Key Points
- To determine whether sympathetic nerve activity is elevated in neonatal and juvenile spontaneously hypertensive rats prior to hypertension onset via augmented respiratory-sympathetic coupling.
- Assessed male spontaneously hypertensive (SH) and normotensive Wistar-Kyoto (WKY) rats across three developmental stages: neonates (postnatal days 9–16), 3 weeks old, and 5 weeks old.
- Used an arterially perfused working heart-brainstem preparation to record perfusion pressure, phrenic nerve activity, and thoracic (T8) sympathetic nerve activity.
- Evaluated central and peripheral chemoreflex sensitivity and arterial baroreflex function alongside recovery from hypocapnic-induced apnoea.
- Perfusion pressure and the amplitude of respiratory-related bursts of sympathetic nerve activity were significantly greater in SH rats at all tested ages (P < 0.05).
- Traube-Hering pressure waves were significantly larger in 5-week-old SH rats compared to WKY controls (9.8 ± 1.5 vs. 1.4 ± 0.8 mmHg; n = 5 per group; P < 0.01).
- Reinstatement of Traube-Hering waves after hypocapnic-induced apnoea triggered a significantly larger increase in perfusion pressure in SH rats (P < 0.05), independent of chemoreflex or baroreflex alterations.
Structured PICO
PPopulationMale spontaneously hypertensive (SH) rats and normotensive Wistar-Kyoto (WKY) rats at three ages: neonates (postnatal day 9-16), 3 weeks old and 5 weeks old.
IInterventionAssessment of perfusion pressure, phrenic nerve activity and thoracic (T8) sympathetic nerve activity using the working heart-brainstem preparation
CComparatorNormotensive Wistar-Kyoto (WKY) rats
OOutcomeSympathetic nerve activity (SNA) and perfusion pressuresurrogate
Augmented respiratory-sympathetic coupling is present in spontaneously hypertensive rats early in postnatal life, suggesting it may be causal in the development of hypertension.