Sympathetic influence on cardiovascular responses to sustained head‐up tilt in humans

Sympathetic β‐adrenergic influences on cardiovascular responses to 50d̀ head‐up tilt were evaluated with metoprolol (β₁‐blockade; 0.29 mg kg^‐1) and propranolol (β₁ and β‐₂‐blockade; 0.28 mg kg^‐1) in eight males. A normotensive‐tachycardic phase was followed by a hypotensive‐bradycardic episode associated with presyncopal symptoms after 23pL3 min (control, mean pLSE). Head‐up tilt made thoracic electrical impedance (3.0pL10Ω), mean arterial pressure (MAP, 86pL4‐93pL4 mmHg), heart rate (HR, 63pL3‐99pL10 beats min^‐1) and total peripheral resistance (TPR, 15pL1‐28pL4 mmHg min L^‐1) increase, while central venous oxygen saturation (74pL2‐58pL4%), cardiac output (5.7pL0.1–3.1pL0.3 L min^‐1), stroke volume (95pL6‐41pL5 mL) and pulse pressure (55pL4‐49pL4 mmHg) decreased (P < 0.05). Central venous pressure decreased during head‐up tilt (7pL2‐0pL1 mmHg), but it remained stable during the sustained tilt. At the appearance of preswyncopal symptoms MAP (49pL3 mmHg), HR (66pL4 beats min^‐1) and TPR (15pL3 mmHg min L^‐1) decreased (P < 0.05). Neither metoprolol or propranolo changed tilt tolerance or cardiovascular variables, except for HR that remained at 57pL2 (metoprolol) and 55pL3 beats min^‐1 (propranolol), and MAP that remained at 87pL5 mmHg during the first phase with metoprolol. In conclusion, sympathetic activation was crucial for the heart rate elevation during normotensive head‐up tilt, but not for tilt tolerance or for the associated hypotension and bradycardia.