These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Altered ion transport in aortic smooth muscle during deoxycorticosterone acetate hypertension in the rat. Author: Jones AW, Hart RG. Journal: Circ Res; 1975 Sep; 37(3):333-41. PubMed ID: 1157222. Abstract: Change in aortic water and electrolyte distribution and in ion turnover were studied during the development of deoxycorticosterone acetate (DOCA) hypertension in the rat. Treatment with DOCA plus saline during the prehypertensive phase was associated with increases in 42K turnover (0.0142 +/- 0.0005 vs. 0.0102 +/- 0.0003 min-1), cell water (0.89 +/- 0.03 vs 0.76 +/- 0.02 kg/kg dry weight), and the ratio of weight to length. These parameters were further increased during the development of hypertension. Significant increases were also observed in total K, Ca, and Mg contents and in Na and C1 contents corrected for the extracellular space. The turnover of 36Cl was increased (0.230 +/- 0.006 vs. 0.136 +/- 0.004 min-1) in DOCA hypertensive rats as was the content of slowly exchanging Cl. Removal of extracellular Ca greatly increased the steady-state turnover of 42K. For control rats, a Ca concentration of 0.1 mM reduced the rate of 42K turnover to less than 50% of the Ca-free value (0.063 +/- 0.004 min-1), whereas DOCA hypertensive rats exhibited only a 10% reduction. At the highest Ca concentration, 5 mM, the 42K turnover was greater in DOCA-treated rats with the hypertensives operating at 67% of maximum efflux or about twice the efflux in controls. It is concluded that significant alterations in ion transport by vascular smooth muscle occur before and during the development of hypertension induced by treatment with DOCA plus saline. Such changes may result from a reduced ability of Ca to stabilize the membrane. It is proposed that such alterations contribute to the changes in vascular reactivity and the hypertrophy associated with hypertension.[Abstract] [Full Text] [Related] [New Search]