Amplified respiratory-sympathetic coupling in neonatal and juvenile spontaneously hypertensive rats

University of Leeds (2008) Proc Physiol Soc 10, PC1

Poster Communications: Amplified respiratory-sympathetic coupling in neonatal and juvenile spontaneously hypertensive rats

A. Simms1, J. Paton2, A. M. Allen1, A. E. Pickering3

1. Department of Physiology, University of Melbourne, Melbourne, Victoria, Australia. 2. Physiology and Pharmacology, University of Bristol, Bristol, United Kingdom. 3. Anaesthesia, University of Bristol, Bristol, United Kingdom.

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Sympathetic nerve activity (SNA) is elevated in mature spontaneously hypertensive (SH) rats compared to their normotensive Wistar-Kyoto (WKY) controls [1, 2]. However, it is unclear whether altered sympathetic activity is a cause or a consequence of hypertension. We tested the hypothesis that sympathetic nerve activity is elevated in pre-hypertensive neonate and juvenile SH rats, and that this may be due to augmented respiratory-sympathetic coupling. Using the working heart brainstem preparation [3], perfusion pressure, phrenic nerve and thoracic (T8) SNA were recorded in male SH and WKY rats at three ages; neonates (postnatal day 9-14), 3-week-old and 5-week-old (n=30). At comparable perfusion flow rates, pressures were higher in SH rats at all ages. Although the mean level of SNA was only higher in neonatal SH rats the amplitude of respiratory-related bursts of SNA were significantly greater in SH rats of all age groups (p<0.05). This was reflected in significantly larger respiratory-related oscillations in perfusion pressure (so called Traube-Hering waves) in SH than WKY rats at all ages (neonates 0.6±0.4 vs. 1.8±0.4mmHg; 3-week-old 2.8±0.7 vs. 5.6±1.5mmHg; 5-week-old 1.5±0.8 vs. 9.8±1.5mmHg, WKY v SHR respectively; Students t test, n=5/group, p<0.05). We assessed the respiratory-sympathetic coupling using phrenic-triggered averaging of the integrated sympathetic nerve recordings across 20 phrenic cycles. This revealed a shift in the peak of respiratory-sympathetic coupling from the post-inspiratory to the inspiratory period with increasing age in SH rats. Thus, increased SNA is already present in SH rats in early postnatal life and they show augmented respiratory modulation at all ages. This is reflected in altered vascular function, even in the “pre-hypertensive” phase, with elevated perfusion pressure and increased magnitude of Traube-Hering waves. We speculate that the amplified respiratory-related bursts of SNA seen in the neonate and juvenile SH rat may be a causal factor in the development of neurogenic hypertension in adulthood.



Where applicable, experiments conform with Society ethical requirements.

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