07.01.2 Effects of the Sympathetic Nervous System
Figure 7.4 Sympathetic NS and kidney (Copyright QUT, Sheila Doggrell)
Angiotensin II acts on blood vessels to cause vasoconstriction. Aldosterone acts on the kidney to promote salt and water retention. Both of these hormonal effects lead to an increase in blood pressure.
On the urinary bladder, noradrenaline acts at a1- adrenoceptors in the neck and sphincters to promote contraction, and contraction in these areas promotes urinary retention.
On the prostate, noradrenaline acts at a1- adrenoceptors, which are the a1A-adrenoceptor subtype, to contract the smooth muscle in the prostrate capsule.
The effects of adrenaline released from adrenal medulla include those on the lung, where the tracheal and bronchial smooth muscle contains b2-adrenoceptors, and adrenaline stimulates these to cause bronchodilation. The bronchial glands also have b2-adrenoceptors, and stimulation of these receptors leads to a decrease in secretions.
On the eye, adrenaline may act at b2-adrenoceptors on ciliary epithelium to increase aqueous humour formation.
Adrenaline has some major effects on metabolism. On the liver, adrenaline stimulates β2-adrenoceptors to activate the enzyme glycogen phosphorylase which catalyses glycogenolysis, which is the breakdown of glycogen to glucose. Also on the liver, adrenaline stimulates β2-adrenoceptors to promote the process of gluconeogenesis, which is the conversion of amino acids to glucose.
These effects of noradrenaline and adrenaline can be mimicked by drugs known as sympathomimetics, or inhibited by antagonists at the adrenoceptors, the adrenoceptor antagonists.
Figure 7.3 Noradrenaline on cardiovascular system
Noradrenaline stimulates the β1-adrenoceptors of the sino-atrial node (pacemaker region of the atria) to increase the heart rate. Noradrenaline also stimulates the β1-adrenoceptors of the ventricles to increase the force at which the heart beats. This combination of increased heart rate and increased heart force leads to an increase in the cardiac output. On release from the sympathetic nervous system, noradrenaline also stimulates the α1-adrenoceptors on the blood vessels. On the veins, noradrenaline causes venoconstriction, and noradrenaline also constricts the arterioles in the skin and mucous membranes. The noradrenaline β1-adrenoceptor-induced increase in cardiac output and α1-adrenoceptor-mediated vasoconstriction combine to give an increase in blood pressure.
Adrenaline released from the adrenal medulla part of the sympathetic nervous system also has effects on the cardiovascular system. The effects of adrenaline on the cardiovascular system are different to those of noradrenaline, and also depend on the concentration of adrenaline. Low concentrations of adrenaline stimulate a-adrenoceptors on arterioles in the skin and mucous membranes to cause vasoconstriction, which is similar to noradrenaline. But in contrast to noradrenaline, adrenaline also stimulates b2-adrenoceptors on blood vessels in skeletal muscle and coronary arteries to cause vasodilation. This mix of vasodilation and vasoconstriction with adrenaline means there may be no effect overall on blood pressure. Instead, with adrenaline, there is a redistribution of blood from cutaneous vessels to heart and skeletal muscle. Low concentrations of adrenaline have little effect on the heart.
With higher concentrations of adrenaline, the fight or flight response is observed. These responses are similar to those observed when adrenaline is being used as drug, as the higher concentrations of adrenaline are used as a medicine. With the higher concentration of adrenaline, all of the effects observed with low concentrations of adrenaline persist and may intensify, plus a more pronounced effect on heart is observed. High concentrations of adrenaline stimulate the cardiac b1- adrenoceptors to induce a racey heart, a high heart rate.
Sympathetic nerves innervate the kidney, and when these nerves are activated, noradrenaline is released and acts on β1-adrenoceptors to induce the secretion of renin into the blood stream (Figure 7.4). Once renin has been secreted the hormones angiotensin II and aldosterone are formed and carried in the blood stream.
The effects of the sympathetic nervous system are exerted on most end organs/systems. The discussion of effects given here is limited to those we modify commonly with drugs, and we need to know these to understand how the drugs work. On the cardiovascular system, activation of the sympathetic nervous system leads to the release of noradrenaline that goes on to stimulate the β1-adrenoceptors of the heart and the α1-adrenoceptors on the blood vessels (Figure 7.3).
