Metabolic Effects of Salbutamol Infusion During Premature Labour

Thomas, D. J. B.; Dove, A F; Alberti, K. G. M. M.

doi:10.1111/j.1471-0528.1977.tb12632.x

Cited by 49 publications

(19 citation statements)

References 7 publications

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“…57,58 The observed rise in blood pressure is thought to be because of vascular ␤ 2 and/or cardiac ␤ 1 receptor-mediated actions, whereas the fall in serum potassium has been attributed to cellular influx related to changes in glucose and insulin metabolism. 59 Our work, however, suggests a potential alternate and/or additional effect related to ALDO.…”

Section: Discussionmentioning

confidence: 99%

β-2 Adrenergic Receptor Diplotype Defines a Subset of Salt-Sensitive Hypertension

et al. 2006

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Abstract-Two genetic variants of the ␤-2 adrenergic receptor, 46GϾA and 79CϾG, affect agonist-mediated receptor downregulation and vascular reactivity. We determined whether these variants were associated with hypertension, per se, blood pressure response to dietary sodium, 2 forms of salt-sensitive hypertension (low renin and nonmodulation), and the activity of the renin-angiotensin-aldosterone system. Included are 280 hypertensive and 65 normotensive white subjects who had the 2 ␤-2 adrenergic receptor genotypes available. Of all subjects, 171 hypertensive and 48 normotensive subjects had complete data for intermediate phenotyping and blood pressure evaluation on high-and low-sodium balance. The ␤-2 adrenergic receptor variants were not associated with hypertension per se. However, among hypertensive subjects, the change (from low to high sodium balance) in mean arterial pressure differed significantly by genotype and by diplotype. Compared with all of the other diplotypes combined, 46AA/79CC was associated with a greater change in blood pressure. Furthermore, this diplotype was associated with low-renin (LR) hypertension (identifying 32% of the LR hypertensives), higher plasma aldosterone, and lower plasma renin and serum potassium levels. In conclusion, the 46AA/79CC diplotype is associated with greater blood pressure response to dietary sodium and higher odds of LR hypertension. We propose that the mechanism for the observed association is inadequate suppression of aldosterone with salt intake, implicating the ␤-2 adrenergic receptor in the regulation of aldosterone secretion. This hypothesis was confirmed in isolated glomerulosa cells, where ␤-2 adrenergic receptor stimulation increased aldosterone secretion, whereas blockade reduced the stimulated aldosterone response. Key Words: ␤-2 adrenergic receptor Ⅲ hypertension Ⅲ salt-sensitive hypertension Ⅲ low-renin hypertension Ⅲ single nucleotide polymorphisms Ⅲ haplotypes Ⅲ diplotypes T he ␤ 2 -adrenergic receptor (␤ 2 AR) is generally thought to influence blood pressure homeostasis through sympathetic nervous system-mediated effects on vascular tone and cardiac contractility. 1 The ␤ 2 AR gene is located on the distal segment of the long arm of chromosome 5 (5q33.3 to 34); this region has been identified as a susceptibility locus for blood pressure and hypertension in several genome-wide scans. [2][3][4][5] Two common, nonsynonymous, coding single nucleotide polymorphisms (SNPs) from this gene, 46GϾA (Gly16Arg) and 79CϾG (Gln27Glu), have been shown to affect agonistmediated receptor desensitization and downregulation, 6 -8 as well as vascular reactivity. 9 -11 Because of these findings, these and other polymorphisms in the ␤ 2 AR gene have been extensively investigated in linkage and association studies with human hypertension, with conflicting results. 10 -24 As has been observed with other complex diseases, conflicting findings have been the norm in genetic studies of hypertension, particularly when a distant phenotype (eg, hypertension) has been used. 25...

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Section: Discussionmentioning

confidence: 99%

β-2 Adrenergic Receptor Diplotype Defines a Subset of Salt-Sensitive Hypertension

et al. 2006

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“…The increase in free fatty acid concentrations and hepatic ketogenesis might be even greater in patients with decreased insulin reserve and those receiving drugs which increase lipolysis such as theophylline or steroids (Robinson, Butcher & Sutherland, 1968). Furthermore, labour and asthma may be associated with increased free fatty acid (Thomas, Dove, et al, 1977) and lactate concentrations (Kashyap, Sivisamboo, Soothy, Cheah & Gartside, 1976). It is not surprising therfore that lactic acidosis Chapman, 1977) and ketoacidosis have been reported in patients receiving /2 agonists.…”

Section: Methodsmentioning

confidence: 99%

“…The lack of electrocardiographic changes attributable to hypokalaemia may be explained by the normal cell potassium content (Surawicz, 1967). In patients with premature labour receiving salbutamol, hypokalaemia persists for many hours (Thomas, Dove, et al, 1977) and in asthmatics it might be expected to predispose to arrhythmias especially when combined with stress, hypoxia, acidosis and drugs which might include theophylline and digoxin. The initial decrease in plasma phosphate may be caused by cellular uptake mediated by insulin (Lindsay, 1976).…”

Section: Methodsmentioning

confidence: 99%

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Metabolic and cardiovascular side effects of the beta 2‐adrenoceptor agonists salbutamol and rimiterol.

Phillips¹,

Vedig²,

Jones³

et al. 1980

Brit J Clinical Pharma

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The metabolic and cardiovascular side‐effects of intravenous infusions of therapeutic doses of beta 2‐adrenoceptor agonists salbutamol and rimiterol have been determined in four healthy male subjects. There were dose‐related increases in plasma glucose, renin activity, serum insulin and heart rate, and significant hyperlactataemia and ketonaemia. There were dose‐related decreases in plasma potassium, phosphate and corticosteroids and significant hypocalcaemia and hypomagnesaemia. The effects of equivalent molar amounts of salbutamol and rimiterol were similar. Whichever drug is used, special care is required with patients who may have abnormal glucose tolerance, potassium depletion, or be predisposed to lactic acidosis. Rimiterol may be preferable for infusion because of its short plasma half‐life.

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“…Several alterations in fetal and maternal glucose homeostasis may be related to this development. Maternal and fetal hyperglycemia has been reported to develop with the administration of B sympathomimetics to women [18,26]. The increase in fetal glucose may be a direct drug effect upon the fetus äs suggested by the observation that fetal hyperglycemia develops during infusion of fenoterol directly to the sheep fetus [6].…”

Section: Introductionmentioning

confidence: 99%

Isoxsuprine Infusion in the rat: Alterations in maternal, fetal and neonatal glucose homeostasis

Ogata¹

1981

Journal of Perinatal Medicine

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Metabolic Effects of Salbutamol Infusion During Premature Labour

Cited by 49 publications

References 7 publications

β-2 Adrenergic Receptor Diplotype Defines a Subset of Salt-Sensitive Hypertension

β-2 Adrenergic Receptor Diplotype Defines a Subset of Salt-Sensitive Hypertension

Metabolic and cardiovascular side effects of the beta 2‐adrenoceptor agonists salbutamol and rimiterol.

Isoxsuprine Infusion in the rat: Alterations in maternal, fetal and neonatal glucose homeostasis

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