Pressor response to pulsatile compression of the rostral ventrolateral medulla mediated by nitric oxide and c‐fos expression

It has been reported that neurovascular compression of the rostral ventrolateral medulla might be causally related to essential hypertension. Recently, we found that pulsatile compression of the rostral ventrolateral medulla increases sympathetic nerve activity and elevates arterial pressure via act...

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Published inBritish journal of pharmacology Vol. 129; no. 5; pp. 859 - 864
Main Authors Morimoto, Satoshi, Sasaki, Susumu, Miki, Shigeyuki, Kawa, Tetsuyoshi, Itoh, Hiroshi, Nakata, Tetsuo, Takeda, Kazuo, Nakagawa, Masao
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.03.2000
Nature Publishing
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Summary:It has been reported that neurovascular compression of the rostral ventrolateral medulla might be causally related to essential hypertension. Recently, we found that pulsatile compression of the rostral ventrolateral medulla increases sympathetic nerve activity and elevates arterial pressure via activation of glutamate receptors in rats. We also found that increases in sympathetic and cardiovascular activities by microinjection of L‐glutamate into the rostral ventrolateral medulla are mediated by c‐fos expression‐related substance(s) following activation of the nitric oxide‐cyclic GMP pathway. Herein, we investigated whether responses to pulsatile compression are mediated by local activation of the nitric oxide‐cyclic GMP pathway and/or c‐fos expression‐related substance(s) in rats. 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 microinjection of a nitric oxide synthase inhibitor, L‐NG‐nitroarginine methyl ester (8±2 mmHg, 1±1 b.p.m., 4.0±1.3%; P<0.05 vs compression without pretreatment) or 7‐nitroindazole (7±2 mmHg, 2±1 b.p.m., 4.0±1.5%; P<0.05), or 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 oligodeoxynucleotide to c‐fos mRNA (2±2 mmHg, 2±1 b.p.m., 1.0±1.0%; P<0.05 vs sense oligodeoxynucleotide). These results suggest that increases in sympathetic and cardiovascular activities induced by pulsatile compression of the rostral ventrolateral medulla 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. British Journal of Pharmacology (2000) 129, 859–864; doi:10.1038/sj.bjp.0703121
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ISSN:0007-1188
1476-5381
DOI:10.1038/sj.bjp.0703121