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*Not currently available in the United States, where most are under investigation for use.

*Not currently available in the United States, where most are under investigation for use.

Vasodilation

FIGURE 10-4 Mechanisms underlying actions of vasodilating ft blockers in blood vessels. ROS, reactive oxygen species; sGC, soluble guanylyl cyclase; AC, adenylyl cyclase; L-type VGCC, L-type voltage-gated Ca2+ channel.

Vasodilation

FIGURE 10-4 Mechanisms underlying actions of vasodilating ft blockers in blood vessels. ROS, reactive oxygen species; sGC, soluble guanylyl cyclase; AC, adenylyl cyclase; L-type VGCC, L-type voltage-gated Ca2+ channel.

Propranolol and other nonselective b receptor antagonists inhibit the vasodilation caused by isoproterenol and augment the pressor response to Epi. This action is significant in patients with pheochromocytoma, in whom b receptor antagonists should be used only after adequate a receptor blockade has been established. This sequence avoids uncompensated a receptor-mediated vasoconstriction caused by catecholamines secreted by the tumor.

PULMONARY SYSTEM Nonselective b receptor antagonists such as propranolol block b2 receptors in bronchial smooth muscle, with little effect on pulmonary function in normal individuals. In patients with COPD, such blockade can lead to life-threatening bronchoconstriction. Although bj-selective antagonists or antagonists with intrinsic sympathomimetic activity are less likely than propranolol to increase airway resistance, these drugs should be used only with great caution, if at all, in patients with bronchospastic diseases. Drugs with bj selectivity and b2 receptor partial agonism (e.g., celiprolol) have potential here, although clinical experience is limited.

METABOLIC EFFECTS Catecholamines promote glycogenolysis and mobilize glucose in response to hypoglycemia. Nonselective b blockers blunt these responses and may delay recovery from hypoglycemia in type 1 (insulin-dependent) diabetes mellitus, but infrequently in type 2 diabetes mellitus. b receptor antagonists can interfere with the counterregulatory effects of cate-cholamines secreted during hypoglycemia by blunting the perception of symptoms such as tremor, tachycardia, and nervousness. Thus, b adrenergic receptor antagonists should be used with great caution in patients with labile diabetes and frequent hypoglycemic reactions; if a b antagonist must be used, a ^-selective antagonist is preferred. In contrast to classical b blockers, which decrease insulin sensitivity, the vasodilating b receptor antagonists increase insulin sensitivity in patients with insulin resistance.

b Receptor antagonists can reduce activation of hormone-sensitive lipase and attenuate the release of free fatty acids from adipose tissue. Nonselective b receptor antagonists consistently reduce HDL cholesterol, increase LDL cholesterol, and increase triglycerides. In contrast, bj-selective antagonists improve the serum lipid profile of dyslipidemic patients. Propranolol and atenolol increase triglycerides, whereas chronic celiprolol, carvedilol, and carteolol reduce plasma triglycerides.

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