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Epinephrine blood pressure response

Figure 10-2. The effects of an alpha-blocker, eg, phentolamine, on the blood pressure responses to epinephrine and phenylephrine. The epinephrine response exhibits reversal of the mean blood pressure change from a net increase (the alpha response) to a net decrease (the beta response). The response to phenylephrine is suppressed but not reversed, because phenylephrine is a pure" alpha agonist without beta action. Figure 10-2. The effects of an alpha-blocker, eg, phentolamine, on the blood pressure responses to epinephrine and phenylephrine. The epinephrine response exhibits reversal of the mean blood pressure change from a net increase (the alpha response) to a net decrease (the beta response). The response to phenylephrine is suppressed but not reversed, because phenylephrine is a pure" alpha agonist without beta action.
Few studies have examined noradrenergic function in patients with phobic disorders. In patients with specific phobias, increases in subjective anxiety and increased heart rate, blood pressure, plasma NE, and epinephrine have been associated with exposure to the phobic stimulus (Nesse et al. 1985). This finding may be of interest from the standpoint of the model of conditioned fear, reviewed above, in which a potentiated release of NE occurs in response to a reexposure to the original stressful stimulus. Patients with social phobia have been found to have greater increases in plasma NE in comparison to healthy controls and patients with panic disorder (Stein et al. 1992). In contrast to panic disorder patients, the density of lymphocyte a-adrenoceptors is normal in social phobic patients (Stein et al. 1993). The growth hormone response to intravenous clonidine (a marker of central a2-receptor function) is blunted in social phobia patients (Tancer et al. 1990). [Pg.217]

A dose of 1 at 30 mg/kg increased the effects of intravenous doses of epinephrine at 5 g/kg and of dl-noreplnephrine at 10 ug/kg on both blood flow and blood pressure. Intravenous phenoxybenzamine at 15 mg/kg plus tolazollne at 2 mg/kg prevented almost completely the actions of I on blood pressure and blood flow Intravenous reserpine at 2 mg/kg increased markedly the effects of I at 30 mg/kg on blood pressure and peripheral resistance, but converted the usual immediate, small, temporary increase in blood flow into an immediate, small, temporary decrease. These various responses would be expected from either a mild sympathomimetic amine or an inhibitor of the breakdown of endogenous catecholamines Indeed, I at 10 M, was found to inhibit the monoamlneoxldase of the rat s liver. If the dose of I used in these experiments were distributed into the same fraction of the body water as that estimated for the human body,the concentration in the plasma would be about 9 times that stated above as the effective concentration for inhibiting the mono amine oxIdase. It is possible that inhibition of monoamlneoxldase by I plays a part in inducing the effects of the oxime on blood vessels and blood pressure. It is possible also that I interferes with reuptake of catecholamines by nerve endings this possibility seems not to have been explored. [Pg.290]

Top Effects of phentolamine, an a-receptor-blocking drug, on blood pressure in an anesthetized dog. Epinephrine reversal is demonstrated by tracings showing the response to epinephrine before (middle) and after (bottom) phentolamine. All drugs given intravenously. BP, blood pressure HR, heart rate. [Pg.200]

The action of epinephrine illustrates the principles by which cyclic AMP mediates hormone action. Epinephrine is the flight or fight hormone that the adrenal glands release in response to stress. The hormone causes an increase in blood pressure and the breakdown of... [Pg.126]

Despite the apparent importance of the adrenal medulla in homeostasis, particularly regulation of metabolism, the medulla in contrast to the adrenal cortex is not vital for survival. Studies in adrenalectomized subjects clearly show that both hemodynamic and glucose-counter-regulatory responses to insulin-hypoglycemia, exercise, and other manipulations remain intact despite absence of epinephrine responses. This contrasts with the severe disturbances of blood pressure regulation accompanying loss of sympathetic nerves. [Pg.1043]

Systemic adverse effects of epinephrine include headache, faintness, increased blood pressure, tachycardia, arrhythmias, tremor, pallor, anxiety, and increased perspiration. Epinephrine should be used with caution in patients with cardiovascular diseases, cerebrovascular diseases, aphakia, CAG, hyperthyroidism, and diabetes melhtus, as well as in patients undergoing anesthesia with halogenated hydrocarbon anesthetics. Using NLO with epinephrine and dipivefrin wiU improve therapeutic response and reduce the risk of systemic adverse effects. ... [Pg.1725]

The neurotransmitter agent that is normally released in the sinoatrial node of the heart in response to a blood pressure increase is (A) Acetylcholine Dopamine Epinephrine Glutamate N orepinephrine... [Pg.56]


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See also in sourсe #XX -- [ Pg.85 , Pg.117 ]




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