Key result
Short-term changes in salt intake, blockade of NO synthase, or cyclooxygenase did not alter basal mean circulatory filling pressure or integrated venomotor responses to endothelin-1 or sarafotoxin 6c.
Why the study?
Does salt intake or blockade of NO synthase and cyclooxygenase alter endothelin-induced venous tone in conscious rats?
Does salt intake or blockade of NO synthase and cyclooxygenase alter endothelin-induced venous tone in conscious rats?
Short-term changes in salt intake, NO synthase blockade, or cyclooxygenase blockade do not alter endothelin-induced venous tone in conscious rats.
No effect of salt or NO/COX blockade on endothelin venomotor responses in rats; leaves open translation to human venous tone regulation.
There may be a relation between altered venous function, endothelin (ET)-1, and an impairment in the activity of endothelial-derived nitric oxide (NO) and prostanoids in salt-dependent hypertension. The present study examined the effects of salt intake on ET-induced changes in venomotor tone and the effects of blockade of NO synthase with N(G)-nitro-L-arginine methyl ester (L-NAME) and of cyclooxygenase with indomethacin on venomotor tone caused by the ET(B) selective agonist sarafotoxin 6c (S6c) in awake rats. Rats were anesthetized for permanent placement of catheters for measurements of arterial and venous pressures. A silicone balloon catheter was also fixed in the right atrium to produce brief circulatory arrest. Venomotor tone was estimated from measurements of mean circulatory filling pressure (MCFP) in conscious rats. There were no differences in mean arterial pressure, heart rate, or MCFP responses to short-term administration of ET-1 or S6c at different levels of salt intake. L-NAME or indomethacin did not change MCFP or the response of MCFP to short-term injection of S6c. In conclusion, neither basal MCFP nor integrated venomotor responses to short-term injection of ET-1 or S6c were altered by short-term changes in salt intake, blockade of NO synthase or cyclooxygenase. These data do not support the hypothesis that increased salt intake alters reactivity of veins to ET-1, NO, or prostanoids.
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Johnson et al. (2001) studied salt-dependent hypertension. Salt intake, L-NAME, and indomethacin vs. basal/control conditions was evaluated on mean circulatory filling pressure (MCFP) and venomotor tone. Short-term changes in salt intake, blockade of NO synthase, or cyclooxygenase did not alter basal mean circulatory filling pressure or integrated venomotor responses to endothelin-1 or sarafotoxin 6c.
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