Effects of cilnidipine on sympathetic outflow and sympathetic arterial pressure and heart rate regulations in rats

Hiromi Yamamoto, Toru Kawada, Shuji Shimizu, Atsunori Kamiya, Shunichi Miyazaki, Masaru Sugimachi

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Aims Cilnidipine is a unique Ca2+ channel blocker that inhibits both L-type and N-type Ca2+ channels. The present study aimed to assess the effects of intravenous cilnidipine on sympathetic outflow and sympathetic arterial pressure (AP) and heart rate (HR) regulations. Main methods Carotid sinus baroreceptor regions were isolated from the systemic circulation in anesthetized and vagotomized Wistar Kyoto rats. Changes in efferent sympathetic nerve activity (SNA), AP and HR in response to a stepwise input of carotid sinus pressure were examined before and during intravenous cilnidipine administration (30 μg/kg bolus + 100 μg kg- 1 h- 1 infusion, n = 6). Key findings Cilnidipine significantly reduced the AP response range (from 68.0 ± 10.2 to 34.6 ± 4.1 mmHg, P = 0.007) but did not affect the SNA response range (from 90.4 ± 10.3 to 84.7 ± 9.5%, P = 0.297) or the HR response range (from 50.4 ± 10.1 to 48.1 ± 6.2 beats/min, P = 0.719). Significance Cilnidipine, at a depressor dose used in the present study, does not acutely suppress sympathetic outflow from the central nervous system. Also, it spared the sympathetic HR response, suggesting that N-type Ca2+ channel blocking action at the cardiac sympathetic nerve endings may be a modest one.

Original languageEnglish
Pages (from-to)1202-1207
Number of pages6
JournalLife Sciences
Volume92
Issue number24-26
DOIs
Publication statusPublished - Jul 10 2013
Externally publishedYes

Fingerprint

Rats
Arterial Pressure
Heart Rate
Carotid Sinus
Pressoreceptors
Nerve Endings
Inbred WKY Rats
Neurology
Intravenous Administration
Central Nervous System
cilnidipine
Pressure

Keywords

  • Carotid sinus baroreflex
  • Cilnidipine
  • Open-loop systems analysis
  • Sympathetic nerve activity

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Effects of cilnidipine on sympathetic outflow and sympathetic arterial pressure and heart rate regulations in rats. / Yamamoto, Hiromi; Kawada, Toru; Shimizu, Shuji; Kamiya, Atsunori; Miyazaki, Shunichi; Sugimachi, Masaru.

In: Life Sciences, Vol. 92, No. 24-26, 10.07.2013, p. 1202-1207.

Research output: Contribution to journalArticle

Yamamoto, Hiromi ; Kawada, Toru ; Shimizu, Shuji ; Kamiya, Atsunori ; Miyazaki, Shunichi ; Sugimachi, Masaru. / Effects of cilnidipine on sympathetic outflow and sympathetic arterial pressure and heart rate regulations in rats. In: Life Sciences. 2013 ; Vol. 92, No. 24-26. pp. 1202-1207.
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AU - Miyazaki, Shunichi

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N2 - Aims Cilnidipine is a unique Ca2+ channel blocker that inhibits both L-type and N-type Ca2+ channels. The present study aimed to assess the effects of intravenous cilnidipine on sympathetic outflow and sympathetic arterial pressure (AP) and heart rate (HR) regulations. Main methods Carotid sinus baroreceptor regions were isolated from the systemic circulation in anesthetized and vagotomized Wistar Kyoto rats. Changes in efferent sympathetic nerve activity (SNA), AP and HR in response to a stepwise input of carotid sinus pressure were examined before and during intravenous cilnidipine administration (30 μg/kg bolus + 100 μg kg- 1 h- 1 infusion, n = 6). Key findings Cilnidipine significantly reduced the AP response range (from 68.0 ± 10.2 to 34.6 ± 4.1 mmHg, P = 0.007) but did not affect the SNA response range (from 90.4 ± 10.3 to 84.7 ± 9.5%, P = 0.297) or the HR response range (from 50.4 ± 10.1 to 48.1 ± 6.2 beats/min, P = 0.719). Significance Cilnidipine, at a depressor dose used in the present study, does not acutely suppress sympathetic outflow from the central nervous system. Also, it spared the sympathetic HR response, suggesting that N-type Ca2+ channel blocking action at the cardiac sympathetic nerve endings may be a modest one.

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