Large vasodilatations in skeletal muscle of resting conscious dogs and their contribution to blood pressure variability

Abstract

Large (up to +400 %) transient (∼20 s) increases of blood flow were observed in the external iliac arteries of resting conscious dogs (n= 10) in the absence of major alerting or muscular activity. At the same time arterial pressure (AP) fellslightly while heart rate (HR) rose. The vasodilatations were resistant to atropine, ganglionic, β‐adrenergic and NO‐synthase inhibition, but were suppressed by spinal or general anaesthesia. Vasodilatations of similar appearance were elicited by an alerting sound; these were abolished by atropine. The spontaneous vasodilatations occurred simultaneously and their magnitudes were well correlated between both legs, but were not correlated to the amount of concomitant activation of the surface electromyogram. The duration of this activation almost never outlasted 10 s. The reactive hyperaemia observed after a total occlusion of the artery even for 16 s was not large enough to explain the size of the spontaneous vasodilatations. Occlusion during peak flow of the vasodilatations did not affect the size of the reactive hyperaemia. Spectral analysis made separately for data segments with and without vasodilatation revealed that the vasodilatations substantially enhanced the variability of AP and HR at frequencies below ∼0.1 Hz. In conclusion, large coordinated skeletal muscle vasodilatations were identified in resting conscious dogs, which are initiated neurally, but not by sympathetic‐cholinergic or nitroxidergic fibres and which do not show any clear correlation to muscular contraction. The vasodilatations substantially affect the regulation of skeletal muscle blood flow and explain a significant portion of AP and HR variability.

Dynamic characteristics and underlying mechanisms of renal blood flow autoregulation in the conscious dog

“…Although this does not allow direct conclusions about the autoregulatory efficiency, the finding raises the suspicion that autoregulation in the skeletal muscle circulation might be more efficient than presently believed (11). The estimation of the autoregulatory strength in this vascular bed, however, will remain difficult, as noted by Jones and Berne (25) with respect to the ample distribution of vasodilator fibers in this region, which are in frequent use in the conscious animal (29).…”

Impaired response of cardiac autonomic nervous system to glucose load in severe obesity

“…Nevertheless, decreased LF oscillations in BP may result from the delayed sympathetic vasomotor reaction to BP changes. In fact, the vasodilatations substantially enhanced the variability of BP and HR at frequencies below approximately 0.100 Hz [34]. Table 4 High-frequency spectral components of HR and BP during controlled breathing and in response to an oral glucose load (bpm min À1 Hz À0.5 and mm Hg min À1 Hz À0.5 )…”

The renin-angiotensin system and the third mechanism of renal blood flow autoregulation

“…In contrast to the kidney, dilation was stronger during the upward than the downward limb. Because both vasoconstrictive ANG II and local dilatory metabolites will increase with time, the positive hysteresis indicates the stronger effect of the latter, resulting in reactive hyperemia (5,6,28). The renal circulation revealed a positive hysteresis only during the ANG II clamp.…”

“…On the basis of the frequency of the MR in the HQ reported by Just and Arendshorst (24) and the negative amplitudes that indicate initial vasoconstriction, we assume that the high-frequency oscillations represent the MR. The initial vasodilatory effect (positive amplitudes) and the very low frequency of the other oscillations lead us to assume that these oscillations represent the metabolic component of pressure-dependent HQF control that is related to the phenomenon of reactive hyperemia (5,6,28).…”

“…This was one of the reasons we used both total and partial occlusions, and why we compared the renal responses with those of the HQ, a vascular bed known to elicit metabolite-driven reactive hyperemia (28). The initial response of the very low-frequency mechanism in the HQ was uniformly dilatory (Fig.…”