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. 1991 Nov 1;88(21):9848–9852. doi: 10.1073/pnas.88.21.9848

Inverse changes in erythroid cell volume and number regulate the hematocrit in newborn genetically hypertensive rats.

J W Boylan 1, J B Van Liew 1, P U Feig 1
PMCID: PMC52818  PMID: 1946411

Abstract

Erythrocytosis and microcytosis have been described in strains of genetically hypertensive rats and in essentially hypertensive humans. Published discussion of these phenomena has centered around their relationship to observed alterations in ionic transport and the pathogenesis of hypertension. In presenting data for another strain of spontaneously hypertensive rats in which these findings are exhibited, we note that erythroid cell size decreases concurrently with the increase in cell numbers so that the hematocrit and the mean corpuscular hemoglobin concentration remain constant. Data from the literature support the hypothesis that erythroid cell size is inversely proportional to cell count in a large number of species. Erythrocytosis, as it develops in the neonatal rat, is a consequence of the marked immaturity of this species at birth. Erythrocytosis in the spontaneously hypertensive rat is not due to a difference in the affinity of its hemoglobin for oxygen or to significant tissue anorexia. Microcytosis in the spontaneously hypertensive rat is the consequence of a continuation of the linear volume decrease with age of its erythroid cells seen in the normotensive animals and may be accounted for by the production of smaller cells with concomitant regulation of individual cell volume.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Bianchi G., Ferrari P., Trizio D., Ferrandi M., Torielli L., Barber B. R., Polli E. Red blood cell abnormalities and spontaneous hypertension in the rat. A genetically determined link. Hypertension. 1985 May-Jun;7(3 Pt 1):319–325. [PubMed] [Google Scholar]
  2. Bruschi G., Minari M., Bruschi M. E., Tacinelli L., Milani B., Cavatorta A., Borghetti A. Similarities of essential and spontaneous hypertension. Volume and number of blood cells. Hypertension. 1986 Nov;8(11):983–989. doi: 10.1161/01.hyp.8.11.983. [DOI] [PubMed] [Google Scholar]
  3. Feig P. U., Mitchell P. P., Boylan J. W. Erythrocyte membrane transport in hypertensive humans and rats. Effect of sodium depletion and excess. Hypertension. 1985 May-Jun;7(3 Pt 1):423–429. [PubMed] [Google Scholar]
  4. Feld L. G., Van Liew J. B., Brentjens J. R., Boylan J. W. Renal lesions and proteinuria in the spontaneously hypertensive rat made normotensive by treatment. Kidney Int. 1981 Nov;20(5):606–614. doi: 10.1038/ki.1981.183. [DOI] [PubMed] [Google Scholar]
  5. Ferrari P., Ferrandi M., Torielli L., Canessa M., Bianchi G. Relationship between erythrocyte volume and sodium transport in the Milan hypertensive rat and age-dependent changes. J Hypertens. 1987 Apr;5(2):199–206. doi: 10.1097/00004872-198704000-00011. [DOI] [PubMed] [Google Scholar]
  6. Kregenow F. M. Osmoregulatory salt transporting mechanisms: control of cell volume in anisotonic media. Annu Rev Physiol. 1981;43:493–505. doi: 10.1146/annurev.ph.43.030181.002425. [DOI] [PubMed] [Google Scholar]
  7. Kregenow F. M. The response of duck erythrocytes to nonhemolytic hypotonic media. Evidence for a volume-controlling mechanism. J Gen Physiol. 1971 Oct;58(4):372–395. doi: 10.1085/jgp.58.4.372. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Matoth Y., Zaizov R., Varsano I. Postnatal changes in some red cell parameters. Acta Paediatr Scand. 1971 May;60(3):317–323. doi: 10.1111/j.1651-2227.1971.tb06663.x. [DOI] [PubMed] [Google Scholar]
  9. Orlov S. N., Pokudin N. I., Kotelevtsev Y. V., Gulak P. V. Volume-dependent regulation of ion transport and membrane phosphorylation in human and rat erythrocytes. J Membr Biol. 1989 Feb;107(2):105–117. doi: 10.1007/BF01871716. [DOI] [PubMed] [Google Scholar]
  10. Reeves R. B., Park J. S., Lapennas G. N., Olszowka A. J. Oxygen affinity and Bohr coefficients of dog blood. J Appl Physiol Respir Environ Exerc Physiol. 1982 Jul;53(1):87–95. doi: 10.1152/jappl.1982.53.1.87. [DOI] [PubMed] [Google Scholar]
  11. Sen S., Hoffman G. C., Stowe N. T., Smeby R. R., Bumpus F. M. Erythrocytosis in spontaneously hypertensive rats. J Clin Invest. 1972 Mar;51(3):710–714. doi: 10.1172/JCI106860. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Stockman J. A., 3rd, Garcia J. F., Oski F. A. The anemia of prematurity. Factors governing the erythropoietin response. N Engl J Med. 1977 Mar 24;296(12):647–650. doi: 10.1056/NEJM197703242961202. [DOI] [PubMed] [Google Scholar]
  13. Valet G., Hanser G., Ruhenstroth-Bauer G. Ein neues Konzept der Hämatopoese im Säugetier-organismus während der Nachgeburtsphase: Nachweis mehrerer Volumenpopulationen der Erythrozyten bei Ratten, Mäusen, Meerschweinchen, Kaninchen, Schafen und Ziegen. Blut. 1977 May;34(5):413–418. doi: 10.1007/BF00996087. [DOI] [PubMed] [Google Scholar]
  14. Valet G., Metzger H., Kachel V., Ruhenstroth-Bauer G. Der Nachweis verschiedener Erythrozytenpopulationen bei der Ratte. Blut. 1972 Jan;24(1):42–53. doi: 10.1007/BF01633141. [DOI] [PubMed] [Google Scholar]
  15. Yonemitsu H., Yamaguchi K., Shigeta H., Okuda K., Takaku F. Two cases of familial erythrocytosis with increased erythropoietin activity in plasma and urine. Blood. 1973 Nov;42(5):793–797. [PubMed] [Google Scholar]
  16. van de Ven C. J., Bohr D. F. Intrinsic difference in erythrocyte membrane in spontaneously hypertensive rats characterized by Na+ and K+ fluxes. Pflugers Arch. 1983 Sep;399(1):74–78. doi: 10.1007/BF00652525. [DOI] [PubMed] [Google Scholar]

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