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Published on: September 28, 2015
Angiotensin II does not mediate the pressor response to PGD2 (icv)
A Kershenovich1, M L Terrell, J Y Summy-Long
1The University of Texas Medical Branch, Galveston, TX 77555-0517, USA.
Journal of the Renin-Angiotensin-Aldosterone System : JRAAS
|April 23, 2002
Summary
Brain prostaglandins maintain blood pressure and are essential for the pressor effects of angiotensin II (Ang II). Inhibiting prostaglandin synthesis lowers blood pressure and blocks Ang II
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Pharmacology
Background:
- Brain-derived angiotensin II (Ang II) and prostaglandins are key neuroregulators of blood pressure.
- The precise interaction and mediating mechanisms between these substances require elucidation.
Purpose of the Study:
- To investigate the interplay between central Ang II and prostaglandins.
- To identify the mechanisms underlying the pressor response mediated by these neuroregulators.
Main Methods:
- Administered indomethacin (prostaglandin synthesis inhibitor) intracerebroventricularly (icv) to rats.
- Administered Ang II and prostaglandin D(2) (PGD(2)) icv.
- Utilized losartan (Ang II AT(1)-receptor antagonist) in conjunction with PGD(2).
Main Results:
- Intracerebroventricular indomethacin reduced basal blood pressure and abolished the pressor response to Ang II.
- The pressor effect of PGD(2) was not blocked by the Ang II AT(1)-receptor antagonist losartan.
- Prostaglandins are tonically produced in the brain, maintaining resting arterial blood pressure.
Conclusions:
- Brain prostaglandins play a crucial role in maintaining basal arterial blood pressure.
- The pressor action of central Ang II is critically dependent on the synthesis of prostaglandins.
- Prostaglandins and Ang II signaling pathways interact to regulate blood pressure.
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