Effect of DOCA-salt treatment duration and anteroventral third ventricle lesions on a plasma-borne sodium pump inhibitor in rats

Emel Songu-Mize, Steven L. Bealer, Robert William Caldwell

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

We determined the effect of plasma obtained from rats treated with DOCA-salt for 6 and 28 days on sodium pump activity, measured as ouabain-sensitive Rb+ uptake in tail arteries from these rats. The effect of an electrolytic lesion in the area of the anteroventral third cerebral ventricle (AV3V) before DOCA-salt treatment was investi¬gated in relation to the ability of plasma to inhibit vascular Na+ pump activity. Systolic blood pressures, plasma sodium and potassium concentrations, body weights and haematocrit were also measured. Six days after DOCA-salt treatment, there was a 22% suppression of vascular Na+ pump activity in these rats. This suppression was due to a plasma factor since plasma from these rats produced a similar degree of suppression in arteries isolated from untreated control rats. Furthermore, tail arteries from DOCA-salt rats treated for 6 days displayed normal Na+ pump activity when incubated in plasma from control rats or in Krebs-Henseleit buffer. There was no elevation of systolic blood pressure at the end of 6 days of treatment with DOCA-salt. Placement of an electrolytic brain lesion in the AV3V area before treatment with DOCA-salt abolished the ability of plasma to inhibit the vascular Na+ pump. Treatment with DOCA-salt for 28 days resulted in a significant increase in systolic blood pressure, a decrease in plasma potassium concentration, and a significant increase in vascular Na+ pump activity (26%). This elevation in pump activity appears to be due to a change in the artery rather than a stimulating factor in the plasma, since incubation of the arteries in both Krebs-Henseleit buffer and in plasma taken from control rats still resulted in increased Na+ pump activity. Our data indicate that, 6 days after DOCA-salt treatment there appears to be an inhibitor of the vascular Na+ pump in the plasma which is undetectable by bio-assay if the rats are lesioned in the AV3V region before this treatment. Twenty-eight days after DOCA-salt treatment, the vascular Na+ pump is stimulated; this is due not to a plasma factor, but to a change in the artery.

Original languageEnglish (US)
Pages (from-to)461-467
Number of pages7
JournalJournal of Hypertension
Volume5
Issue number4
StatePublished - Jan 1 1987
Externally publishedYes

Fingerprint

Desoxycorticosterone Acetate
Sodium-Potassium-Exchanging ATPase
Third Ventricle
Salts
Blood Vessels
Arteries
Blood Pressure
Tail
Potassium
Cerebral Ventricles
Ouabain
Hematocrit

Keywords

  • DOCA-salt hypertension
  • Early and late stages of hypertension
  • Endogenous Na<sup>+</sup>
  • K<sup>+</sup>adenosine triphosphatase
  • K<sup>+</sup>pump
  • K<sup>+</sup>pump inhibitor
  • Na<sup>+</sup>
  • Na<sup>+</sup>pump
  • Vascular Na<sup>+</sup>

ASJC Scopus subject areas

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Effect of DOCA-salt treatment duration and anteroventral third ventricle lesions on a plasma-borne sodium pump inhibitor in rats. / Songu-Mize, Emel; Bealer, Steven L.; Caldwell, Robert William.

In: Journal of Hypertension, Vol. 5, No. 4, 01.01.1987, p. 461-467.

Research output: Contribution to journalArticle

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AB - We determined the effect of plasma obtained from rats treated with DOCA-salt for 6 and 28 days on sodium pump activity, measured as ouabain-sensitive Rb+ uptake in tail arteries from these rats. The effect of an electrolytic lesion in the area of the anteroventral third cerebral ventricle (AV3V) before DOCA-salt treatment was investi¬gated in relation to the ability of plasma to inhibit vascular Na+ pump activity. Systolic blood pressures, plasma sodium and potassium concentrations, body weights and haematocrit were also measured. Six days after DOCA-salt treatment, there was a 22% suppression of vascular Na+ pump activity in these rats. This suppression was due to a plasma factor since plasma from these rats produced a similar degree of suppression in arteries isolated from untreated control rats. Furthermore, tail arteries from DOCA-salt rats treated for 6 days displayed normal Na+ pump activity when incubated in plasma from control rats or in Krebs-Henseleit buffer. There was no elevation of systolic blood pressure at the end of 6 days of treatment with DOCA-salt. Placement of an electrolytic brain lesion in the AV3V area before treatment with DOCA-salt abolished the ability of plasma to inhibit the vascular Na+ pump. Treatment with DOCA-salt for 28 days resulted in a significant increase in systolic blood pressure, a decrease in plasma potassium concentration, and a significant increase in vascular Na+ pump activity (26%). This elevation in pump activity appears to be due to a change in the artery rather than a stimulating factor in the plasma, since incubation of the arteries in both Krebs-Henseleit buffer and in plasma taken from control rats still resulted in increased Na+ pump activity. Our data indicate that, 6 days after DOCA-salt treatment there appears to be an inhibitor of the vascular Na+ pump in the plasma which is undetectable by bio-assay if the rats are lesioned in the AV3V region before this treatment. Twenty-eight days after DOCA-salt treatment, the vascular Na+ pump is stimulated; this is due not to a plasma factor, but to a change in the artery.

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