Calcium channels and regulation of vascular tone in hypertension

2004 ◽  
pp. 151-159
Author(s):  
Théophile Godfraind
Keyword(s):  
Calcium Channels ◽  
Vascular Tone ◽  
Regulation Of Vascular Tone

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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