(Hypertension. 1997;30:585.)
© 1997 American Heart Association, Inc.
Articles |
Nitric Oxide Blunts Sympathetic Response of Pregnant Normotensive and Hypertensive Rat Arteries
From the Departments of Pharmacology and Internal Medicine (E.B.C.), School of Medicine of Ribeirão Preto, University of São Paulo, Brazil.
Correspondence to Dr Maria Cristina O. Salgado, Department of Pharmacology, School of Medicine, University of São Paulo, 14049-900 Ribeirão Preto, São Paulo, Brazil. E-mail mcdosalg{at}fmrp.usp.br
Abstract Rat pregnancy is associated with a blunted response
to vasocontrictors both in vivo and in vitro as well as a decrease in
arterial pressure. We examined the influence of pregnancy
on neurally induced vasoconstrictor and vasodilator responses of the
isolated mesenteric arterial bed from normotensive Wistar
and spontaneously hypertensive nonpregnant and 20-day pregnant rats and
determined the possible role of nitric oxide (NO) in modulating these
responses. MAP (mm Hg) in pregnant normotensive (98±1, n=13) and
hypertensive (136±5, n=13) rats was lower (P<.05) than in
nonpregnant controls (114±2, n=14, and 174±3, n=12, respectively). In
isolated mesenteric arterial beds, electrical field
stimulation (EFS; 34 V, 3 ms, 10-64 Hz) of perivascular nerves at basal
tone induced a frequency-dependent increase in perfusion pressure that
was significantly (P<.001) greater in preparations from
hypertensive compared with normotensive rats. Pregnancy was associated
with a significant decrease in the maximal vasoconstrictor response
elicited by EFS in both normotensive and hypertensive groups compared
with their nonpregnant controls. In
phenylephrine-preconstricted mesenteric beds, EFS (60 V, 1
ms, 1-8 Hz) elicited a similar frequency-dependent decrease in
perfusion pressure in normotensive and hypertensive groups, but
pregnancy did not influence these responses. In the presence of the NO
synthase inhibitor
N
-nitro-L-arginine (200
µmol/L), the maximal vasoconstrictor response induced by EFS was
significantly (P<.001) augmented in both normotensive and
hypertensive groups, and the differences observed between pregnant and
nonpregnant groups were abolished. Responses to sodium nitroprusside
were not affected by pregnancy, although they were greater in
preparations from hypertensive rats. These results indicate that NO
contributes to pregnancy-associated diminished vasoconstrictor response
to sympathetic stimulation in the mesenteric arterial bed
of both normotensive and hypertensive rats.
Key Words: nitric oxide • vasoconstriction • rats, inbred SHR • vasodilation • mesenteric arteries