S. Morimoto et al., Presser response to pulsatile compression of the rostral ventrolateral medulla mediated by nitric oxide and c-fos expression, BR J PHARM, 129(5), 2000, pp. 859-864
1 It has been reported that neurovascular compression of the rostral ventro
lateral medulla might be causally related to essential hypertension. Recent
ly, we found that pulsatile compression of the rostral ventrolateral medull
a increases sympathetic nerve activity and elevates arterial pressure via a
ctivation of glutamate receptors in rats. We also found that increases in s
ympathetic and cardiovascular activities by microinjection of L-glutamate i
nto the rostral ventrolateral medulla are mediated by c-fos expression-rela
ted substance(s) following activation of the nitric oxide-cyclic GMP pathwa
y.
2 Herein, we investigated whether responses to pulsatile compression are me
diated by local activation of the nitric oxide-cyclic GMP pathway and/or c-
Sos expression-related substance(s) in rats.
3 Increases in arterial pressure (15+/-1 mmHg), heart rate (9+/-1 b.p.m.),
and sympathetic nerve activity (% change: 8.5+/-1.1%) induced by pulsatile
compression were partially but significantly inhibited after local microinj
ection of a nitric oxide synthase inhibitor, L-NG-nitroarginine methyl este
r (8+/-2 mmHg, 1+/-1 b.p.m., 4.0+/-1.3%; P<0.05 vs compression without pret
reatment) or 7-nitroindazole (7+/-2 mmHg, 2+/-1 b.p.m., 4.0+/-1.5%; P<0.05)
, pr a soluble guanylate cyclase inhibitor, methylene blue (9+/-1 mmHg, 4+/
-1 b.p.m., 4.1+/-1.4%; P<0.05). In addition, increases in arterial pressure
, heart rate, and sympathetic nerve activity by pulsatile compression were
significantly reduced 6 h after microinjection of antisense oligodeoxynucle
otide to c-fos mRNA (2+/-2 mmHg, 2+/-1 b.p.m., 1.0+/-1.0%; P<0.05 vs sense
oligodeoxynucleotide).
4 These results suggest that increases in sympathetic and cardiovascular ac
tivities induced by pulsatile compression of the rostral ventrolateral medu
lla are mediated, at least in part, by local activation of the nitric oxide
-cyclic GMP pathway and c-fos expression-related substance(s) in rats.