Sympathetic nerve activity (SNA) is elevated in established hypertension. We tested the hypothesis that SNA is elevated in neonate and juvenile spontaneously hypertensive (SH) rats prior to the development of hypertension, and that this may be due to augmented respiratory–sympathetic coupling. Using the working heart–brainstem preparation, perfusion pressure, phrenic nerve activity and thoracic (T8) SNA were recorded in male SH rats and normotensive Wistar–Kyoto (WKY) rats at three ages: neonates (postnatal day 9–16), 3 weeks old and 5 weeks old. Perfusion pressure was higher in SH rats at all ages reflecting higher vascular resistance. The amplitude of respiratory-related bursts of SNA was greater in SH rats at all ages (P < 0.05). This was reflected in larger Traube–Hering pressure waves in SH rats (1.4 ± 0.8 versus 9.8 ± 1.5 mmHg WKY versus SH rat, 5 weeks old, n= 5 per group, P < 0.01). Recovery from hypocapnic-induced apnoea and reinstatement of Traube–Hering waves produced a significantly greater increase in perfusion pressure in SH rats (P < 0.05). Differences in respiratory–sympathetic coupling in the SH rat were not secondary to changes in central or peripheral chemoreflex sensitivity, nor were they related to altered arterial baroreflex function. We have shown that increased SNA is already present in SH rats in early postnatal life as revealed by augmented respiratory modulation of SNA. This is reflected in an increased magnitude of Traube–Hering waves resulting in elevated perfusion pressure in the SH rat. We suggest that the amplified respiratory-related bursts of SNA seen in the neonate and juvenile SH rat may be causal in the development of their hypertension
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