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Angiotensin II does not mediate the pressor response to PGD2 (icv)

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

Journal of Renin-Angiotensin-Aldosterone System, Vol. 1, No. 2, 195-200 (2000)
DOI: 10.3317/jraas.2000.025


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