Isoproterenol and propranolol: ability to cross the blood-brain barrier and effects on cerebral circulation in man.

Olesen, Jes; Hougård, K; Hertz, Marianne M.

doi:10.1161/01.str.9.4.344

Cited by 79 publications

(39 citation statements)

References 26 publications

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“…In the pheochromocytoma-positive patient group, there was no significant correlation between anxiety, as measured by four standard scales, and plasma NE or E levels. Somatic symptoms, however, were correlated with plasma E levels, which is consonant with our knowledge of the peripheral effects of E. Since systemic catecholamines do not cross the blood-brain barrier in physiologically significant amounts (23)(24)(25), these results suggest that increased peripheral catecholamines secreted by a source autonomous of nervous system control and stimulation are not sufficient to elicit severe anxiety as defined by DSM-III criteria in the majority of patients, even though considerable physical symptoms are experienced.…”

Section: Discussionsupporting

confidence: 76%

“…They do so autonomously and not through autonomic nervous system stimulation, responding instead to such stimuli as change in position. Since peripheral catecholamines do not appear to cross the blood-brain barrier in physiologically significant amounts (23)(24)(25), these patients provide an opportunity to study the effect of autonomously secreted elevated peripheral catecholamine levels on symptoms of anxiety. The second group of subjects were patients with hypertension and/or elevated catecholamine levels, who were initially suspected of having a pheochromocytoma but were subsequently shown not to have such a tumor.…”

Section: Introductionmentioning

confidence: 99%

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Peripheral catecholamine levels and the symptoms of anxiety: studies in patients with and without pheochromocytoma.

Starkman

Cameron

Nesse³

et al. 1990

Psychosomatic Medicine

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We studied the correlation of plasma and urinary epinephrine (E) and norepinephrine (NE) levels with anxiety symptoms in three patient groups: 1) pheochromocytoma (PH+) (n = 17); 2) hypertensives with elevated catecholamine levels shown not to have a PH (PH-) (n = 25); and 3) patients with panic disorder (PD) (n = 23). Structured interviews and four self-rated anxiety scales were used, the SCL-90R Anxiety and Phobic Anxiety scales, and the Spielberger State/Trait Anxiety Inventories. The SCL-90R Somatization scale (which measures 12 somatic symptoms) was also utilized. None of the PH+ patients met DSM-III criteria for PD. Two met criteria for generalized anxiety disorder (GAD). Of the PH-patients, two had PD, two had GAD. and three had both. Urinary and plasma E did not show significant positive correlations with any of the four anxiety scales in any of the three patient groups. In both the PH+ and PH-groups, E was significantly correlated with the SCL-90R Somatization scale. NE was not significantly correlated with any of the four anxiety scales in the PH+ group. In contrast, in the PH-group, plasma NE was significantly correlated with anxiety on all anxiety scales (r = +0.55 to +0.77, p < 0.05). Furthermore, in the PH-group, plasma NE was significantly correlated with those items of the SCL-90R Anxiety scale measuring the cognitive rather than the noncognitive symptoms of anxiety. In the PD group as well, plasma NE showed a significant correlation with the SCL-90R Anxiety Scale (r = +0.67, p < 0.05). Taken together, our observations suggest that: 1) the effects of catecholamines in the periphery derived from a source independent of nervous system control (such as a PH) are not sufficient to elicit an anxiety disorder meeting DSM-III criteria; and 2) in patients without an autonomous source of peripheral catecholamines, NE in the periphery results from sympathetic nervous system activation and probably reflects, rather than causes, anxiety.

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Section: Discussionsupporting

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Peripheral catecholamine levels and the symptoms of anxiety: studies in patients with and without pheochromocytoma.

Starkman

Cameron

Nesse³

et al. 1990

Psychosomatic Medicine

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“…Whereas blood glucose levels fell with sympathetic blockade, blood glucose levels following LPS treatment were similar in control, parasympathetic, and ganglionic blocker-treated mice. Propranolol crosses the bloodbrain barrier, whereas phentolamine, atropine, and chlorisondamine do not (34). Thus, propranolol delivery may have resulted in off-target effects in the brain.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-6 amplifies glucagon secretion: coordinated control via the brain and pancreas

