Muscle mechanoreflex induces the pressor response by resetting the arterial baroreflex neural arc
ABSTRACT 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.
- SourceAvailable from: Naoto Fujii[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
- [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
- [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