Chronic adrenergic receptor blockade does not prevent hyperinsulinemia-induced hypertension in rats

Henry L. Keen, Michael W. Brands, Magdalena Alonso-Galicia, John E. Hall

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Increased adrenergic activity has been suggested to mediate the hypertension associated with hyperinsulinemia. This study tested whether combined α1- and β-adrenergic receptor blockade would prevent insulin-induced hypertension when euglycemia was maintained by continuous intravenous glucose infusion. Sprague-Dawley rats (n = 16) were instrumented with artery and vein catheters and placed in metabolic cages. Propranolol and prazosin (10 mg/kg/day each) were infused continuously intravenously in 9 rats and 7 other rats received vehicle. Mean arterial pressure (MAP) and heart rate (HR) were measured 24 h per day using computerized methods. After a control period, a 7-day intravenous infusion of insulin (1.5 mU/kg/min) was begun and glucose was coadministered intravenously at 23 mg/kg/min to prevent hypoglycemia. The MAP averaged 93 ± 1 mm Hg in the blockade rats during the control period, which was significantly lower than the 98 ± 1 mm Hg in the normal rats. During insulin infusion, MAP increased similarly in both groups, with a 10 ± 2 mm Hg and 11 ± 1 mm Hg increase in normal and blockade rats, respectively, by day 7. The HR also increased in both groups: from 417 ± 8 beats/min to 426 ± 13 beats/min (P = NS) in normal rats and from 379 ± 10 beats/min to 419 ± 10 beats/min (P < .05) in blockade rats. Control sodium excretion averaged 2.5 ± 0.1 mEq/day in both groups and no significant change in sodium balance was measured in either group. All variables returned toward control after stopping insulin. These results suggest that increased adrenergic activity is not required for chronic hyperinsulinemia to raise blood pressure in rats.

Original languageEnglish (US)
Pages (from-to)1192-1199
Number of pages8
JournalAmerican journal of hypertension
Volume9
Issue number12 I
DOIs
StatePublished - Dec 1 1996

Fingerprint

Hyperinsulinism
Adrenergic Receptors
Hypertension
Insulin
Arterial Pressure
Intravenous Infusions
Adrenergic Agents
Heart Rate
Sodium
Glucose
Prazosin
Hypoglycemia
Propranolol
Sprague Dawley Rats
Veins
Catheters
Arteries
Blood Pressure

Keywords

  • blood pressure
  • insulin
  • sympathetic nervous system

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Chronic adrenergic receptor blockade does not prevent hyperinsulinemia-induced hypertension in rats. / Keen, Henry L.; Brands, Michael W.; Alonso-Galicia, Magdalena; Hall, John E.

In: American journal of hypertension, Vol. 9, No. 12 I, 01.12.1996, p. 1192-1199.

Research output: Contribution to journalArticle

Keen, Henry L. ; Brands, Michael W. ; Alonso-Galicia, Magdalena ; Hall, John E. / Chronic adrenergic receptor blockade does not prevent hyperinsulinemia-induced hypertension in rats. In: American journal of hypertension. 1996 ; Vol. 9, No. 12 I. pp. 1192-1199.
@article{fc3ea52491894fc299a6b922ea9f0ddf,
title = "Chronic adrenergic receptor blockade does not prevent hyperinsulinemia-induced hypertension in rats",
abstract = "Increased adrenergic activity has been suggested to mediate the hypertension associated with hyperinsulinemia. This study tested whether combined α1- and β-adrenergic receptor blockade would prevent insulin-induced hypertension when euglycemia was maintained by continuous intravenous glucose infusion. Sprague-Dawley rats (n = 16) were instrumented with artery and vein catheters and placed in metabolic cages. Propranolol and prazosin (10 mg/kg/day each) were infused continuously intravenously in 9 rats and 7 other rats received vehicle. Mean arterial pressure (MAP) and heart rate (HR) were measured 24 h per day using computerized methods. After a control period, a 7-day intravenous infusion of insulin (1.5 mU/kg/min) was begun and glucose was coadministered intravenously at 23 mg/kg/min to prevent hypoglycemia. The MAP averaged 93 ± 1 mm Hg in the blockade rats during the control period, which was significantly lower than the 98 ± 1 mm Hg in the normal rats. During insulin infusion, MAP increased similarly in both groups, with a 10 ± 2 mm Hg and 11 ± 1 mm Hg increase in normal and blockade rats, respectively, by day 7. The HR also increased in both groups: from 417 ± 8 beats/min to 426 ± 13 beats/min (P = NS) in normal rats and from 379 ± 10 beats/min to 419 ± 10 beats/min (P < .05) in blockade rats. Control sodium excretion averaged 2.5 ± 0.1 mEq/day in both groups and no significant change in sodium balance was measured in either group. All variables returned toward control after stopping insulin. These results suggest that increased adrenergic activity is not required for chronic hyperinsulinemia to raise blood pressure in rats.",
keywords = "blood pressure, insulin, sympathetic nervous system",
author = "Keen, {Henry L.} and Brands, {Michael W.} and Magdalena Alonso-Galicia and Hall, {John E.}",
year = "1996",
month = "12",
day = "1",
doi = "10.1016/S0895-7061(96)00254-3",
language = "English (US)",
volume = "9",
pages = "1192--1199",
journal = "American Journal of Hypertension",
issn = "0895-7061",
publisher = "Oxford University Press",
number = "12 I",

