Cholinergic Manifestations of the Acute Autonomic Reaction to Hypoglycaemia in Man

Corrall, R. J. M.; Frier, B M; Davidson, Neil; Hopkins, W. M.; French, E. B.

doi:10.1042/cs0640049

Cited by 43 publications

(29 citation statements)

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“…In our study sweating, a sympathetic cholinergic response to hypoglycaemia (Corrall et al, 1983), was enhanced by pre-treatment with all three P-adrenoceptor blockers probably as a result of increased at-adrenoceptor stimulation (Foster et al, 1971) from higher plasma levels of adrenaline. Both subjective and objective enhancement of sweating during hypoglycaemia have been reported previously in normal subjects and diabetic patients using propranolol (Abramson et al, 1966;Deacon & Barnett, 1976;Schluter et al, 1982) and metoprolol (Schluter et al, 1982;Viberti et al, 1980).…”

Section: Resultsmentioning

confidence: 76%

Beta‐adrenoceptor blockade and hypoglycaemia. A randomised, double‐ blind, placebo controlled comparison of metoprolol CR, atenolol and propranolol LA in normal subjects.

Kerr¹,

Macdonald²,

Heller³

et al. 1990

Brit J Clinical Pharma

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1. The effect of 1 week of treatment with propranolol LA (160 mg), atenolol (100 mg) and metoprolol CR (100 mg) on awareness of and the physiological responses to moderate hypoglycaemia were compared with placebo using a randomised, cross‐over design in 12 healthy volunteers. 2. All three beta‐adrenoceptor antagonists reduced resting heart rate, systolic blood pressure and heart rate responses to submaximal exercise compared with placebo. 3. Under hyperinsulinaemic (60 mu m‐2 min‐1) clamp conditions, at a blood glucose of 2.5 mmol l‐1, atenolol prevented the rise in systolic and atenolol and metoprolol CR prevented the fall in diastolic blood pressure usually associated with hypoglycaemia. At this level of hypoglycaemia, the expected increase in heart rate was inhibited by atenolol but not metoprolol CR. Pre‐ treatment with propranolol LA resulted in a significant pressor response and a bradycardia during hypoglycaemia. In addition the normal increase in finger tremor was abolished by propranolol LA. 4. During hypoglycaemia all three beta‐adrenoceptor blockers augmented sweating compared with placebo but hypoglycaemic symptoms, awareness and slowing of reaction time were the same with drugs and placebo. 5. The rise in plasma adrenaline and other counter‐regulatory hormones during hypoglycaemia was enhanced by beta‐adrenoceptor blockade. 6. We conclude that beta‐adrenoceptor antagonists modify the physiological and hormonal responses to, but do not adversely affect awareness of, moderate hypoglycaemia in healthy volunteers.

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Section: Resultsmentioning

confidence: 76%

Beta‐adrenoceptor blockade and hypoglycaemia. A randomised, double‐ blind, placebo controlled comparison of metoprolol CR, atenolol and propranolol LA in normal subjects.

Kerr¹,

Macdonald²,

Heller³

et al. 1990

Brit J Clinical Pharma

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“…Although a symptom such as palpitations might be attributable to circulating catecholamines, sweating, a prominent symptom, is at best partially explicable on this basis (32,33). It is largely attributable to sympathetic postganglionic cholinergic activation (32)(33)(34).…”

Section: Resultsmentioning

confidence: 99%

Glycemic thresholds for activation of glucose counterregulatory systems are higher than the threshold for symptoms.

Schwartz¹,

Clutter²,

Shah³

et al. 1987

J. Clin. Invest.

386

232

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To define glycemic thresholds for activation of glucose counterregulatory systems and for symptoms of hypoglycemia, we measured these during stepped reductions in the plasma glucose concentration (in six 10-mg/dl hourly steps) from 90 to 40 mg/dl under hyperinsulinemic clamp conditions, and compared these with the same measurements during euglycemia (90 mg/dl) under the same conditions over 6 h in 10 normal humans. Arterialized venous plasma glucose concentrations were used to calculate glycemic thresholds of 69±2 mg/dl for epinephrine secretion, 68±2 mg/dl for glucagon secretion, 66±2 mg/dl for growth hormone secretion, and 58±3 mg/dl for cortisol secretion. In contrast, the glycemic threshold for symptoms was 53±2 mg/dl, significantly lower than the thresholds for epinephrine (P < 0.001), glucagon (P < 0.001), and growth hormone (P < 0.01) secretion. Thus, the glycemic thresholds for activation of glucose counterregulatory systems during decrements in plasma glucose lie within or just below the physiologic plasma glucose concentration range, and are substantially higher than the threshold for hypoglycemic symptoms in normal humans. These findings provide further support for the concept that glucose counterregulatory systems are involved in the prevention, as well as the correction, of hypoglycemia.

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“…Based on the velocity of ophthalmic arterial flow (38) Attenuation in responses from both limbs of the autonomic nervous system was evident during our study. The glucose concentration required to cause epinephrine secretion (mediated by CNS sympathetic outflow) (4, 5), pancreatic polypeptide release (from vagally innervated PP cells in the pancreas) (39), and sweating (a postganglionic cholinergic event) (40) decreased from day 1 to day 4. Because many of the fundamental warning signs of incipient hypoglycemia (shakiness, heart pounding, nervousness, and sweating) are triggered by autonomic nervous system activation, subjects were dependent on neuroglycopenic symptoms to identify hypoglycemia.…”

Section: Discussionmentioning

confidence: 99%

Adaptation in brain glucose uptake following recurrent hypoglycemia.

Boyle

Nagy

O’Connor

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

202

160

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Brain glucose metabolism is impaired during hypoglycemia, but, if sined, brain metabolism reverts to normal in animal models-data in man are lacking. We tested the hypothesis that adaptations occur to allow maintenance of normal rates of brain gluc uptake (BGU) following recurrent hypoglycemia in man. Twelve normal humans were studied over 4 days. (6). Based on the preceding series of facts, we presume that in sustained human hypoglycemia, normal increments in epinephrine and glucagon will fail to occur, reflecting a normalization ofglucose availability to the brain secondary to improved glucose uptake.We tested the hypothesis that the systemic glucose concentration required to impair brain glucose uptake (BGU) would occur near the usual basal glucose concentration in nondiabetic subjects but that after 56 hr of interprandial hypoglycemia, BGU would remain normal even at very subbasal glucose levels. Further, we hypothesized that increments in counterregulatory hormones, symptoms of hypoglycemia, and impairment in cognitive functions tests would be delayed until critically low arterial glucose levels were reached after the period of interprandial hypoglycemia. METHODS 9352The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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Cholinergic Manifestations of the Acute Autonomic Reaction to Hypoglycaemia in Man

Cited by 43 publications

References 0 publications

Beta‐adrenoceptor blockade and hypoglycaemia. A randomised, double‐ blind, placebo controlled comparison of metoprolol CR, atenolol and propranolol LA in normal subjects.

Beta‐adrenoceptor blockade and hypoglycaemia. A randomised, double‐ blind, placebo controlled comparison of metoprolol CR, atenolol and propranolol LA in normal subjects.

Glycemic thresholds for activation of glucose counterregulatory systems are higher than the threshold for symptoms.

Adaptation in brain glucose uptake following recurrent hypoglycemia.

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