Literature DB >> 1730459

Hypertension during chronic hyperinsulinemia in rats is not salt-sensitive.

M W Brands1, D A Hildebrandt, H L Mizelle, J E Hall.   

Abstract

The goal of this study was to examine the chronic blood pressure and renal actions of insulin in conscious rats and to determine whether the blood pressure response to insulin is salt-sensitive. The effects of chronic hyperinsulinemia were examined in three groups of Sprague-Dawley rats given low sodium (LS rats, 0.6 meq/day), normal sodium (NS rats, 3.0 meq/day), or high sodium (HS rats, 11.4 meq/day) intakes. After 5-7 days of acclimation and 4 days of control measurements, insulin was infused 24 hr/day (1.5 milliunit/kg/min i.v.) for 7 days, and euglycemia was maintained by infusion of glucose (22 mg/kg/min i.v.). Mean arterial pressure was recorded continuously 19 hr/day, using computerized techniques, from chronically implanted aortic catheters. Chronic insulin infusion increased arterial pressure similarly in the three groups of rats, from 91 +/- 2 to 104 +/- 4 mm Hg in LS rats (n = 6), from 86 +/- 2 to 104 +/- 4 mm Hg in NS rats (n = 5), and from 91 +/- 2 to 105 +/- 8 mm Hg in HS rats (n = 5). There were no significant changes in plasma renin activity or glucose concentration in any group during insulin infusion. Control sodium excretions were 0.5 +/- 0.1, 2.3 +/- 0.1, and 9.3 +/- 0.6 meq/day in LS, NS, and HS rats, respectively, and there were no significant changes in urinary sodium excretion or cumulative sodium balance during 7 days of insulin infusion in any of the groups. These observations indicate that chronic hyperinsulinemia in rats produced hypertension that was not salt-sensitive and not dependent on sodium retention or increased renin secretion. Moreover, insulin-induced hypertension was associated with a shift of renal pressure natriuresis, since sodium balance was maintained at elevated arterial pressures.

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Year:  1992        PMID: 1730459     DOI: 10.1161/01.hyp.19.1_suppl.i83

Source DB:  PubMed          Journal:  Hypertension        ISSN: 0194-911X            Impact factor:   10.190


  9 in total

1.  Physiological hyperinsulinemia caused by acute hyperglycemia minimizes renal sodium loss by direct action on kidneys.

Authors:  Debra L Irsik; Michael W Brands
Journal:  Am J Physiol Regul Integr Comp Physiol       Date:  2018-05-23       Impact factor: 3.619

Review 2.  Role of Hyperinsulinemia and Insulin Resistance in Hypertension: Metabolic Syndrome Revisited.

Authors:  Alexandre A da Silva; Jussara M do Carmo; Xuan Li; Zhen Wang; Alan J Mouton; John E Hall
Journal:  Can J Cardiol       Date:  2020-02-12       Impact factor: 5.223

3.  The normal increase in insulin after a meal may be required to prevent postprandial renal sodium and volume losses.

Authors:  Debra L Irsik; Bonnie L Blazer-Yost; Alexander Staruschenko; Michael W Brands
Journal:  Am J Physiol Regul Integr Comp Physiol       Date:  2017-03-22       Impact factor: 3.619

Review 4.  Cardiometabolic Features of Polycystic Ovary Syndrome: Role of Androgens.

Authors:  Licy L Yanes Cardozo; Damian G Romero; Jane F Reckelhoff
Journal:  Physiology (Bethesda)       Date:  2017-09

Review 5.  Sodium-retaining effect of insulin in diabetes.

Authors:  Michael W Brands; M Marlina Manhiani
Journal:  Am J Physiol Regul Integr Comp Physiol       Date:  2012-10-03       Impact factor: 3.619

Review 6.  The inter-relationship between insulin resistance and hypertension.

Authors:  A Salvetti; G Brogi; V Di Legge; G P Bernini
Journal:  Drugs       Date:  1993       Impact factor: 9.546

7.  Chronic renal artery insulin infusion increases mean arterial pressure in male Sprague-Dawley rats.

Authors:  Debra L Irsik; Jian-Kang Chen; Michael W Brands
Journal:  Am J Physiol Renal Physiol       Date:  2017-09-27

8.  The Relation between Fructose-Induced Metabolic Syndrome and Altered Renal Haemodynamic and Excretory Function in the Rat.

Authors:  Mohammed H Abdulla; Munavvar A Sattar; Edward J Johns
Journal:  Int J Nephrol       Date:  2011-07-12

9.  Chronic Insulin Infusion Down-Regulates Circulating and Urinary Nitric Oxide (NO) Levels Despite Molecular Changes in the Kidney Predicting Greater Endothelial NO Synthase Activity in Mice.

Authors:  Maurice B Fluitt; Sophia Rizvi; Lijun Li; Ashley Alunan; Hwal Lee; Swasti Tiwari; Carolyn M Ecelbarger
Journal:  Int J Mol Sci       Date:  2018-09-22       Impact factor: 5.923

  9 in total

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