Barnes

Otero

Elliott

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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Barnes TM, Otero YF, Elliott AD, Locke AD, Malabanan CM, Coldren AG, Brissova M, Piston DW, McGuinness OP. Interleukin-6 amplifies glucagon secretion: coordinated control via the brain and pancreas. Am J Physiol Endocrinol Metab 307: E896 -E905, 2014. First published September 9, 2014; doi:10.1152/ajpendo.00343.2014.-Inappropriate glucagon secretion contributes to hyperglycemia in inflammatory disease. Previous work implicates the proinflammatory cytokine interleukin-6 (IL-6) in glucagon secretion. IL-6-KO mice have a blunted glucagon response to lipopolysaccharide (LPS) that is restored by intravenous replacement of IL-6. Given that IL-6 has previously been demonstrated to have a transcriptional (i.e., slow) effect on glucagon secretion from islets, we hypothesized that the rapid increase in glucagon following LPS occurred by a faster mechanism, such as by action within the brain. Using chronically catheterized conscious mice, we have demonstrated that central IL-6 stimulates glucagon secretion uniquely in the presence of an accompanying stressor (hypoglycemia or LPS). Contrary to our hypothesis, however, we found that IL-6 amplifies glucagon secretion in two ways; IL-6 not only stimulates glucagon secretion via the brain but also by direct action on islets. Interestingly, IL-6 augments glucagon secretion from both sites only in the presence of an accompanying stressor (such as epinephrine). Given that both adrenergic tone and plasma IL-6 are elevated in multiple inflammatory diseases, the interactions of the IL-6 and catecholaminergic signaling pathways in regulating GCG secretion may contribute to our present understanding of these diseases. glucagon; inflammation; interleukin-6; hypoglycemia; endotoxemia INFLAMMATORY DISEASE CAUSES PROFOUND ALTERATIONS in glucose homeostasis and accompanying insulin resistance. Exquisite control of insulin (INS) and glucagon (GCG) secretion from the pancreas maintains euglycemia in healthy individuals (56). However, this balance is altered in inflammatory disease. The bulk of glucoregulatory research has focused on the INS side of the story for some years, whereas less research has focused on therapies to attenuate GCG secretion or action. Demonstrating the importance of GCG, hyperglycemia associated with INS deficiency does not manifest in the absence of GCGdependent signaling in rodent models of diabetes (52). Moreover, in models of type 2 diabetes, inhibition of GCG also improves glucose homeostasis (44). Although diabetes and acute or chronic inflammation are vastly different in etiology and pathology, they have some similarities; hyperglycemia is associated with either a rise in absolute levels of GCG or in the ratio of GCG to INS as well as in proinflammatory cytokines.

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“…Propranolol crosses the blood-brain barrier rapidly. 11 Thus, full pharmacological effect on the brain can be expected at the time of the study, because propranolol had been infused over a period of 1 hour. Propranolol per se has only little, if any, effect on baseline CBF.…”

Section: Discussionmentioning

confidence: 99%

Activation-Induced Resetting of Cerebral Metabolism and Flow Is Abolished by β-Adrenergic Blockade With Propranolol

Schmalbruch

Linde

Paulson

et al. 2002

Stroke

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Background and Purpose-It has previously been shown that activation will increase cerebral blood flow (CBF) and cerebral glucose uptake (CMR glc ) in excess of cerebral oxygen uptake (CMRO 2 ).Our purpose was to investigate the influence of ␤-adrenergic blockade with propranolol on the activation-induced uncoupling of cerebral glucose and oxygen metabolism. Methods-Using awake rats, we determined the cerebral arteriovenous differences of oxygen [(aϪv) and lactate [(aϪv) lac ] both under baseline conditions and during activation. The molar ratio between CMRO 2 and CMR glc , the oxygen-glucose index (OGI), was calculated. Results-Without ␤-adrenergic blockade, activation decreased the (aϪv) O2 but not the (aϪv) glc , reducing the OGI from 6.1 during baseline conditions to 4.0 under activation (PϽ0.01). The (aϪv) O2 decreased, indicating that the ratio CBF/CMRO 2 had increased. Under baseline conditions, a slight flux of lactate from the brain was observed. Activation increased the arterial lactate concentration, and during this condition, the lactate flux from the brain was reversed into a slight lactate uptake. Propranolol administration did not change the behavior of the animals during activation. After administration of propranolol, baseline values were unaffected, but ␤-adrenergic blockade totally abolished the activation-induced uncoupling of (aϪv) O2 from (aϪv) glc , because both remained constant with an unchanged OGI. The unchanged (aϪv) O2 indicates that CBF remained unchanged compared with CMRO 2 . Conclusions-␤-Adrenergic

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Isoproterenol and propranolol: ability to cross the blood-brain barrier and effects on cerebral circulation in man.

Cited by 79 publications

References 26 publications

Peripheral catecholamine levels and the symptoms of anxiety: studies in patients with and without pheochromocytoma.

Peripheral catecholamine levels and the symptoms of anxiety: studies in patients with and without pheochromocytoma.

Interleukin-6 amplifies glucagon secretion: coordinated control via the brain and pancreas

Activation-Induced Resetting of Cerebral Metabolism and Flow Is Abolished by β-Adrenergic Blockade With Propranolol

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