Mechanisms of Structural Vascular Changes in Genetic Hypertension: Analyses on Cultured Vascular Smooth Muscle Cells from Spontaneously Hypertensive Rats

1981 ◽  
Vol 61 (s7) ◽  
pp. 121s-123s ◽  
Author(s):  
Yukio Yamori ◽  
Takehiro Igawa ◽  
Toshimi Kanbe ◽  
Masahiro Kihara ◽  
Yasuo Nara ◽  
...  

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 β-adrenergic neurohumoral mechanism accelerates SMC growth independently of blood pressure.

1992 ◽  
Vol 70 (9) ◽  
pp. 1261-1270 ◽  
Author(s):  
Robert M. K. W. Lee ◽  
Jim Tsoporis ◽  
Roger R. J. Wang

Chronic treatment of spontaneously hypertensive rats (SHR) and Kyoto–Wistar normotensive rats (WKY) with nadolol was carried out from gestation until 28 weeks of age. Nadolol treatment caused some lowering of blood pressure but did not prevent the development of hypertension or cardiac hypertrophy in the SHR, in spite of significant β-blockade. The lumen of large mesenteric arteries from control SHR was smaller than from WKY, and nadolol treatment increased the lumen size in the SHR. An increased number of smooth muscle cell layers present in the control SHR as compared with WKY was reduced slightly by nadolol treatment. However, the changes produced by nadolol did not reach the levels of control and treated WKY. In the aorta, the incidence of polyploid smooth muscle cells was higher in the SHR than the WKY in the control group. Nadolol treatment reduced the percentage of polyploid cells in both SHR and WKY, so that the difference between these two groups of animals was eliminated in the treated groups. The tissue level of norepinephrine in the plasma, heart, mesenteric arteries, and adrenal glands in the SHR and WKY was not affected by the treatment. We suggest that the ineffectiveness of nadolol in preventing hypertension development may be due to its lack of effect in preventing primary changes in the resistance arteries, and that the development of polyploidy of smooth muscle cells may be mediated by β-receptors.Key words: nadolol, vascular changes, hypertension, spontaneously hypertensive rats, β-receptor, catecholamines.


Hypertension ◽  
1998 ◽  
Vol 32 (1) ◽  
pp. 166-169 ◽  
Author(s):  
Yvonnick Bezie ◽  
Patrick Lacolley ◽  
Stéphane Laurent ◽  
Giorgio Gabella

Sign in / Sign up

Export Citation Format

Share Document