1. Neurohumoral mechanisms regulate blood pressure and blood volume to ensure adequate blood flow for all body organs. 2. The autonomic nervous system affects the cardiovascular system through the release of epinephrine, norepinephrine, and acetylcholine. 3. The arterial baroreceptor reflex regulates arterial blood pressure. 4. The atrial volume receptor reflex regulates blood volume and helps to stabilize blood pressure. 5. The cardiovascular state of conscious subjects is determined by an ongoing and ever-changing mixture of reflex effects and psychogenic responses. TABLE 25-1 Receptors Involved in Autonomic Control of the Cardiovascular System Sympathetic control of the heart is exerted through the β1-adrenergic receptors, which are found on every cardiac muscle cell. These beta receptors are activated by norepinephrine or epinephrine. Chapters 19 and 21 discuss the effects of activation of the cardiac β-adrenergic receptors. In brief, pacemaker rate increases, cell-to-cell conduction velocity increases, and refractory period decreases. In addition, contractility is increased, so the cardiac contractions are quicker and stronger. The overall effect is increased heart rate and increased stroke volume.
Neural and Hormonal Control of Blood Pressure and Blood Volume
The Autonomic Nervous System Affects the Cardiovascular System Through the Release of Epinephrine, Norepinephrine, and Acetylcholine
Receptor Type
Location
Usual Activator
Effect of Activation
Function
α Adrenergic
α1 and α2
Arterioles (all organs)
Norepinephrine from sympathetic neurons, or circulating epinephrine and norepinephrine
Vasoconstriction
Decreases blood flow to organs; increases total peripheral resistance (major effect)
Veins (abdominal organs)
Norepinephrine from sympathetic neurons, or circulating epinephrine and norepinephrine
Venoconstriction
Displaces venous blood toward heart
β Adrenergic
β1
Heart (all cardiac muscle cells)
Norepinephrine from sympathetic neurons, or circulating epinephrine and norepinephrine
Increased pacemaker rate; faster speed of conduction; decreased refractory period; quicker, stronger contractions
Increases heart rate, stroke volume, and cardiac output (major effects)
β2
Arterioles (coronary and skeletal muscle)
Circulating epinephrine and norepinephrine
[β2 receptors not innervated]
Vasodilation
Increases coronary blood flow; increases skeletal muscle blood flow
Muscarinic Cholinergic
M2
Heart (all cardiac muscle cells, but sparse direct innervation of ventricular muscle cells)
Acetylcholine from parasympathetic neurons
Opposite of β1
Decreases heart rate and cardiac output (major effect)
Sympathetic nerve endings at ventricular muscle cells
Acetylcholine from parasympathetic neurons
Inhibition of norepinephrine release from sympathetic neurons
Decreases magnitude of sympathetic effects on ventricular muscle cells
M3
Arterioles (coronary)
Acetylcholine from parasympathetic neurons
Vasodilation (mediated via nitric oxide)
Increases coronary blood flow (minor effect)
Arterioles (genitals)
Acetylcholine from parasympathetic neurons
Vasodilation (mediated via nitric oxide)
Causes engorgement and erection
Arterioles (skeletal muscle)
Acetylcholine from specialized sympathetic neurons
Vasodilation (mediated via nitric oxide)
Increases muscle blood flow (in anticipation of exercise)
Arterioles (most other organs)
[Receptors not innervated; normal activator unknown]
Vasodilation (mediated via nitric oxide)
Function unknown
You may also need

Full access? Get Clinical Tree

