(Hypertension. 1997;30:942-947.)
© 1997 American Heart Association, Inc.
Articles |
Impaired Nitric Oxide– and Prostaglandin-Mediated Responses to Flow in Resistance Arteries of Hypertensive Rats
From the Institut National de la Santé et de la Recherche Médicale (INSERM) U141 and U348 (J.M.), IFR Circulation Lariboisière, Université Paris VII, Paris, France.
Correspondence to D. Henrion, PhD, INSERM U141, Hôpital Lariboisière, 41 Bd de la Chapelle, 75475 Paris, Cedex 10, France. E-mail daniel.henrion{at}inserm.lrb.ap-hop-paris.fr
Abstract In human and experimental hypertension, flow (shear
stress)–induced dilation in large arteries is attenuated and
resistant to nitric oxide blockade. We tested the hypothesis
that a defect in nitric oxide–and/or
prostaglandin-dependent flow-induced dilation might occur
in mesenteric resistance arteries from spontaneously hypertensive rats
(SHR). We measured resistance mesenteric artery diameter in situ by
intravital microscopy and simultaneously measured
mesenteric arterial pressure in a collateral artery. The
flow-diameter-pressure relationship was established in normotensive
Wistar-Kyoto rats (WKY) and in SHR under control conditions and after
endothelium removal, inhibition of nitric oxide
synthesis with N
-nitro-L-arginine
methyl ester (10 µmol/L), or inhibition of
prostaglandin synthesis with indomethacin
(10 µmol/L). Production of prostaglandins
was determined in the perfusate. Endothelium
removal decreased artery diameter by 14±1.6% in WKY and 5±0.5%
(P<.01 versus WKY) in SHR at a flow rate of 400 µL/min.
In WKY, N-nitro-L-arginine methyl
ester and indomethacin decreased resistance artery
diameter by 12±3% (P<.001) and 5±2%
(P<.01), respectively, at a flow rate of 400 µL/min;
neither substance had any significant effect in SHR. In both strains,
flow induced the production of 6-keto-prostaglandin
F1
, the metabolite of prostacyclin;
prostaglandin F2; and
thromboxane B2, the stable metabolite of
thromboxane A2. Production of
6-keto-prostaglandin F1 and
prostaglandin F2 was
significantly lower in SHR than WKY, and TxB2
production was significantly higher in SHR than WKY. The
present findings suggest that in SHR mesenteric resistance
arteries, dilation in response to increases in flow was
resistant to nitric oxide and prostaglandin
synthesis blockade. A modification of the ratio of vasodilator to
vasoconstrictor prostaglandins might be at least partly
responsible for the decreased dilator response to flow in SHR.
Key Words: blood vessels • nitric oxide • rats, inbred SHR • prostaglandins
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