Muscle mechanoreflex induces the pressor response by resetting the arterial baroreflex neural arc

Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka 565-8565, Japan.
AJP Heart and Circulatory Physiology (Impact Factor: 3.84). 05/2004; 286(4):H1382-8. DOI: 10.1152/ajpheart.00801.2003
Source: PubMed


The effects of the muscle mechanoreflex on the arterial baroreflex neural control have not previously been analyzed over the entire operating range of the arterial baroreflex. In anesthetized, vagotomized, and aortic-denervated rabbits (n = 8), we isolated carotid sinuses and changed intracarotid sinus pressure (CSP) from 40 to 160 mmHg in increments of 20 mmHg every minute while recording renal sympathetic nerve activity (SNA) and arterial pressure (AP). Muscle mechanoreflex was induced by passive muscle stretch (5 kg of tension) of the hindlimb. Muscle stretch shifted the CSP-SNA relationship (neural arc) to a higher SNA, whereas it did not affect the SNA-AP relationship (peripheral arc). SNA was almost doubled [from 63 +/- 15 to 118 +/- 14 arbitrary units (au), P < 0.05] at the CSP level of 93 +/- 8 mmHg, and AP was increased approximately 50% by muscle stretch. When the baroreflex negative feedback loop was closed, muscle stretch increased SNA from 63 +/- 15 to 81 +/- 21 au (P < 0.05) and AP from 93 +/- 8 to 109 +/- 12 mmHg (P < 0.05). In conclusion, the muscle mechanoreflex resets the neural arc to a higher SNA, which moves the operating point towards a higher SNA and AP under baroreflex closed-loop conditions. Analysis of the baroreflex equilibrium diagram indicated that changes in the neural arc induced by the muscle mechanoreflex might compensate for pressure falls resulting from exercise-induced vasodilatation.

