(Hypertension. 1997;30:1105-1111.)
© 1997 American Heart Association, Inc.
Articles |
Role of Endothelial Kinins in Control of Coronary Nitric Oxide Production
From the Departments of Physiology (X.Z., X.X., T.H.H.) and Pharmacology (A.N.), New York Medical College, Valhalla, NY, and Henry Ford Hospital (G.A.S.), Detroit, Mich.
Abstract The purpose of the present study was to
determine whether interventions that promote kinin production
or decrease kinin inactivation affect nitric oxide production
in isolated canine coronary microvessels. Accordingly,
bradykinin (10-8 to
10-5 mol/L), ramiprilat
(10-10 to 10-8
mol/L), A23187 (10-8 to
10-6 mol/L), kallikrein (1 to 20 U/mL), and
kininogen (0.5 to 10 µg/mL) were used to stimulate
endothelium-dependent nitric oxide production.
Receptor antagonists, serine protease
inhibitors, and a kinin antibody were used to
inactivate local kallikrein-kinin activity. Nitrite, the
metabolite of nitric oxide in aqueous solution, was measured using the
Griess reaction. All the agonists significantly increased nitrite
release. For instance, the highest dose of bradykinin,
ramiprilat, A23187, kallikrein, and kininogen markedly
increased nitrite production, from 60±10 to 156±12, 153±11,
161±15, 176±15, and 168±16 pmol/mg (all P<.05),
respectively. The increased nitrite production caused by these
agents was not only blocked by
N
-nitro-L-arginine methyl ester
(L-NAME) and HOE 140 (which blocks B2 kinin receptor) but
by the kinin antibody also. For instance, nitrite production
elicited by bradykinin, ramiprilat, A23187, and kininogen
was reduced to 95±8, 87±8, 94±11, and 85±11 pmol/mg (all
P<.05), respectively, by the kinin antibody.
Carbachol-induced nitrite production (from 66±8 to 144±13)
was blocked by L-NAME but not by HOE 140 or the kinin antibody. These
results suggest that either increasing kininogen to promote
endogenous kinin formation or inhibiting
angiotensin-converting enzyme to decrease kinin breakdown,
increases nitric oxide production in isolated coronary
microvessels. These data indicate that a microvessel kallikrein-kinin
system has an important role in the control of nitric oxide
production in coronary microvessels.
Key Words: nitric oxide synthase • serine protease inhibitors • kallikrein-kinin system • kininogen
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