Experimental Physiology : Translation and Integration Carotid baroreflex (CBR) function has been extensively studied in humans by the application of neck pressure (NP) and neck suction (NS) to the carotid sinus using the variable pressure neck chamber (Eckberg, 1977b; Mancia et al. 1978, 1985; Wallin & Eckberg, 1982; Strange et al. 1990; Potts et al. 1993; Papelier et al. 1994; Sundblad & Linnarsson, 1996; Fadel et al. 2001a; Ogoh et al. 2002). While this technique has provided important information regarding CBR control, questions remain as to the extent to which CBR adaptation may occur with the use of NP and NS. Eckberg (1977b) has previously reported that in humans constant-intensity stimulation resulted in significant adaptation of the CBR-mediated heart rate (HR) response. Other investigations (Eckberg, 1977a; Potts et al. 1993; Potts & Raven, 1995; Ogoh et al. 2002) have also indicated that alterations in R–R interval or HR are transient with the application of NS for 5 s during a held expiration. These findings have lead to the speculation that alterations in afferent nerve traffic from the carotid baroreceptors are not maintained during sustained stimuli (Eckberg & Sleight, 1992). However, Mancia et al. (1978, 1985) have reported that HR responses were well maintained during 2 min of NP and over the first 15 s of NS. In addition, Wallin & Eckberg (1982) reported that cardiac responses to 5 s of NP and NS were well maintained until the stimulus was terminated; however, muscle sympathetic nerve activity (MSNA) responses were only transitory. These disparate findings have been difficult to reconcile and they continually raise the question as to whether or not baroreceptor adaptation occurs with NP and NS. The application of NP and NS during held expiration, a common manoeuvre to limit respiratory-related fluctuations in HR (Potts et al. 1993), limits the time period during which CBR responses can be assessed. Therefore, even though the greatest changes in HR and MSNA occur early in response to NP and NS, possibly even before the stimulus is terminated, it may be that extension of the stimulus for a longer period (i.e. without a breath hold) may maintain CBR-mediated responses. Alternatively, considering that animal investigations have shown that baroreflex responses Does pulsatile and sustained neck pressure or neck suction produce differential cardiovascular and sympathetic responses in humans? Shigehiko Ogoh *, Paul J. Fadel †, Janelle M. Hardisty, Wendy L. Wasmund, David M. Keller, Peter B. Raven and Michael L. Smith Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA (Manuscript received 7 April 2003; accepted 30 June 2003) Although square-wave sustained and R wave-triggered pulsatile stimuli have been used to assess carotid baroreflex (CBR) function in humans, it remains unclear whether these different stimulus protocols elicit comparable responses and whether CBR responses adapt during prolonged stimulation. Thus, we measured muscle sympathetic nerve activity (MSNA), heart rate (HR) and mean arterial pressure (MAP) in response to +30 Torr neck pressure (NP) and _30 Torr neck suction (NS) delivered for 20 s either as a sustained or pulsatile stimulus. CBR-mediated changes in MSNA, HR and MAP were similar with sustained and pulsatile stimuli. The time course of MSNA and HR responses identified that significant changes occurred during the initial 5 s and were better maintained over 20 s with NP than with NS. Changes in MAP exhibited a slower onset with the peak increase during NP occurring at 10 s (sustained, 7 ± 1 mmHg; pulsatile, 7 ± 1 mmHg; P > 0.05) and the nadir during NS occurring at 20 s (sustained, _7 ± 1 mmHg; pulsatile, _9 ± 2 mmHg; P > 0.05). These data demonstrate that sustained and pulsatile NP and NS produce comparable CBR-mediated responses. Furthermore, despite MSNA and HR returning towards baseline during NS, CBR-mediated changes in MAP are well maintained over 20 s of NS and NP. Experimental Physiology (2003) 88.5, 595–601. 2586 † Present address: Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-8586, USA. Publication of The Physiological Society * Corresponding author: sogoh@hsc.unt.edu ) by guest on April 12, 2012 ep.physoc.org Downloaded from Exp Physiol (