3 Reads
  • Source
    • "It may well be that the intensities of the dynamic exercise employed in those earlier studies, in which ABR control of MSNA was unchanged, did not fully activate the muscle metaboreflex (Fadel et al. 2001; Keller et al. 2004; Ogoh et al. 2007), and that dynamic exercise at a workload high enough to activate the muscle metaboreflex would increase the sensitivity of ABR control of MSNA in humans. In addition, several other factors that reportedly influence ABR function, including central command, the muscle mechanoreflex, body temperature, and central venous pressure (CVP) (Iellamo et al. 1997; Potts & Mitchell, 1998; Gallagher et al. 2001; McIlveen et al. 2001; Cui et al. 2002; Ogoh et al. 2002; Kamiya et al. 2003; Charkoudian et al. 2004; Yamamoto et al. 2004), would also be progressively activated or altered as exercise intensity increased (Rowell et al. 1996). Moreover, the responses to dynamic exercise of the factors that affect ABR function would differ considerably from their responses to isometric exercise (Rowell, 1993; Rowell et al. 1996). "
    [Show abstract] [Hide abstract]
    ABSTRACT: We tested the hypotheses that arterial baroreflex (ABR) control over muscle sympathetic nerve activity (MSNA) in humans does not remain constant throughout a bout of leg cycling ranging in intensity from very mild to exhausting. ABR control over MSNA (burst incidence, burst strength and total MSNA) was evaluated by analysing the relationship between beat-to-beat spontaneous variations in diastolic arterial pressure (DAP) and MSNA in 15 healthy subjects at rest and during leg cycling in a seated position at five workloads: very mild (10 W), mild (82 +/- 5.0 W), moderate (126 +/- 10.2 W), heavy (156 +/- 14.3 W), and exhausting (190 +/- 21.2 W). The workload was incremented every 6 min. The linear relationships between DAP and MSNA variables were significantly shifted downward during very mild exercise, but then shifted progressively upward as exercise intensity increased. During heavy and exhausting exercise, moreover, the DAP-MSNA relationships were also significantly shifted rightward from the resting relationship. The sensitivity of ABR control over burst incidence and total MSNA was significantly lower during very mild exercise than during rest, and the sensitivity of the burst incidence control remained lower than the resting level at all higher exercise intensities. By contrast, the sensitivity of the total MSNA control recovered to the resting level during mild and moderate exercise, and was significantly increased during heavy and exhausting exercise (versus rest). We conclude that, in humans, ABR control over MSNA is not uniform throughout a leg cycling exercise protocol in which intensity was varied from very mild to exhausting. We suggest that this non-uniformity of ABR function is one of the mechanisms by which sympathetic and cardiovascular responses are matched to the exercise intensity.
    The Journal of Physiology 07/2008; 586(Pt 11):2753-66. DOI:10.1113/jphysiol.2007.150060 · 5.04 Impact Factor
  • Source
    • "Thus, activation of muscle mechanoreflex can mediate vagal inhibition and sympathoexcitation in absence of central command and muscle metaboreflex. This shifting of the sympathovagal balance is not counteracted by the baroreflex because the neural input from the muscle mechanoreflex resets the baroreflex operating point to a higher operating pressure (Potts & Mitchell 1998, Yamamoto et al. 2004), in a manner similar to that of central command (Dicarlo & Bishop 2001). This functional resetting allows the baroreflex to operate at the prevailing pressure evoked by exercise (Raven et al. 2006). "
    [Show abstract] [Hide abstract]
    ABSTRACT: This study evaluated the influence of muscle mechanical afferent stimulation on the integrated arterial baroreflex control of the sinus node during dynamic exercise. Systolic blood pressure (SBP) and pulse interval (PI) were measured continuously and non-invasively in 15 subjects at rest and during passive cycling. The arterial baroreflex was evaluated with the cross-correlation method (xBRS) for the computation of time-domain baroreflex sensitivity on spontaneous blood pressure and PI variability. xBRS computes the greatest positive correlation between beat-to-beat SBP and PI, and when significant at P = 0.01, slope and delay are recorded as one xBRS value. Heart rate variability (HRV) was evaluated in the frequency domain. Compared with rest, passive exercise resulted in a parallel increase in heart rate (67 +/- 3.2 vs. 70 +/- 3.6 beats min(-1); P < 0.05) and mean arterial pressure (87 +/- 2 vs. 95 +/- 2 mmHg; P < 0.05), and a significant decrease in xBRS (13.1 +/- 1.8 vs. 10.5 +/- 1.7 ms mmHg(-1); P < 0.01) with an apparent rightward shift in the regression line relating SBP to PI. Also low frequency power of HRV increased while high frequency power decreased (56.7 +/- 3.5 vs. 62.7 +/- 4.8 and 43.2 +/- 3.4 vs. 36.9 +/- 4.9 normalized units respectively; P < 0.05). These data suggest that the stimulation of mechanosensitive stretch receptors is capable of modifying the integrated baroreflex control of sinus node function by decreasing the cardiac vagal outflow during exercise.
    Acta Physiologica 03/2008; 192(3):351-7. DOI:10.1111/j.1748-1716.2007.01766.x · 4.38 Impact Factor
  • Source
    • "In addition, the muscle reflex has been reported to interact with the baroreflex (Potts & Mitchell, 1998), and contribute to the central resetting of the baroreflex during exercise (DiCarlo & Bishop, 2001; Miki et al. 2003). We have recently reported that passive stretch of the triceps surae muscles shifts the CSP–SNA relationship to a higher SNA using the baroreflex equilibrium diagram analysis (Yamamoto et al. 2004). Further studies are necessary to address the mechanism for the resetting during upright tilt. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Since humans are under ceaseless orthostatic stress, the mechanism to maintain arterial pressure (AP) under orthostatic stress against gravitational fluid shift is of great importance. We hypothesized that (1) orthostatic stress resets the arterial baroreflex control of sympathetic nerve activity (SNA) to a higher SNA, and (2) resetting of the arterial baroreflex contributes to preventing postural hypotension. Renal SNA and AP were recorded in eight anaesthetized, vagotomized and aortic-denervated rabbits. Isolated intracarotid sinus pressure (CSP) was increased stepwise from 40 to 160 mmHg with increments of 20 mmHg (60 s for each CSP level) while the animal was placed supine and at 60 deg upright tilt. Upright tilt shifted the CSP-SNA relationship (the baroreflex neural arc) to a higher SNA, shifted the SNA-AP relationship (the baroreflex peripheral arc) to a lower AP, and consequently moved the operating point to marked high SNA while maintaining AP. A simulation study suggests that resetting in the neural arc would double the orthostatic activation of SNA and increase the operating AP in upright tilt by 10 mmHg, compared with the absence of resetting. In addition, upright tilt did not change the CSP-AP relationship (the baroreflex total arc). A simulation study suggests that although a downward shift of the peripheral arc could shift the total arc downward, resetting in the neural arc would compensate this fall and prevent the total arc from shifting downward to a lower AP. In conclusion, upright tilt increases SNA by resetting the baroreflex neural arc. This resetting may compensate for the reduced pressor responses to SNA in the peripheral cardiovascular system and contribute to preventing postural hypotension.
    The Journal of Physiology 08/2005; 566(Pt 1):237-46. DOI:10.1113/jphysiol.2005.086512 · 5.04 Impact Factor
Show more