Mechanisms of structural vascular changes in genetic hypertension: analyses on cultured vascular smooth muscle cells from spontaneously hypertensive rats.

نویسندگان

  • Y Yamori
  • T Igawa
  • T Kanbe
  • M Kihara
  • Y Nara
  • R Horie
چکیده

1. The basic mechanism underlying the structural vascular changes occurring in hypertension was studied in cultured aortic smooth muscle cells (SMC) obtained by an explant method from spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) and compared with that in normotensive Wistar--Kyoto (WKY) rats. 2. The growth rate of SMC from SHR and SHRSP at the age of 2.5--11 months was greater than that of SMC from WKY rats even after repeated passages. 3. [3H]Thymidine and [14C]leucine incorporation, and ornithine decarboxylase (ODC) activity of SMC were increased in SHR and SHRSP in comparison with WKY rats. 4. The application of isoprenaline but not noradrenaline to the culture media increased ODC activity acutely in SMC from WKY rats and this increase was blocked by propranolol. 5. These results indicate that SMC from SHR and SHRSP are more prone to proliferate than those from WKY rats and that a beta-adrenergic neurohumoral mechanism accelerates SMC growth independently of blood pressure.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Studies of hypertension-induced vascular hypertrophy in cultured smooth muscle cells from spontaneously hypertensive rats.

Mechanisms of vascular hypertrophy induced by hypertension were studied in cultured aortic smooth muscle cells from spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) and compared with those from normotensive Wistar-Kyoto (WKY) rats. Fetal calf serum-stimulated ornithine decarboxylase (ODC) activity of cultured smooth muscle cells was greater in SHR and SHRSP than in WKY. Beta- ...

متن کامل

Lipid bilayer in genetic hypertension.

Membrane microviscosity, phospholipid composition, and turnover were measured in cultured vascular smooth muscle cells isolated from mesenteric arteries of stroke-prone spontaneously hypertensive and age-matched, normotensive Wistar-Kyoto rats. Membrane microviscosity, measured with fluorescence polarization, revealed greater microviscosity (lower fluidity) of the membranes isolated from smooth...

متن کامل

Augmented vascular smooth muscle cell stiffness and adhesion when hypertension is superimposed on aging.

Hypertension and aging are both recognized to increase aortic stiffness, but their interactions are not completely understood. Most previous studies have attributed increased aortic stiffness to changes in extracellular matrix proteins that alter the mechanical properties of the vascular wall. Alternatively, we hypothesized that a significant component of increased vascular stiffness in hyperte...

متن کامل

c-Src-dependent nongenomic signaling responses to aldosterone are increased in vascular myocytes from spontaneously hypertensive rats.

Aldosterone plays an important role in the pathogenesis of hypertension. We previously demonstrated that nongenomic signaling by aldosterone in vascular smooth muscle cells occurs through c-Src-dependent pathways. Here we tested the hypothesis that upregulation of c-Src by aldosterone plays a role in increased mitogen-activated protein (MAP) kinase activation, [3H]-proline incorporation, and NA...

متن کامل

Na(+)-H+ exchanger expression in vascular smooth muscle of spontaneously hypertensive and Wistar-Kyoto rats.

The Na(+)-H+ exchanger has important modulatory effects on vascular smooth muscle cell proliferation and contractility. Increased Na(+)-H+ exchange activity is a general property of many tissues, including mesenteric artery and cultured vascular smooth muscle cells, in the spontaneously hypertensive rat (SHR). In the present work, we investigated whether alterations in the steady-state levels o...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Clinical science

دوره 61 Suppl 7  شماره 

صفحات  -

تاریخ انتشار 1981