Acute metabolic effects of clonidine and adenosine in man

Arthur L Swislocki, R. E. Vestal, G. M. Reaven, B. B. Hoffman

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Insulin resistance may contribute to non-insulin-dependent diabetes mellitus, hypertension, and dyslipidemia; increased free fatty acid concentrations could both promote and maintain this state of insulin resistance. Therefore, agents that inhibit lipolysis and decrease plasma concentrations of free fatty acids could be of therapeutic interest. We have measured metabolic effects of clonidine, an alpha2 adrenergic agonist, and adenosine in healthy human subjects since human fat cells have alpha2 and adenosine A1 receptors, which inhibit lipolysis in vitro. Clonidine, as expected, significantly lowered systolic and diastolic blood pressure; clonidine also decreased the plasma concentration of free fatty acids. Although clonidine caused a transient mild increase in plasma glucose, insulin and triglyceride concentrations were unchanged. The metabolic effects of adenosine were examined with two protocols. In the first study, volunteers received a graded infusion of adenosine (at 0, 10, 20, 50 and 100 ug/kg · min, for 30 min/dose), and glucose, insulin, free fatty acids, as well as respiratory rate, systolic and diastolic blood pressures, and heart rate were measured. There was no change in glucose, insulin, or free fatty acid concentrations. In the second study a graded infusion was used and was maintained at 100 ug/kg/min for 120 minutes. Heart rate and respiratory rate significantly increased. Glucose and free fatty acid concentrations were unchanged, while insulin concentrations were significantly increased. All subjects had significant symptomatic complaints (dyspnea, chest pressure) during the adenosine infusion. We conclude that while clonidine lowered free fatty acids and increased plasma glucose, we were unable to demonstrate an effect of adenosine on circulating free fatty acids and glucose, despite doses that were sufficient to provoke hemodynamic and symptomatic changes.

Original languageEnglish (US)
Pages (from-to)90-95
Number of pages6
JournalHormone and Metabolic Research
Volume25
Issue number2
StatePublished - 1993
Externally publishedYes

Fingerprint

Clonidine
Nonesterified Fatty Acids
Adenosine
Insulin
Glucose
Blood Pressure
Plasmas
Lipolysis
Blood pressure
Respiratory Rate
Insulin Resistance
Adrenergic alpha-2 Receptor Agonists
Heart Rate
Adenosine A1 Receptors
Hemodynamics
Medical problems
Dyslipidemias
Adipocytes
Dyspnea
Type 2 Diabetes Mellitus

Keywords

  • adenosine
  • clonidine
  • fatty acids
  • hypertension therapy
  • insulin

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

Cite this

Swislocki, A. L., Vestal, R. E., Reaven, G. M., & Hoffman, B. B. (1993). Acute metabolic effects of clonidine and adenosine in man. Hormone and Metabolic Research, 25(2), 90-95.

Acute metabolic effects of clonidine and adenosine in man. / Swislocki, Arthur L; Vestal, R. E.; Reaven, G. M.; Hoffman, B. B.

In: Hormone and Metabolic Research, Vol. 25, No. 2, 1993, p. 90-95.

Research output: Contribution to journalArticle

Swislocki, AL, Vestal, RE, Reaven, GM & Hoffman, BB 1993, 'Acute metabolic effects of clonidine and adenosine in man', Hormone and Metabolic Research, vol. 25, no. 2, pp. 90-95.
Swislocki, Arthur L ; Vestal, R. E. ; Reaven, G. M. ; Hoffman, B. B. / Acute metabolic effects of clonidine and adenosine in man. In: Hormone and Metabolic Research. 1993 ; Vol. 25, No. 2. pp. 90-95.
@article{fa5862711feb4b65ac6ce7ab122a5930,
title = "Acute metabolic effects of clonidine and adenosine in man",
abstract = "Insulin resistance may contribute to non-insulin-dependent diabetes mellitus, hypertension, and dyslipidemia; increased free fatty acid concentrations could both promote and maintain this state of insulin resistance. Therefore, agents that inhibit lipolysis and decrease plasma concentrations of free fatty acids could be of therapeutic interest. We have measured metabolic effects of clonidine, an alpha2 adrenergic agonist, and adenosine in healthy human subjects since human fat cells have alpha2 and adenosine A1 receptors, which inhibit lipolysis in vitro. Clonidine, as expected, significantly lowered systolic and diastolic blood pressure; clonidine also decreased the plasma concentration of free fatty acids. Although clonidine caused a transient mild increase in plasma glucose, insulin and triglyceride concentrations were unchanged. The metabolic effects of adenosine were examined with two protocols. In the first study, volunteers received a graded infusion of adenosine (at 0, 10, 20, 50 and 100 ug/kg · min, for 30 min/dose), and glucose, insulin, free fatty acids, as well as respiratory rate, systolic and diastolic blood pressures, and heart rate were measured. There was no change in glucose, insulin, or free fatty acid concentrations. In the second study a graded infusion was used and was maintained at 100 ug/kg/min for 120 minutes. Heart rate and respiratory rate significantly increased. Glucose and free fatty acid concentrations were unchanged, while insulin concentrations were significantly increased. All subjects had significant symptomatic complaints (dyspnea, chest pressure) during the adenosine infusion. We conclude that while clonidine lowered free fatty acids and increased plasma glucose, we were unable to demonstrate an effect of adenosine on circulating free fatty acids and glucose, despite doses that were sufficient to provoke hemodynamic and symptomatic changes.",
keywords = "adenosine, clonidine, fatty acids, hypertension therapy, insulin",
author = "Swislocki, {Arthur L} and Vestal, {R. E.} and Reaven, {G. M.} and Hoffman, {B. B.}",
year = "1993",
language = "English (US)",
volume = "25",
pages = "90--95",
journal = "Hormone and Metabolic Research",
issn = "0018-5043",
publisher = "Georg Thieme Verlag",
number = "2",

