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Present data demonstrated that TCDD may lead to an increase in blood pressure via increased renal oxidative stress and vascular reactivity.
Thus, endothelin increases the blood pressure mainly by vasoconstriction.
Through a variety of mechanisms related to prostaglandin inhibition, including sodium retention and vasoconstriction, these agents may increase blood pressure.
These data suggest that Ca supplements may acutely influence blood pressure and blood coagulation.
We conclude that central aldosterone infusion initiates an increase in blood pressure by a mechanism independent of Na retention.
Open accessJournal ArticleDOI
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We suggest that a small increase in plasma sodium may be part of the mechanisms whereby dietary salt increases the blood pressure.
These data suggest that stimulation of PVN glutamatergic neurons is sufficient to cause autonomic dysfunction and drive the increase in blood pressure during hypertension.
5-HT may be important in the maintenance of blood pressure but alternative mechanisms for the action of ketanserin in reducing blood pressure require investigation.
Ketanserin effectively lowers arterial blood pressure.