Advertisement

Increased Sodium Appetite and Polydipsia in Goldblatt Hypertension

  • Manuel Vijande
  • Marina Costales
  • James T. Fitzsimons
Part of the NATO ASI Series book series (NSSA, volume 105)

Abstract

Two kidney Goldblatt hypertension can be induced in the rat by complete ligation of the aorta between the renal arteries1. The ischaemic (left) kidney secretes excessive amounts of renin, resulting in plasma renin concentrations which peak during the first week after operation and return to near normal after about a month2. Occlusion of the aorta leads to polydipsia and polyuria3, with reduced preference for NaCl in the chronic stages of hypertension 4–6 weeks postoperatively4. Partial aortic occlusion, which is less lethal than complete occlusion but which produces a similar sequence of changes, was introduced in order to examine the polydipsia and changes in Na appetite that occur in renal hypertension5. The relation between blood pressure and spontaneous fluid intake was also investigated.

Keywords

Renal Artery Arterial Blood Pressure Flame Photometry Renin Secretion Aortic Occlusion 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    J. M. Rojo-Ortega and J. Genest, A method for production of experimental hypertension in rats, Can. J. of Physiol. Pharmacol. 46: 883–885 (1968).CrossRefGoogle Scholar
  2. 2.
    M. Fernandes, G. Onesti, A. Weder, R. Dykyj, A. B. Gould, K. E. Kim and C. Swartz, Experimental model of severe renal hypertension, J. Lab. Clin. Med. 87: 561–567 (1976).PubMedGoogle Scholar
  3. 3.
    J.M. Rojo-Ortega, F. P. Queiroz and J. Genest, Effects of sodium chloride on early and chronic phases of malignant hypertension in rats, Am. J. Physiol. 236: H665–H671 (1979).PubMedGoogle Scholar
  4. 4.
    S. Forman and J. L. Falk, NaCl solution ingestion in genetic (SHR) and aortic-ligation hypertension, Physiol. & Behav. 22: 371–377 (1979).CrossRefGoogle Scholar
  5. 5.
    Marina Costales, J. T. Fitzsimons and M. Vijande, Increased sodium appetite and polydipsia induced by partial aortic occlusion in the rat, J. Physiol. 352: 467–481 (1984).PubMedGoogle Scholar
  6. 6.
    J. Mohring, Maria Petri and Barbel Mohring, Salt appetite during the early phase of renal hypertension in rats, Pflugers Arch. 356: 153–158 (1975).PubMedCrossRefGoogle Scholar
  7. 7.
    J. D. Swales, H. Thurston, F. P. Queiroz and A. Medina, Sodium balance during the development of experimental hypertension, J. Lab. Clin. Med. 80: 539–547 (1972).PubMedGoogle Scholar
  8. 8.
    J.T. Fitzsimons, “The Physiology of Thirst and Sodium Appetite,” Monographs of the Physiological Society, No. 35, Cambridge University Press, Cambridge (1979).Google Scholar
  9. 9.
    D. B. Avrith and J. T. Fitzsimons, Increased sodium appetite in the rat induced by intracranial administration of components of the renin-angiotensin system, J. Physiol. 301: 349–364 (1980).PubMedGoogle Scholar
  10. 10.
    R. M. Elfont and J. T. Fitzsimons, The role of angiotensin in increased sodium appetite after adrenalectomy, J. Physiol. 320: 70P (1981).Google Scholar
  11. 11.
    R. G. Bengis, T. G. Coleman, D. B. Young and R. E. McCaa, Long-term blockade of angiotensin formation in various normotensive and hypertensive rat models using converting enzyme inhibitor (SQ 14, 225), Circ. Res. 43: suppl. I, 145–153 (1978).Google Scholar

Copyright information

© Springer Science+Business Media New York 1986

Authors and Affiliations

  • Manuel Vijande
    • 1
    • 2
  • Marina Costales
    • 1
    • 2
  • James T. Fitzsimons
    • 1
    • 2
  1. 1.Department of PhysiologyUniversity of OviedoSpain
  2. 2.The Physiological LaboratoryCambridgeEngland

Personalised recommendations