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Hypertension. 2001;37:894-897

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(Hypertension. 2001;37:894.)
© 2001 American Heart Association, Inc.


Scientific Contributions

Abnormal Renal Vascular Responses to Dipyridamole-Induced Vasodilation in Spontaneously Hypertensive Rats

Dinko Susic; Jasmina Varagic; Edward D. Frohlich

From the Hypertension Research Laboratory, Alton Ochsner Medical Foundation, New Orleans, La.

Correspondence to Edward D. Frohlich, MD, Alton Ochsner Distinguished Scientist, Alton Ochsner Medical Foundation, 1516 Jefferson Highway, New Orleans, LA 70121.

The objective of this study was to determine whether there were differences in hemodynamic responses of different vascular beds to systemic administration of dipyridamole between spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. To this end, systemic hemodynamics and organ blood flows (using labeled microspheres) were determined in conscious rats before and 10 minutes after dipyridamole (4 mg · kg-1 · min-1) infusion. In both the normotensive and hypertensive rats, the dipyridamole infusion reduced arterial pressure by {approx}20 mm Hg, associated with a decreased total peripheral resistance and an increased cardiac output. Renal blood flow decreased significantly in SHR after dipyridamole but remained unchanged or increased slightly in the WKY rats. There were no other differences in regional hemodynamics, including those of brain, liver, skin, and muscle, between the WKY and SHR. Antihypertensive treatment completely restored normal renal vascular response to dipyridamole. Previous reports had demonstrated an abnormal coronary hemodynamic response of the SHR. Our data demonstrate that, as with coronary hemodynamics, hypertension selectively induced alterations in renal vasculature. These findings may be of importance in identifying the earliest hemodynamic evidence of developing hypertensive nephrosclerosis.


Key Words: hypertension • renal vasculature • dipyridamole • regional hemodynamics