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       SNS stimulation increases cardiac contractility and systemic vascular resistance, which usually causes the arterial pressure to increase greatly.

       PNS stimulation decreases cardiac contractility, but has virtually no effect on systemic vascular resistance.

       The usual effect of PNS stimulation is a slight fall in pressure.

       Arterial baroreceptors are stretch receptors located in the carotid sinus and aortic arch to detect changes in arterial blood pressure.

       When arterial blood pressure increases, arterial baroreceptors are stretched and signals are transmitted to the brain stem, which inhibit the SNS impulses to the heart and blood vessels, and increase vagal tone on the SA node of the heart, which results in bradycardia to correct the increase in pressure (baroreceptor reflex).

       When arterial blood pressure decreases, arterial baroreceptors sense the decrease in tension and signal the vasomotor center to facilitate SNS activity in the heart and blood vessels and decrease vagal tone, causing an increase in heart rate to correct the decrease in pressure.

       Venous baroreceptors, located in the right atrium and great veins, increase heart rate when the right atrium is stretched by increased filling pressure (Bainbridge reflex).

       Muscarinic receptors mediate bronchoconstriction and increase mucus secretion.

       β2 receptors mediate bronchial smooth muscle relaxation and increase mucus secretion (see Table 7.2).

       Adrenergic agonists include vasopressors (e.g. phenylephrine) and inotropes (e.g. dobutamine).

       Most adrenergic agonists activate both α and β receptors, with the predominant pharmacologic effect being the expression of this mixed receptor activation (see Table 7.3).Table 7.2 Comparative pharmacology of selective β2 adrenergic bronchodilators.Agentβ2 selectivityPeak effect (minutes)Duration of action (hours)Albuterol+++++30–604Metaproterenol+++30–603–4Terbutaline++++604Salmeterol++++60>12Clenbuterol++++30–608–12Table 7.3 Principal sites of action of adrenergic agonists.Agentα1α2β1β2DA1DA2MechanismPhenylephrine+++++?±000directNorepinephrine+++++++++++++000directEpinephrine+++++++++++++++00directEphedrine++?+++++00indirect + directDopamine+ to +++++?+++++00directDobutamine±?++++++00directIsoproterenol00++++++++++00direct+ = increase, − = decrease, 0 = no change.

       Hemodynamic effects evoked by adrenergic agonists include changes in heart rate (chronotropism), cardiac contractility (inotropism), conduction velocity of the cardiac impulse (dromotropism), cardiac rhythm, and systemic vascular resistance (see Table 7.4).

       The effects of these drugs on capacitance veins (venous return) may be as important as their inotropic actions and more important than arteriolar effects.

       Certain drugs have an indirect sympathomimetic action, rather than directly exciting adrenergic effector organs, and cause release of NE from its storage vesicles in the SNS nerve endings (e.g. ephedrine).

       These drugs inhibit acetylcholinesterase, preventing rapid destruction of ACh so that it accumulates at muscarinic and nicotinic receptors.

       Neostigmine and edrophonium are mainly used for reversal of non‐depolarizing neuromuscular blockade (nicotinic effect). Neostigmine has also been administered parenterally to promote GI motility in horses.

       Simultaneous administration of an anticholinergic prevents unwanted muscarinic signs (bradycardia, salivation, bronchospasm, intestinal hypermotility) without preventing the nicotinic effects of ACh.

       These drugs block the action of ACh on the muscarinic type of cholinergic effector organs, but do not affect the nicotinic action of ACh on the postganglionic neurons or on skeletal muscle (e.g. atropine, glycopyrrolate).