scholarly journals Impaired Regulation of Vascular Tone by Endothelial Cells in Atherosclerosis

1997 ◽  
Vol 24 (9) ◽  
pp. 443-448
Author(s):  
Ken-ichi HIRATA ◽  
Seinosuke KAWASHIMA ◽  
Mitsuhiro YOKOYAMA
Keyword(s):  
Endothelial Cells ◽  
Vascular Tone ◽  
Regulation Of Vascular Tone

scholarly journals L-Arginine/Nitric Oxide Pathway and KCa Channels in Endothelial Cells: A Mini-Review

2020 ◽  
Author(s):  
Marcelo González ◽  
José Carlos Rivas
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Function ◽  
Vascular Tone ◽  
Molecular Mechanisms ◽  
Cardiovascular Health ◽  
Kca Channels ◽  
Subsequent Activation ◽  
Regulation Of Vascular Tone

The endothelium is an organ with a key role in the maintenance of cardiovascular health through the regulation of vascular tone, vascular resistance, blood flow, and arterial pressure. These functions are related with the synthesis and release of vasoactive molecules, mainly vasodilators like nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). Both factors are released and diffused from endothelial cells to the smooth muscle cells, where there is a subsequent activation of signaling pathways that finally decrease the intracellular calcium to induce the vascular relaxation. The study of the molecular mechanisms that underlie the endothelial function still is in development, but from the evidence obtained from the endothelial cells in vitro studies are possible to partially describe the pathways to regulate the physiological endothelial function and the disturbances in pathological conditions. In this mini-review, we describe the main mechanisms for NO synthesis and the role of potassium channels related with EDHF. We include schemes and graphical summaries for better understanding of the molecular regulation of vascular tone in the human cardiovascular system.

scholarly journals Can Endothelial Glycocalyx Be A Major Morphological Substrate in Pre-Eclampsia?

2020 ◽  
Vol 21 (9) ◽  
pp. 3048 ◽  
Author(s):  
Marina M. Ziganshina ◽  
Ekaterina L. Yarotskaya ◽  
Nicolai V. Bovin ◽  
Stanislav V. Pavlovich ◽  
Gennady T. Sukhikh
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Vascular Tone ◽  
Endothelial Activation ◽  
Endothelial Glycocalyx ◽  
Pathogenic Factor ◽  
New Approach ◽  
Pathological Conditions ◽  
Key Factor ◽  
Regulation Of Vascular Tone

Today pre-eclampsia (PE) is considered as a disease of various theories; still all of them agree that endothelial dysfunction is the leading pathogenic factor. Endothelial dysfunction is a sequence of permanent immune activation, resulting in the change of both the phenotype and the functions of an endothelial cell and of the extracellular layer associated with the cell membrane—endothelial glycocalyx (eGC). Numerous studies demonstrate that eGC mediates and regulates the key functions of endothelial cells including regulation of vascular tone and thromboresistance; and these functions are disrupted during PE. Taking into account that eGC and its components undergo alterations under pathological conditions leading to endothelial activation, it is supposed that eGC plays a certain role in pathogenesis of PE. Envisaging the eGC damage as a key factor of PE, might be a new approach to prevention, treatment, and rehabilitation of patients with PE. This approach could include the development of drugs protecting eGC and promoting regeneration of this structure. Since the issue of PE is far from being solved, any effort in this direction might be valuable.

Neural regulation of vascular tone and cold induced vasoconstriction in human finger skin

1990 ◽  
Vol 30 (2) ◽  
pp. 169-173 ◽  
Author(s):  
Lars Erik Lindblad ◽  
Lena Ekenvall ◽  
Christer Klingstedt
Keyword(s):  
Vascular Tone ◽  
Neural Regulation ◽  
Human Finger ◽  
Finger Skin ◽  
Regulation Of Vascular Tone

Endothelial regulation of vascular tone

1993 ◽  
Vol 17 (6) ◽  
pp. 1143-1144
Author(s):  
John P. Cooke
Keyword(s):  
Vascular Tone ◽  
Regulation Of Vascular Tone

Cardiovascular and renal control in NOS-deficient mouse models

2003 ◽  
Vol 284 (3) ◽  
pp. R628-R638 ◽  
Author(s):  
Pablo A. Ortiz ◽  
Jeffrey L. Garvin
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Cardiac Function ◽  
Knockout Mice ◽  
Vascular Tone ◽  
Single Gene ◽  
No Production ◽  
Compensatory Mechanisms ◽  
Nos Isoforms ◽  
Regulation Of Vascular Tone

Nitric oxide (NO) plays an essential role in the maintenance of cardiovascular and renal homeostasis. Endogenous NO is produced by three different NO synthase (NOS) isoforms: endothelial NOS (eNOS), inducible NOS (iNOS), and neuronal NOS (nNOS). To investigate which NOS is responsible for NO production in different tissues, NOS knockout (−/−) mice have been generated for the three isoforms. This review focuses on the regulation of cardiovascular and renal function in relation to blood pressure homeostasis in the different NOS−/− mice. Although regulation of vascular tone and cardiac function in eNOS−/− has been extensively studied, far less is known about renal function in these mice. eNOS−/− mice are hypertensive, but the mechanism responsible for their high blood pressure is still not clear. Less is known about cardiovascular and renal control in nNOS−/− mice, probably because their blood pressure is normal. Recent data suggest that nNOS plays important roles in cardiac function, renal homeostasis, and regulation of vascular tone under certain conditions, but these are only now beginning to be studied. Inasmuch as iNOS is absent from the cardiovascular system under physiological conditions, it may become important to blood pressure regulation only during pathological conditions related to inflammatory processes. However, iNOS is constitutively expressed in the kidney, where its function is largely unknown. Overall, the study of NOS knockout mice has been very useful and produced many answers, but it has also raised new questions. The appearance of compensatory mechanisms suggests the importance of the different isoforms to specific processes, but it also complicates interpretation of the data. In addition, deletion of a single gene may have physiologically significant effects in addition to those being studied. Thus the presence or absence of a specific phenotype may not reflect the most important physiological function of the absent gene.

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