Vascular smooth muscle cells from the Milan hypertensive rat exhibit decreased functional angiotensin II receptors.

Socorro, Lilian; Vallega, Gino; Nunn, Amelia; Moore, Thomas J.; Canessa, Mitzy

doi:10.1161/01.hyp.15.6.591

Cited by 17 publications

(8 citation statements)

References 29 publications

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“…The second important observation of our report is the distinctly increased proliferation of cell lines of hypertensive origin, and similar findings have so far only been reported for animal models of genetic hypertension (22,23). The association of altered Na+/H+ exchange in "hypertensive" cell lines with enhanced proliferation is of special interest since current hypothesis suggest that the enhanced peripheral resistance in essential hypertension partially develops on the basis of an increased proliferation of vascular smooth muscle cells in resistance vessels (24,25).…”

Section: Resultssupporting

confidence: 85%

Hypertensive sodium-proton exchanger phenotype persists in immortalized lymphoblasts from essential hypertensive patients. A cell culture model for human hypertension.

Rosskopf¹,

Frömter²,

Siffert

1993

J. Clin. Invest.

122

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Section: Resultssupporting

confidence: 85%

Hypertensive sodium-proton exchanger phenotype persists in immortalized lymphoblasts from essential hypertensive patients. A cell culture model for human hypertension.

Rosskopf¹,

Frömter²,

Siffert

1993

J. Clin. Invest.

122

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“…These results suggest that platelet factor BB plays an important role in the proliferation of hypertensive vascular cells. VSMCs from hypertensive rats also exhibited enhanced proliferation, 7 -10 with spontaneously hypertensive rats (SHR) having a higher number of EGF receptors 8 and enhanced responsiveness of Na + -H + exchange to angiotensin II (Ang II). 10 This abnormality may be responsible for the greater vascular hyperplasia observed in genetic models of rat hypertension and partially account for the high vascular resistance to blood flow.…”

Section: Cell Growth and Na-k-cl Cotransport Responses Of Vascular Smmentioning

confidence: 99%

“…The MHS strain is a low-renin hypertensive model with kidney abnormalities and blunted vessel response to vasoconstrictors. 7 The present study was designed to investigate in VSMCs from Milan rats the role of serum and PDGF BB in cellular proliferation and expression of Na-K-Cl cotransport activity.…”

Section: Cell Growth and Na-k-cl Cotransport Responses Of Vascular Smmentioning

confidence: 99%

“…The radioactive solution was removed at different times, the dishes were rapidly washed three times with ice-cold 100 mmol/L MgCl 2 , and cells were extracted with 1.5 mL of 0.1% SDS for -y-radioactivity counting and protein content as described. 7 The cell-associated counts per minute was divided by the specific activity of the ^Rb-K* influx solution to normalize the flux in nanomoles per milligram protein per 5 minutes. The influx was found to be linear up to 15 minutes.…”

Section: Na-k-cl Cotransport and Na-k Pump Activitiesmentioning

confidence: 99%

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Cell growth and Na-K-Cl cotransport responses of vascular smooth muscle cells of Milan rats.

