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This Article Full Text Full Text (PDF) All Versions of this Article: 93/9/1058    most recent expphysiol.2008.043216v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Flanagan, E. T. Articles by Johns, E. J. PubMed PubMed Citation Articles by Flanagan, E. T. Articles by Johns, E. J. Related Collections Cardiovascular control

¹ Department of Physiology, University College Cork, Cork, Republic of Ireland ² School of Pharmacy, Universiti Sains Malaysia, Penang, Malaysia

This study aimed to quantify the effect of cardiac hypertrophy induced with isoprenaline and caffeine on reflex regulation of renal sympathetic nerve activity by the arterial and cardiopulmonary baroreceptors. Male Wistar rats, untreated or given water containing caffeine and subcutaneous (S.C.) isoprenaline every 72 h for 2 weeks or thyroxine S.C. for 7 days, were anaesthetized and prepared for measurement of renal sympathetic nerve activity or cardiac indices. Both isoprenaline–caffeine and thyroxine treatment blunted weight gain but increased heart weight and heart weight to body weight ratio by 40 and 14% (both P < 0.01), respectively. In the isoprenaline–caffeine group, the maximal rate of change of left ventricular pressure and the contractility index were higher by 17 and 14% (both P < 0.01), respectively, compared with untreated rats. In the isoprenaline–caffeine-treated rats, baroreflex gain curve sensitivity was depressed by approximately 30% (P < 0/05), while the mid-point blood pressure was lower, by 15% (P < 0/05), and the range of the curve was 60% (P < 0.05) greater than in the untreated rats. An acute intravenous infusion of a saline load decreased renal sympathetic nerve activity by 42% (P < 0.05) in the untreated rats but had no effect in the isoprenaline–caffeine- or the thyroxine-treated groups. The isoprenaline–caffeine treatment induced cardiac hypertrophy with raised cardiac performance and an associated depression in the reflex regulation of renal sympathetic nerve activity by both high- and low-pressure baroreceptors. The thyroxine-induced cardiac hypertrophy also blunted the low-pressure baroreceptor-mediated renal sympatho-inhibition. These findings demonstrate that in cardiac hypertrophy without impaired cardiac function, there is a blunted baroreceptor control of renal sympathetic outflow.

(Received 10 May 2008; accepted after revision 15 May 2008; first published online 16 May 2008)
Corresponding author E. J. Johns: Department of Physiology, Aras Windle, University College Cork, Western Road, Cork, Republic of Ireland. Email: e.j.johns{at}ucc.ie