}

TY - JOUR

T1 - Acute metabolic effects of clonidine and adenosine in man

AU - Swislocki, Arthur L

AU - Vestal, R. E.

AU - Reaven, G. M.

AU - Hoffman, B. B.

PY - 1993

Y1 - 1993

N2 - Insulin resistance may contribute to non-insulin-dependent diabetes mellitus, hypertension, and dyslipidemia; increased free fatty acid concentrations could both promote and maintain this state of insulin resistance. Therefore, agents that inhibit lipolysis and decrease plasma concentrations of free fatty acids could be of therapeutic interest. We have measured metabolic effects of clonidine, an alpha2 adrenergic agonist, and adenosine in healthy human subjects since human fat cells have alpha2 and adenosine A1 receptors, which inhibit lipolysis in vitro. Clonidine, as expected, significantly lowered systolic and diastolic blood pressure; clonidine also decreased the plasma concentration of free fatty acids. Although clonidine caused a transient mild increase in plasma glucose, insulin and triglyceride concentrations were unchanged. The metabolic effects of adenosine were examined with two protocols. In the first study, volunteers received a graded infusion of adenosine (at 0, 10, 20, 50 and 100 ug/kg · min, for 30 min/dose), and glucose, insulin, free fatty acids, as well as respiratory rate, systolic and diastolic blood pressures, and heart rate were measured. There was no change in glucose, insulin, or free fatty acid concentrations. In the second study a graded infusion was used and was maintained at 100 ug/kg/min for 120 minutes. Heart rate and respiratory rate significantly increased. Glucose and free fatty acid concentrations were unchanged, while insulin concentrations were significantly increased. All subjects had significant symptomatic complaints (dyspnea, chest pressure) during the adenosine infusion. We conclude that while clonidine lowered free fatty acids and increased plasma glucose, we were unable to demonstrate an effect of adenosine on circulating free fatty acids and glucose, despite doses that were sufficient to provoke hemodynamic and symptomatic changes.

AB - Insulin resistance may contribute to non-insulin-dependent diabetes mellitus, hypertension, and dyslipidemia; increased free fatty acid concentrations could both promote and maintain this state of insulin resistance. Therefore, agents that inhibit lipolysis and decrease plasma concentrations of free fatty acids could be of therapeutic interest. We have measured metabolic effects of clonidine, an alpha2 adrenergic agonist, and adenosine in healthy human subjects since human fat cells have alpha2 and adenosine A1 receptors, which inhibit lipolysis in vitro. Clonidine, as expected, significantly lowered systolic and diastolic blood pressure; clonidine also decreased the plasma concentration of free fatty acids. Although clonidine caused a transient mild increase in plasma glucose, insulin and triglyceride concentrations were unchanged. The metabolic effects of adenosine were examined with two protocols. In the first study, volunteers received a graded infusion of adenosine (at 0, 10, 20, 50 and 100 ug/kg · min, for 30 min/dose), and glucose, insulin, free fatty acids, as well as respiratory rate, systolic and diastolic blood pressures, and heart rate were measured. There was no change in glucose, insulin, or free fatty acid concentrations. In the second study a graded infusion was used and was maintained at 100 ug/kg/min for 120 minutes. Heart rate and respiratory rate significantly increased. Glucose and free fatty acid concentrations were unchanged, while insulin concentrations were significantly increased. All subjects had significant symptomatic complaints (dyspnea, chest pressure) during the adenosine infusion. We conclude that while clonidine lowered free fatty acids and increased plasma glucose, we were unable to demonstrate an effect of adenosine on circulating free fatty acids and glucose, despite doses that were sufficient to provoke hemodynamic and symptomatic changes.

KW - adenosine

KW - clonidine

KW - fatty acids

KW - hypertension therapy

KW - insulin

UR - http://www.scopus.com/inward/record.url?scp=0027475759&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027475759&partnerID=8YFLogxK

M3 - Article

VL - 25

SP - 90

EP - 95

JO - Hormone and Metabolic Research

JF - Hormone and Metabolic Research

SN - 0018-5043

IS - 2

ER -