When the sympathetic constrictor tone is high, the decrease in blood flow caused by occlusion of the common carotid artery is minimal, but there is a significant increase in flow after the occlusion is released. The dilation of blood vessels due to baroreceptor stimulation occurs because it inhibits the activity of sympathetic vasoconstrictors.

The resistance vessels in skeletal muscle play a crucial role in maintaining arterial blood pressure because skeletal muscle makes up a large part of the body's mass, making it the largest vascular bed. The involvement of skeletal muscle vessels in vascular reflexes is essential for maintaining normal arterial blood pressure.

A summary of the effects of sympathetic neural activity on the blood vessels in muscle and skin can be seen in Fig. 17.39. It is important to note that the lower the basal tone of the skin vessels, the stronger their constrictor response. Additionally, active cutaneous vasodilation is absent.

In active skeletal muscle, blood flow is regulated by metabolic factors. In resting muscle, neural factors are more dominant. Cutting the sympathetic nerves to the muscle eliminates the neural component of vascular tone and reveals the intrinsic basal tone of the blood vessels. The neural and local mechanisms that regulate blood flow oppose each other, and during muscle contraction, the local vasodilator mechanism becomes predominant. However, during exercise, strong sympathetic nerve stimulation slightly reduces the vasodilation induced by locally released metabolites.

Fig. 17.38 provides evidence of the involvement of the muscle vascular bed in vasoconstriction and vasodilation mediated by the carotid sinus baroreceptors after occlusion and release of the common carotid artery. In this experimental setup, the sciatic and femoral nerves were the only direct innervation of the hind leg muscle mass. The muscle was perfused with blood at a constant pressure.

Blood reaches the brain through the internal carotid and vertebral arteries. The vertebral arteries combine to form the basilar artery, which, along with branches of the internal carotid arteries, forms the circle of Willis. Arteries on the surface of the brain differ from those that penetrate the brain tissue. Pial arteries and arterioles receive extrinsic innervation, such as via the superior cervical ganglion, sphenopalatine nerves, and trigeminal nerve. On the other hand, parenchymal arterioles have intrinsic innervation through cerebral neurons. Pial arteries have more smooth muscle cells compared to parenchymal arterioles. Additionally, pial arteries and arterioles have collateral branches, while parenchymal arterioles do not. As a result, parenchymal arterioles regulate blood flow to specific cortical regions, and their occlusion can significantly decrease blood flow.
Fig. 17.38 ). When sympathetic constrictor tone is high, the decrease in blood flow evoked by common carotid artery occlusion is small, but the increase in flow after the release of occlusion is large. The vasodilation produced by baroreceptor stimulation is caused by inhibition of sympathetic vasoconstrictor activity.
The resistance vessels in skeletal muscle contribute significantly to maintenance of arterial blood pressure because skeletal muscle constitutes a large fraction of the body’s mass, and the muscle vasculature thus constitutes the largest vascular bed. Participation of the skeletal muscle vessels in vascular reflexes is important in maintaining normal arterial blood pressure.
A comparison of the sympathetic neural effects on the blood vessels of muscle and skin is summarized in
Fig.
17.39.
Note that the lower the basal tone of the skin vessels, the greater their constrictor response; also note the absence of active cutaneous vasodilation.
In active skeletal muscle, blood flow is regulated by meta- bolic factors. In resting muscle, neural factors predominate,
Fig. 17.39 ). Cutting of the sympathetic nerves to muscle abolishes the neural component of vascular tone, and it unmasks the intrinsic basal tone of the blood vessels. The neural and local mechanisms that regulate blood flow oppose each other, and during muscle contraction, the local vasodilator mechanism supervenes. However, during exercise, strong sympathetic nerve stimulation slightly attenuates the vasodilation induced by locally released metabolites.
•Fig. 17.38 Evidence of Participation of the Muscle Vascular Bed in Vasoconstriction and Vasodilation Mediated by the Carotid Sinus Baroreceptors After Occlusion and Release of the Common Carotid Artery. Inthispreparation,thesciaticandfemoralnervesconstitutedtheonlydirectinnervationofthehindlegmusclemass.Themusclewasperfusedwithbloodataconstantpressure.(RedrawnfromJonesRD,BerneRM.Am J Physiol. 1963;204:461.)
Blood reaches the brain through the internal carotid and vertebral arteries. The vertebral arteries join to form the basilar artery, which, in conjunction with branches of the •Fig. 17.39 Basaltoneandtherangeofresponseofresistancevesselsinmuscle(dashed lines) andskin(shaded areas) tostimulationandsectionofsympatheticnerves.Peripheralresistanceisplottedonalogarithmicscale.(RedrawnfromCelanderO,FolkowB.Acta Physiol Scand. 1953;29:241.) internal carotid arteries, forms the circle of Willis. Arteries on the brain surface differ from those that penetrate the brain parenchyma. Pial arteries and arterioles have an extrinsic innervation (e.g., via superior cervical ganglion, sphenopalatine nerves, trigeminal nerve); parenchymal arterioles have an intrinsic innervation (via cerebral neurons). Pial arteries have more smooth muscle cells than do parenchymal arterioles. Also, pial arteries and arterioles have collateral branches, whereas parenchymal arterioles do not. Therefore, parenchymal arterioles regulate blood flow to discrete cortical regions, and their occlusion can reduce blood flow significantly.