et al. 1994

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The present study examines the role of serum growth factors in the proliferative response and Na-K-Cl cotransport activity of vascular smooth muscle cells from Milan normotensive (MNS) and hypertensive (MHS) rats. Cells from thoracic aorta of both strains were cultured in 10% serum medium and made quiescent by 72 hours in 0.3% serum medium. MHS cells grown with 10% serum had a shorter population doubling time than MNS cells between passages 8 and 12 (13.8±1.7 versus 20.1±1.6 hours, P<.01, n=4). MHS cells also exhibited a higher response of thymidine incorporation into nucleic acid to serum, epidermal, and platelet-derived growth factor BB. In MHS cells epidermal (100 ng/mL) and platelet (50 ng/mL) growth factors increased thymidine incorporation 2-and 10-fold, respectively. In MNS cells epidermal factor did not induce a significant response, and that of platelet factor was twofold lower than in MHS cells. Binding curves revealed a higher number of receptors for platelet than epidermal growth factor in both strains and a similar number of both receptors in MHS and MNS cells. Quantitative immunoblots of these recep-V ascular smooth muscle cells (VSMCs) within the tunica media of adult arteries are in quiescent state of growth, with the cell cycle reversibly arrested in the Gi/G 0 phase. In rats, the replication rate is approximately 0.02%, but this slow growth rate can be altered by mechanical injury and the release of growth factors by platelets, monocytes, and endothelial cells. The initiation of the proliferative cycle and the rate of growth are controlled by autocrine and paracrine secretion of growth factors and the expression of these receptors.1 Platelet-derived growth factor (PDGF), isoform BB, is the most powerful mitogenic for the initiation of the proliferative cycle in VSMCs, 2 and it may play a role in the hyperplasia of the tunica media in hypertension. Stimulation of ion fluxes is among the earliest changes induced by growth factor addition to Go-arrested cells. Activation of Na + -H + exchange by several mitogens has been well characterized in various cell types, 3 and stimulation of Ca 2+ -Na + exchange by PDGF BB 4 and of Na-K-Cl cotransport by epidermal growth factor (EGF) has been reported in VSMCs 5 and fibroblasts.6 Previous investigations have shown thatFrom the Endocrine-Hypertension Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass (M.C., G.V.), and Departamento de Inmunologia Ginica y Reumatologia, Facultad de Medicina, Universidad Catolica de Chile, Santiago (G.S., E.W., A.G.).Correspondence to Mitzy Canessa, PhD, Endocrine-Hypertension Division, Brigham and Women's Hospital, 221 Longwood Ave, Boston, MA 02115. tor proteins confirmed the observation that the greater proliferation of MHS cells could not be related to a higher number of growth factor receptors. Cotransport activity (bumetanide-sensitive M Rb influx in nanomoles per milligram protein per 5 minutes) was found to be significantly higher in MHS cells (16±3, n=18) t...

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“…Other mechanisms possibly responsible for the increased extracellular volume are the actions of vasoactive substances such as vasopressin, PGs and angiotensin. Indeed, cultured smooth muscle cells from MHR exhibit blunted phospholipase C, Nail exchange and cytosolic Ca response to angiotensin II despite having the same number of angiotensin II receptors as MN cells [39]. Bianchi et al [40] found that the defects in the renal tubular cells in MHRs are also present in the red blood cells (RBC) and that bone marrow transplantation from MHRs to F1 hybrids transmitted the RBC Na and Ca abnormalities to the recipient.…”

Section: Milan Hypertensive Strainmentioning

confidence: 99%

Pathogenesis of the essential hypertensions

1991

Pediatr Nephrol

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The pathogenesis of essential hypertension (EH) is reviewed with a special focus on the development phase or the pre-hypertensive period. Three animal models are presented: the spontaneously hypertensive rat, the Dahl's salt-sensitive rat, and the Milan hypertensive rat. Some of the findings in animal models have inspired new fields and technical approaches for studying EH in man. From the original idea of Page, a new mosaic of various etiological parameters serves as a basis for reviewing the multiple facets of EH in man. One must conclude that EH is heterogeneous disease and most likely every single hypertensive patient belongs to a subgroup of the whole population of hypertensives.

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Vascular smooth muscle cells from the Milan hypertensive rat exhibit decreased functional angiotensin II receptors.

Cited by 17 publications

References 29 publications

Hypertensive sodium-proton exchanger phenotype persists in immortalized lymphoblasts from essential hypertensive patients. A cell culture model for human hypertension.

Hypertensive sodium-proton exchanger phenotype persists in immortalized lymphoblasts from essential hypertensive patients. A cell culture model for human hypertension.

Cell growth and Na-K-Cl cotransport responses of vascular smooth muscle cells of Milan rats.

Pathogenesis of the essential hypertensions

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