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Angiotensin II does not mediate the pressor response to PGD2 (icv)
Amir Kershenovich
The University of Texas Medical Branch at Galveston, 301 University Blvd. Galveston, TX 77555-0517, USA
Mary Lee Terrell
The University of Texas Medical Branch at Galveston, 301 University Blvd. Galveston, TX 77555-0517, USA
Joan Y Summy-Long
Pennsylvania State University College of Medicine, 500 University Dr. Hershey, PA 17033, USA
Massako Kadekaro
The University of Texas Medical Branch at Galveston, 301 University Blvd. Galveston, TX 77555-0517, USA, mkutyna{at}utmb.edu
The objective of the present studies was to examine the interaction between brain-derived angiotensin II (Ang II) and prostaglandins in order to identify the mechanisms mediating the pressor response produced by these neuroregulators. Inhibiting synthesis of prostaglandins with indomethacin [indocin, 200 µg/ 5 µl artificial cerebrospinal fluid (aCSF)], administered intracerebroventricularly (icv) to conscious adult male Sprague-Dawley rats, reduced blood pressure to values below basal levels. When injected prior to Ang II (50 ng/5 µl aCSF; icv), indomethacin completely abolished the pressor response induced by the octapeptide. The increase in blood pressure produced by prostaglandin D2 (PGD 2, 20 µg/5 µl; icv), the most prominent prostaglandin in the rat brain, however, was not prevented by losartan (25 µg/5 µl; icv), an Ang II AT 1-receptor antagonist. Collectively, these results indicate that prostaglandins produced tonically in the brain maintain resting arterial blood pressure and that the pressor action of Ang II is dependent on de novo synthesis of a prostaglandin.
Key Words: blood pressure losartan prostaglandin Ang II AT1-receptor
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Journal of Renin-Angiotensin-Aldosterone System, Vol. 1, No. 2,
195-200 (2000)
DOI: 10.3317/jraas.2000.025

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