Материал: 2016_Kaplan_USMLE_Step_1_Lecture_Notes_Pharmacology

SOMATIC

Bridge to Physiology

For a more detailed discussion, see Section II, Chapter 2, in Physiology.

Neurotransmitters

λAcetylcholine (ACh) is the neurotransmitter at both nicotinic and muscarinic receptors in tissues that are innervated. Note that all direct transmission from the CNS (preganglionic and motor) uses ACh, but postganglionic transmission in the SANS system may use one of the organ-specific transmitters described below.

λNorepinephrine (NE) is the neurotransmitter at most adrenoceptors in organs, as well as in cardiac and smooth muscle.

λDopamine (DA) activates D1 receptors, causing vasodilation in renal and mesenteric vascular beds.

λEpinephrine (E, from adrenal medulla) activates most adrenoceptors and is transported in the blood.

BLOOD PRESSURE CONTROL MECHANISMS

Autonomic Feedback Loop

λBlood pressure is the product of total peripheral resistance (TPR) and cardiac output (CO).

λBoth branches of the ANS are involved in the autonomic (or neural) control of blood pressure via feedback mechanisms.

λChanges in mean blood pressure are detected by baroreceptors, which relay information to the cardiovascular centers in the brainstem controlling PANS and SANS outflow. For example, an increase in mean blood

Chapter 1 λ

pressure elicits baroreceptor discharge, resulting in increased PANS activity, leading to bradycardia and decreased SANS activity, which leads, in turn, to decreased heart rate, force of contraction, and vasoconstriction. The resulting decreases in cardiac output and total peripheral resistance

vasoconstriction

B P = T P R ×C O

C O = H R ×S V

Figure II-1-2. Autonomic Feedback Loop

Hormonal Feedback Loop

λBlood pressure is also regulated via the hormonal feedback loop shown in Figure II-1-3.

λThe system is affected only by decreases in mean blood pressure (hypotension), which result in decreased renal blood flow.

λDecreased renal pressure causes the release of renin, which promotes formation of the angiotensins.

λAngiotensin II increases aldosterone release from the adrenal cortex, which, via its mineralocorticoid actions to retain sodium and water, increases blood volume.

λIncreased venous return results in an increase in cardiac output.

λAngiotensin II also causes vasoconstriction, resulting in an increase in TPR.

The Autonomic Nervous System (ANS)

Note

Baroreceptor reflexes can be blocked at the ganglionic synapse with NN receptor antagonists. Alternatively, a reflex bradycardia can be blocked with muscarinic antagonists; a reflex tachycardia can be blocked with β1 antagonists.

Note

Antihypertensive Drugs

Both the ANS (neural) and endocrine feedback loops are invoked when patients are treated with antihypertensive drugs. Such

compensatory mechanisms may result in tachycardia and both salt and water retention.

Muscarinic stimulation

1.Miosis

2.Accommodation (near vision)

Muscarinic antagonism

1.Mydriasis

2.Accommodation to far vision, leading to cycloplegia (paralysis of accommodation)

α1-agonists

1.Mydriasis

2.No cycloplegia