkit under conditions that mimic obesity. Furthermore, we searched for articles discussing how dietary manipulation could be exploited to rescue Ca2+-dependent vasodilation. Results: We found evidence that the endothelial Ca2+ could be severely affected by obese vessels. This rearrangement could contribute to endothelial damage and is likely to be involved in the disruption of vasorelaxant mechanisms. However, several Ca2+-permeable channels, including Vanilloid Transient Receptor Potential (TRPV) 1, 3 and 4 could be stimulated by several food components to stimulate vasorelaxation in obese individuals. Conclusion: The endothelial Ca2+ toolkit could be targeted to reduce vascular damage and rescue endothelium- dependent vasodilation in obese vessels. This hypothesis remains, however, to be probed on truly obese endothelial cells.

Testosterone Induces Dilation of Canine Coronary Conductance and Resistance Arteries In Vivo

Circulation ◽  
1996 ◽  
Vol 94 (10) ◽  
pp. 2614-2619 ◽  
Author(s):  
Tony M. Chou ◽  
Krishnankutty Sudhir ◽  
Stuart J. Hutchison ◽  
Eitetsu Ko ◽  
Thomas M. Amidon ◽  
...  
Keyword(s):  
Resistance Arteries ◽  
Coronary Conductance

Benidipine Improves Endothelial Function in Renal Resistance Arteries of Hypertensive Rats

Hypertension ◽  
1996 ◽  
Vol 28 (1) ◽  
pp. 58-63 ◽  
Author(s):  
Yasuaki Dohi ◽  
Masayoshi Kojima ◽  
Koichi Sato
Keyword(s):  
Endothelial Function ◽  
Resistance Arteries ◽  
Hypertensive Rats

Abnormalities of the lymphatic system and impaired fluid clearance in patients with heart failure with preserved ejection fraction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
G Rossitto ◽  
S Mary ◽  
C McAllister ◽  
K.B Neves ◽  
L Haddow ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Blood Vessels ◽  
Lymphatic System ◽  
Filtration Coefficient ◽  
Funding Source ◽  
Preserved Ejection Fraction ◽  
Resistance Arteries ◽  
Fluid Extravasation ◽  
Capillary Fluid

Abstract Background Coronary and skeletal muscle microvascular dysfunction have been proposed as main factors in the pathogenesis of Heart Failure with Preserved Ejection Fraction (HFpEF). However, assessment of systemic arterial function has only been indirect thus far; most importantly, no direct link between systemic microvasculature and congestion, one of the core characteristics of the syndrome, has yet been investigated. Purpose To provide direct functional and anatomical characterisation of the systemic microvasculature and to explore in vivo parameters of capillary fluid extravasation and lymphatic clearance in HFpEF. Methods In 16 patients with HFpEF and 16 age- and sex-matched healthy controls (72±6 and 68±5 years, respectively) we determined peripheral microvascular filtration coefficient (proportional to vascular permeability and area) and isovolumetric pressure (above which lymphatic drainage cannot compensate for fluid extravasation) by venous occlusion plethysmography and collected a skin biopsy for vascular immunohistochemistry and gene expression analysis (TaqMan). Additionally, we measured brachial flow-mediated dilatation (FMD) and assessed by wire myography the vascular function of resistance arteries isolated from gluteal subcutaneous fat biopsies. Results Skin biopsies in patients with HFpEF showed rarefaction of small blood vessels (82±31 vs 112±21 vessels/mm2; p=0.003) and in ex-vivo analysis (n=6/group) we found defective relaxation of peripheral resistance arteries (p<0.001). Accordingly, post-ischaemic hyperaemic response (fold-change vs baseline, 4.6±1.6 vs 6.7±1.7; p=0.002) and FMD (3.9±2.1 vs 5.6±1.5%; p=0.014) were found to be reduced in patients with HFpEF compared to controls. In the skin of patients with HFpEF we also observed a reduced number (85±27 vs 130±60 vessels/mm2; p=0.012) but larger average diameter of lymphatic vessels (42±19 vs 26±9 μm2; p=0.007) compared to control subjects. These changes were paralleled by reduced expression of LYVE1 (p<0.05) and PROX1 (p<0.001), key determinants of lymphatic differentiation and function. Whilst patients with HFpEF had reduced peripheral capillary fluid extravasation compared to controls (microvascular filtration coefficient, leg 33.1±13.3 vs 48.4±15.2, p<0.01; trend for arm 49.9±20.5 vs 66.3±30.1, p=0.09), they had lower lymphatic clearance (isovolumetric pressure: leg 22±4 vs 16±4 mmHg, p<0.005; arm 25±5 vs 17±4 mmHg, p<0.001). Conclusions We provide direct evidence of systemic dysfunction and rarefaction of small blood vessels in patients with HFpEF. Despite a reduced microvascular filtration coefficient, which is in keeping with microvascular rarefaction, the clearance of extravasated fluid in HFpEF is limited by an anatomically and functionally defective lymphatic system. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): British Heart Foundation Centre of Research Excellence Award

scholarly journals SP284BETA-TRACE PROTEIN CORRELATES WITH ENDOTHELIAL FUNCTION IN PERIPHERAL RESISTANCE ARTERIES IN END STAGE RENAL DISEASE

2017 ◽  
Vol 32 (suppl_3) ◽  
pp. iii202-iii202
Author(s):  
Samsul Arefin ◽  
Amaryllis Van Craenenbroeck ◽  
Neja Mudrovcic ◽  
Ann-Christin Bragfors-Helin ◽  
Peter Stenvinkel ◽  
...  
Keyword(s):  
Renal Disease ◽  
Endothelial Function ◽  
End Stage Renal Disease ◽  
Peripheral Resistance ◽  
Resistance Arteries ◽  
Stage Renal Disease ◽  
End Stage
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