["The Journal of Physiology, EarlyView. ", "\nAbstract figure legend Neonatal spontaneously hypertensive rats (SHRs) exhibit inherent respiratory dysfunction in early life, including oscillatory breathing patterns and apnoeic events that cause oxygen desaturation and brain hypoxia, in addition to an impaired hypoxic ventilatory response. These breathing abnormalities and the consequent postnatal hypoxia are relevant factors that trigger sympathetic hyperactivity in adult life, because hyperoxia treatment during the first 2 weeks of life prevents excessive sympathetic drive in adult SHRs. Created in BioRender.\n\n\n\n\n\n\n\n\n\nAbstract\nEssential hypertension remains a major global health problem with poorly defined mechanisms. Increased vascular sympathetic activity and sleep‐disordered breathing are common features in hypertensive patients and adult spontaneously hypertensive rats (SHRs), an experimental model of essential hypertension. We hypothesized that SHRs exhibit inherent respiratory dysfunctions during postnatal development, leading to irregular breathing and hypoxaemia that contribute to later sympathetic hyperactivity. We assessed pulmonary ventilation, oxygen consumption, systemic and tissue oxygen levels and cardiovascular parameters in male and female normotensive (Wistar–Kyoto and Sprague–Dawley, NT) rats and SHRs from birth to adulthood. Newborn SHRs (0–2 days old) exhibited hypoventilation, fluctuating respiratory frequency and increased episodes of apnoea and breath‐hold, resulting in hypoxaemia and reduced brain oxygen levels in comparison to NT pups. These irregularities and hypoxaemia persisted until postnatal day 12. During hypoxic challenges, SHR pups from 0 to 12 days of life displayed an impaired ventilatory response, contrasting with the developmental increase in hypoxic ventilatory response seen in NT animals. In adult animals, the higher mean arterial pressure levels in SHRs were correlated with postnatal hypoventilation, suggesting a developmental link between postnatal respiratory dysfunction and hypertension. Chronic exposure to hyperoxia (50% O2) during the first 2 weeks of life attenuated respiratory irregularities in neonatal SHRs and reduced sympathetic vasoconstrictor tone in adult SHRs. Our results show that SHRs show early‐life respiratory deficits that lead to breathing irregularities and hypoxaemia during postnatal development, which might contribute to the development of sympathetic hyperactivity in essential hypertension.\n\n\n\n\n\n\n\n\n\nKey points\n\nArterial hypertension is a common cardiovascular disease globally; however, its underlying mechanisms are still not fully understood.\nIn spontaneously hypertensive rats (SHRs), a widely used experimental model of arterial hypertension, we identified inherent respiratory dysfunctions that cause breathing irregularities during the postnatal period.\nNeonatal SHR pups exhibit hypoventilation, fluctuating respiratory frequency and increased episodes of apnoea and breath‐hold, leading to hypoxaemia and reduced oxygen levels in the brain.\nExposure to high oxygen levels during postnatal life attenuates the respiratory irregularities in neonatal SHRs and reduces sympathetic vasoconstrictor tone in adult SHRs.\nOur study shows that early‐life respiratory irregularities and hypoxaemia are present in SHRs from birth and might contribute to the development of sympathetic hyperactivity in arterial hypertension.\n\n\n"]