Carotid-Cardiac Baroreflex Function Does Not Influence Blood Pressure Regulation during Head-Up Tilt in Humans

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  • Ogoh Shigehiko
    Department of Integrative Physiology, University of North Texas Health Science Center Department of Anaesthesia, The Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen
  • Yoshiga Chie C.
    Department of Anaesthesia, The Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen
  • Secher Niels H.
    Department of Anaesthesia, The Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen
  • Raven Peter B.
    Department of Integrative Physiology, University of North Texas Health Science Center

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  • Use of the Ca-Shortening Curve to Estimate the Myofilament Responsiveness to Ca〔2+〕 in Tetanized Rat Ventricular Myocytes
  • Use of the Ca Shortening Curve to Estimate the Myofilament Responsiveness to Ca 2 in Tetanized Rat Ventricular Myocytes

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Abstract

The influence of the carotid-cardiac baroreflex on blood pressure regulation was evaluated during supine rest and 40° head-up tilt (HUT) in 9 healthy young subjects with and without full cardiac vagal blockade. The carotid baroreflex responsiveness, or maximal gain (GMAX), was assessed from the beat-to-beat changes in heart rate (HR) and mean arterial pressure (MAP) by the variable neck pressure and suction technique ranging in pressure from +40 to −80 Torr, with and without glycopyrrolate (12.0 ± 1.0 μg/kg body weight; mean ± SE). In the supine position, glycopyrrolate increased the HR to 91 ± 3 bpm, from 54 ± 3; MAP to 89 ± 2 mmHg, from 76 ± 2; and cardiac output to 6.8 ± 0.3 l·min−1, from 4.9 ± 0.3 (P < 0.05). The GMAX of the carotid baroreflex control of HR was reduced to −0.06 ± 0.01 bpm·mmHg−1, from −0.30 ± 0.02 (P < 0.05) with no significant effect on the GMAX of the carotid baroreflex control of MAP. During HUT the carotid baroreflex control of MAP was unchanged, though the GMAX of the carotid baroreflex control of HR was increased (P < 0.05). During HUT, central blood volume, assessed by electrical thoracic admittance, and total vascular conductance were decreased with and without glycopyrrolate. Furthermore, glycopyrrolate reduced GMAX of the carotid baroreflex control of HR during HUT (P < 0.05) with no significant effect on GMAX of the carotid baroreflex control of MAP. These data suggest that during supine rest and HUT-induced decreases in central blood volume, the carotid baroreflex control of HR is mediated primarily via parasympathetic activity. Furthermore, the maintenance of arterial blood pressure during postural stress is primarily mediated by arterial and cardiopulmonary reflex regulation of sympathetic activity and its effects on the systemic vasculature.<br>

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