The heart and vasculature, as well as the large bowel, are regulated in Chapter 18. It is worth noting that skeletal muscle and skin do not receive parasympathetic innervation. The impact of cholinergic fibers on total vascular resistance is minimal because only a small portion of the body's resistance vessels receive parasympathetic fibers.

During hemorrhagic shock, the resistance vessels constrict to help maintain normal arterial blood pressure. When arterial hypotension occurs, arterioles constrict, causing a slight mobilization of blood from the tissue due to the recoil of post-arteriolar vessels when intraluminal pressure decreases. Additionally, extravascular fluid is mobilized due to increased fluid absorption into the capillaries in response to lowered capillary hydrostatic pressure.

The stimulation of parasympathetic fibers in the salivary glands leads to significant vasodilation. This vasodilation is mediated by a vasodilator polypeptide called bradykinin, which is formed locally when an enzyme acts on a plasma protein substrate in the glandular lymphatic vessels. Bradykinin is also formed in other exocrine glands, such as the lacrimal and sweat glands. Its presence in sweat may contribute to the dilation of cutaneous blood vessels.

Epinephrine and norepinephrine have a potent effect on peripheral blood vessels. In skeletal muscle, low concentrations of epinephrine cause the dilation of resistance vessels (β2-adrenergic effect), while high concentrations result in constriction (α1-adrenergic effect), as indicated in Table 14.1.

The primary effect of norepinephrine in all vascular beds is vasoconstriction. Under physiological conditions, the release of catecholamines from the adrenal medulla is less significant than the release of norepinephrine from sympathetic nerve endings.

Various substances play a role in regulating vascular tone, some of which are released from the endothelium (e.g., nitric oxide, endothelin, thromboxane A2), while others are derived from perivascular tissues (e.g., histamine, adenosine, angiotensin II). These substances are listed in Table 14.1.

The sympathetic and vagal effects in the areas of the cerebral medulla are influenced by neural impulses originating from the baroreceptors, chemoreceptors, hypothalamus, cerebral cortex, and skin. These areas of the medulla are also affected by changes in blood concentrations of CO2 and O2.

The baroreceptors, also known as pressoreceptors, are stretch receptors found in the carotid sinuses and aortic arch (Figs. 18.25 and 18.26). The carotid sinuses are slightly depicted in Fig. 18.25, showing their innervation. Fig. 18.26 illustrates the innervation of the aortic bodies and baroreceptors in the aortic arch.
CHAPTER 18 Regulation of the Heart and Vasculature and large bowel. Skeletal muscle and skin do not receive parasympathetic innervation. The effect of cholinergic fibers on total vascular resistance is small because only a small proportion of the resistance vessels of the body receive parasympathetic fibers.
Inhemorrhagicshock,theresistancevesselsconstrictandtherebyassistinthemaintenanceofnormalarterialbloodpressure.Witharterialhypotension,theenhancedarteriolarconstrictionalsoleadstoasmallmobilizationofbloodfromthetissuebyvirtueofrecoilofthepostarteriolarvesselswhenintraluminalpressureisreduced.Furthermore,extravascularfluidismobilizedbecauseofgreaterfluidabsorptionintothecapillariesinresponsetotheloweredcapillaryhydrostaticpressure.
Stimulation of the parasympathetic fibers to the salivary glands induces marked vasodilation. A vasodilator polypeptide, bradykinin, formed locally from the action of an enzyme on a plasma protein substrate in the glandular lymphatic vessels, mediates this vasodilation. Bradykinin is formed in other exocrine glands, such as the lacrimal and sweat glands. Its presence in sweat may be partly responsible for the dilation of cutaneous blood vessels.
Epinephrine and norepinephrine exert a powerful effect on peripheral blood vessels. In skeletal muscle, low concentrations of epinephrine dilate resistance vessels (β2-adrenergic effect), but high concentrations produce constriction (α1adrenergic effect), as noted in
Table 14.1.
In all vascular beds, the primary effect of norepinephrine is vasoconstriction. When stimulated, the adrenal gland can release epinephrine and norepinephrine into the systemic circulation. However, under physiological conditions, the effect of catecholamine release from the adrenal medulla is less important than norepinephrine release from sympathetic nerve endings.
Table 14.1 ). Some are released from the endothelium (e.g., nitric oxide, endothelin, thromboxane A2), whereas others are derived from perivascular tissues (e.g., histamine, adenosine, angiotensin II).
Areas of the cerebral medulla that mediate sympathetic and vagal effects are under the influence of neural impulses that originate in the baroreceptors, chemoreceptors, hypothalamus, cerebral cortex, and skin. These areas of the medulla are also affected by changes in the blood concentrations of CO2 and O2.
The baroreceptors (or pressoreceptors) are stretch receptors located in the carotid sinuses and in the aortic arch (
Figs. 18.25 18.26 ). The carotid sinuses are the slightly
Fig. 18.25 Diagrammaticrepresentationofthecarotidsinusandcarotidbodyandtheirinnervation.(RedrawnfromAdamsWE.The Comparative Morphology of the Carotid Body and Carotid Sinus.
Fig. 18.26 Anteriorviewoftheaorticarchshowingtheinnervationoftheaorticbodiesandbaroreceptors.(ModifiedfromNonidezJF.Anat Rec. 1937;69:299.)