Blockade of neuronal nitric oxide synthase alters the baroreflex control of heart rate in the rabbit

Hiroshi Murakami, Jun Li Liu, Hirohito Yoneyama, Yasuhiro Nishida, Kenji Okada, Hiroaki Kosaka, Hironobu Morita, Irving H. Zucker

Research output: Contribution to journalArticle

39 Scopus citations

Abstract

In previous studies we used N(G)-nitro-L-arginine (L-NNA) to investigate the role of nitric oxide (NO) in baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA). L-NNA increased resting mean arterial pressure (MAP), decreased HR, and did not change or slightly decreased RSNA. These changes complicated the assessment of the central effects of NO on the baroreflex control of HR and RSNA. Therefore, in the present study the effects of the relatively selective neuronal NO synthase inhibitor 7-nitroindazole (7-NI) on the baroreflex control of HR and RSNA were investigated in rabbits. Intraperitoneal injection of 7-NI (50 mg/kg) had no effect on resting HR, MAP, or RSNA. 7-NI significantly reduced the lower plateau of the HR-MAP baroreflex curve from 140 ± 4 to 125 ± 4 and from 177 ± 10 to 120 ± 9 beats/min in conscious and anesthetized preparations, respectively (P < 0.05). In contrast, there was no significant difference in the RSNA-MAP curves before and afar 7-NI administration in conscious or anesthetized preparations. These data suggest that blockade of neuronal NO synthase influences baroreflex control of HR but not of RSNA in rabbits.

Original languageEnglish (US)
Pages (from-to)R181-R186
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume274
Issue number1 43-1
DOIs
StatePublished - Jan 1998

Keywords

  • Arterial pressure
  • Sympathetic nerve activity
  • Vagus

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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