Calcium and the Production of Endothelium-Derived Vasoactive Factors

Author(s):  
V. B. Schini ◽  
T. Nagao ◽  
S. Illiano ◽  
P. M. Vanhoutte
Keyword(s):  
2006 ◽  
Vol 37 (03) ◽  
Author(s):  
R Trollmann ◽  
K Strasser ◽  
J Soliz ◽  
D Wenzel ◽  
W Rascher ◽  
...  

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 412-P
Author(s):  
PARESH DANDONA ◽  
HUSAM GHANIM ◽  
SCOTT MONTE ◽  
KELLY GREEN ◽  
JOSEPH A. CARUANA

Author(s):  
Husam Ghanim ◽  
Manav Batra ◽  
Kelly Green ◽  
Jeanne Hejna ◽  
Sanaa Abuaysheh ◽  
...  

1995 ◽  
Vol 268 (3) ◽  
pp. H1077-H1085 ◽  
Author(s):  
H. Mori ◽  
M. Chujo ◽  
E. Tanaka ◽  
A. Yamakawa ◽  
Y. Shinozaki ◽  
...  

We examined humoral and/or locally produced vasoactive factors involved in modulating sympathetic coronary vasoconstriction via the ATP-sensitive K (KATP) channel in 42 anesthetized dogs. Glibenclamide (30 micrograms.kg-1.min-1 ic or 0.6 mg.kg-1.min-1 left atrial injection) augmented coronary vascular resistance (CVR) at baseline and during cardiac sympathetic nerve stimulation (2-20 Hz), with a greater increase seen in the subepicardial region than in the subendocardial region both during beta-adrenergic receptor blockade and alpha- and beta-receptor blockade [P < 0.05 and P < 0.05 (n = 6 and 18 dogs), analysis of variance]. In contrast, pinacidil (10 micrograms.kg-1.min-1; n = 8 dogs) suppressed CVR. Glibenclamide enhanced CVR response to locally administered norepinephrine of 0.001–0.1 microgram.kg-1.min-1 (P < 0.05, analysis of covariance; n = 5 dogs) but did not enhance norepinephrine or neuropeptide Y overflow (n = 18 dogs). CVR was not modified by calcitonin gene-related peptide (CGRP) antagonist [CGRP-(8–37)], 8-phenyltheophylline, or N omega-nitro-L-arginine (n = 11 dogs). Thus sympathetic coronary vasoconstriction is modified by coronary vascular KATP channels with a transmural difference. However, CGRP, adenosine, and endothelial nitric oxide production are not involved in the modulation.


1998 ◽  
Vol 78 (1) ◽  
pp. 53-97 ◽  
Author(s):  
FRANK M. FARACI ◽  
DONALD D. HEISTAD

Faraci, Frank M., and Donald D. Heistad. Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels. Physiol. Rev. 78: 53–97, 1998. — Several new concepts have emerged in relation to mechanisms that contribute to regulation of the cerebral circulation. This review focuses on some physiological mechanisms of cerebral vasodilatation and alteration of these mechanisms by disease states. One mechanism involves release of vasoactive factors by the endothelium that affect underlying vascular muscle. These factors include endothelium-derived relaxing factor (nitric oxide), prostacyclin, and endothelium-derived hyperpolarizing factor(s). The normal vasodilator influence of endothelium is impaired by some disease states. Under pathophysiological conditions, endothelium may produce potent contracting factors such as endothelin. Another major mechanism of regulation of cerebral vascular tone relates to potassium channels. Activation of potassium channels appears to mediate relaxation of cerebral vessels to diverse stimuli including receptor-mediated agonists, intracellular second messengers, and hypoxia. Endothelial- and potassium channel-based mechanisms are related because several endothelium-derived factors produce relaxation by activation of potassium channels. The influence of potassium channels may be altered by disease states including chronic hypertension, subarachnoid hemorrhage, and diabetes.


Medicina ◽  
2021 ◽  
Vol 57 (9) ◽  
pp. 884
Author(s):  
Kenneth P. van Knegsel ◽  
Bergita Ganse ◽  
Pascal C. Haefeli ◽  
Filippo Migliorini ◽  
Mario F. Scaglioni ◽  
...  

Background and Objectives: Wound infections provoked by alterations in microcirculation are major complications in the treatment of trochanteric femur fractures. Surgical fracture fixation on a traction table is the gold standard for treatment, but the effect on tissue microcirculation is unknown. Microcirculation could be impaired by the pull on the soft-tissue or by a release of vasoactive factors. We hypothesized that intraoperative traction impairs soft-tissue microcirculation. Materials and Methods: In 22 patients (14 women, eight men), average age 78 years (range 36–96 ± 14), with trochanteric femur fractures, non-invasive laser-Doppler spectrophotometry was used to assess oxygen saturation, hemoglobin content, and blood flow in the skin and subcutaneous tissue before and after application of traction. Measurements were recorded in nine locations around the greater trochanter at a depth of 2, 8, and 15 mm before and after fracture reduction by traction. Results: No differences were found in any depth with traction compared to without (oxygen saturation: p = 0.751, p = 0.308, and p = 0.955, haemoglobin content: p = 0.651, p = 0.928, and p = 0.926, blood flow: p = 0.829, p = 0.866, and p = 0.411). Conclusion: In this pilot study, the application of traction does not affect skin and subcutaneous microcirculation in the surgery of proximal femur fractures.


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