}

TY - JOUR

T1 - Chronic adrenergic receptor blockade does not prevent hyperinsulinemia-induced hypertension in rats

AU - Keen, Henry L.

AU - Brands, Michael W.

AU - Alonso-Galicia, Magdalena

AU - Hall, John E.

PY - 1996/12/1

Y1 - 1996/12/1

N2 - Increased adrenergic activity has been suggested to mediate the hypertension associated with hyperinsulinemia. This study tested whether combined α1- and β-adrenergic receptor blockade would prevent insulin-induced hypertension when euglycemia was maintained by continuous intravenous glucose infusion. Sprague-Dawley rats (n = 16) were instrumented with artery and vein catheters and placed in metabolic cages. Propranolol and prazosin (10 mg/kg/day each) were infused continuously intravenously in 9 rats and 7 other rats received vehicle. Mean arterial pressure (MAP) and heart rate (HR) were measured 24 h per day using computerized methods. After a control period, a 7-day intravenous infusion of insulin (1.5 mU/kg/min) was begun and glucose was coadministered intravenously at 23 mg/kg/min to prevent hypoglycemia. The MAP averaged 93 ± 1 mm Hg in the blockade rats during the control period, which was significantly lower than the 98 ± 1 mm Hg in the normal rats. During insulin infusion, MAP increased similarly in both groups, with a 10 ± 2 mm Hg and 11 ± 1 mm Hg increase in normal and blockade rats, respectively, by day 7. The HR also increased in both groups: from 417 ± 8 beats/min to 426 ± 13 beats/min (P = NS) in normal rats and from 379 ± 10 beats/min to 419 ± 10 beats/min (P < .05) in blockade rats. Control sodium excretion averaged 2.5 ± 0.1 mEq/day in both groups and no significant change in sodium balance was measured in either group. All variables returned toward control after stopping insulin. These results suggest that increased adrenergic activity is not required for chronic hyperinsulinemia to raise blood pressure in rats.

AB - Increased adrenergic activity has been suggested to mediate the hypertension associated with hyperinsulinemia. This study tested whether combined α1- and β-adrenergic receptor blockade would prevent insulin-induced hypertension when euglycemia was maintained by continuous intravenous glucose infusion. Sprague-Dawley rats (n = 16) were instrumented with artery and vein catheters and placed in metabolic cages. Propranolol and prazosin (10 mg/kg/day each) were infused continuously intravenously in 9 rats and 7 other rats received vehicle. Mean arterial pressure (MAP) and heart rate (HR) were measured 24 h per day using computerized methods. After a control period, a 7-day intravenous infusion of insulin (1.5 mU/kg/min) was begun and glucose was coadministered intravenously at 23 mg/kg/min to prevent hypoglycemia. The MAP averaged 93 ± 1 mm Hg in the blockade rats during the control period, which was significantly lower than the 98 ± 1 mm Hg in the normal rats. During insulin infusion, MAP increased similarly in both groups, with a 10 ± 2 mm Hg and 11 ± 1 mm Hg increase in normal and blockade rats, respectively, by day 7. The HR also increased in both groups: from 417 ± 8 beats/min to 426 ± 13 beats/min (P = NS) in normal rats and from 379 ± 10 beats/min to 419 ± 10 beats/min (P < .05) in blockade rats. Control sodium excretion averaged 2.5 ± 0.1 mEq/day in both groups and no significant change in sodium balance was measured in either group. All variables returned toward control after stopping insulin. These results suggest that increased adrenergic activity is not required for chronic hyperinsulinemia to raise blood pressure in rats.

KW - blood pressure

KW - insulin

KW - sympathetic nervous system

UR - http://www.scopus.com/inward/record.url?scp=0030445126&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030445126&partnerID=8YFLogxK

U2 - 10.1016/S0895-7061(96)00254-3

DO - 10.1016/S0895-7061(96)00254-3

M3 - Article

C2 - 8972890

AN - SCOPUS:0030445126

VL - 9

SP - 1192

EP - 1199

JO - American Journal of Hypertension

JF - American Journal of Hypertension

SN - 0895-7061

IS - 12 I

ER -