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Baroreflex sensitivity differs among same strain Wistar rats from the same laboratory

Vitor E. Valenti, Luiz Carlos de Abreu, Hugo Macedo Junior, Oseas F. Moura Filho, Celso Ferreira
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Published Online: Aug 7th 2018 Heart International 2011;6(2):e9 DOI: https://doi.org/10.4081/hi.2011.e9
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Abstract

Overview

Previous studies showed that a proportion
of normotensive Sprague-Dawley rats spontaneously
exhibit lower baroreflex sensitivity.
However, investigations have not yet been carried
out on Wistar rats. We aimed to compare
baroreflex sensitivity among rats from the
same strain and the same laboratory. Male
Wistar normotensive rats (300-400g) were
studied. Cannulas were inserted into the
abdominal aortic artery through the right
femoral artery to measure mean arterial pressure
and heart rate. Baroreflex was calculated
as the derivative of the variation of heart rate
in function of the mean arterial pressure variation
(ΔHR/ΔMAP) tested with a depressor
dose of sodium nitroprusside (50 μg/kg) and
with a pressor dose of phenylephrine (8μg/kg)
in the right femoral venous approach through
an inserted cannula. We divided the rats into
four groups: i) high bradycardic baroreflex,
baroreflex gain less than -2 tested with
phenylephrine; ii) low bradycardic baroreflex,
baroreflex gain between -1 and -2 tested with
phenylephrine; iii) high tachycardic baroreflex,
baroreflex gain less than -3 tested with
sodium nitroprusside; and iv) low tachycardic
baroreflex, baroreflex gain between -1 and -3
tested with sodium nitroprusside.
Approximately 71% of the rats presented a
decrease in bradycardic reflex while around
half showed an increase in tachycardic reflex.
No significant changes in basal mean arterial
pressure and heart rate, tachycardic and
bradycardic peak and heart rate range were
observed. There was a significant change in
baroreflex sensitivity among rats from the
same strain and the same laboratory.

Keywords

Baroreceptors, hypertension, autonomic nervous system, parasympathetic nerve, sympathetic nerve.

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Article Information

Correspondence

Vitor E. Valenti, Departamento de Medicina, Disciplina de Cardiologia, Universidade Federal de São Paulo, UNIFESP, Rua Napoleão de Barros, 715 – Térreo, 04039- 032, São Paulo, SP, Brazil. Tel. +55.11.5572-5462. E-mail: vitor.valenti@gmail.com

Acknowledgements

This research was supported
by public funding from Fundação de Amparo à
Pesquisa do Estado de São Paulo (FAPESP).

Received

2011-05-09T00:00:00

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