This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bianchi, G. Articles by Polli, E. Search for Related Content PubMed PubMed Citation Articles by Bianchi, G. Articles by Polli, E.

Hypertension, Vol 7, 319-325, Copyright © 1985 by American Heart Association

ARTICLES

Red blood cell abnormalities and spontaneous hypertension in the rat. A genetically determined link

G Bianchi, P Ferrari, D Trizio, M Ferrandi, L Torielli, BR Barber and E Polli

The significance of the erythrocyte abnormalities described in rats and humans with spontaneous hypertension is far from clear. This study, in two highly inbred strains of rats, was designed to evaluate whether these abnormalities are primary and thus genetically related to hypertension. The Milan hypertensive strain (MHS) and its normotensive control strain (MNS) were used to carry out two types of experiments. In two groups of lethally irradiated (MHS X MNS) F1 hybrids, bone marrow from MHS or MNS was transplanted. The differences in red cell function between the recipients of bone marrow from MHS and recipients of bone marrow from MNS were similar to those existing between the parental donor MHS and MNS: Na+-K+ cotransport was increased (p less than 0.02) and intracellular Na+ content (p less than 0.05) and cell volume (p less than 0.02) were decreased in MHS. The same pattern was observed when this experiment was repeated in different groups of F1 hybrids. In individuals of the segregating F2 population, obtained by crossing the (MHS X MNS) F1 hybrids, there was a positive correlation (p less than 0.001) between the red blood cell Na+-K+ cotransport and the mean blood pressure. These results indicate that the erythrocyte abnormalities may well be genetically associated with the primary cause of spontaneous hypertension in rats. Because of the many similarities demonstrated when young prehypertensive MHS or humans prone to develop hypertension are compared with their respective controls, it is possible that the findings described here in rats are relevant to human essential hypertension.

This article has been cited by other articles:

				S. N. Orlov and A. A. Mongin Salt-sensing mechanisms in blood pressure regulation and hypertension Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2039 - H2053. [Abstract] [Full Text] [PDF]

				G. Bianchi Genetic variations of tubular sodium reabsorption leading to "primary" hypertension: from gene polymorphism to clinical symptoms Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2005; 289(6): R1536 - R1549. [Abstract] [Full Text] [PDF]

				G. Jiang, F. Akar, S. L. Cobbs, K. Lomashvilli, R. Lakkis, F. J. Gordon, R. L. Sutliff, and W. C. O'Neill Blood pressure regulates the activity and function of the Na-K-2Cl cotransporter in vascular smooth muscle Am J Physiol Heart Circ Physiol, April 1, 2004; 286(4): H1552 - H1557. [Abstract] [Full Text] [PDF]

				J. Zicha and J. Kunes Ontogenetic Aspects of Hypertension Development: Analysis in the Rat Physiol Rev, October 1, 1999; 79(4): 1227 - 1282. [Abstract] [Full Text] [PDF]

				S. N. Orlov, N. C. Adragna, V. A. Adarichev, and P. Hamet Genetic and biochemical determinants of abnormal monovalent ion transport in primary hypertension Am J Physiol Cell Physiol, March 1, 1999; 276(3): C511 - C536. [Abstract] [Full Text] [PDF]