scholarly journals Effect of Euglena cells on blood pressure, cerebral and peripheral vascular changes and life-span in stroke-prone spontaneously hypertensive rats.

1988 ◽  
Vol 41 (2) ◽  
pp. 115-125 ◽  
Author(s):  
Tetsuo MURAKAMI ◽  
Kozo OKAMOTO ◽  
Shozaburo KITAOKA ◽  
Yoshitomi IIZUKA
Keyword(s):  
Blood Pressure ◽  
Life Span ◽  
Spontaneously Hypertensive Rats ◽  
Vascular Changes ◽  
Peripheral Vascular ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Blood pressure control and erythrocytosis in rats: theory and observations

1994 ◽  
Vol 72 (6) ◽  
pp. 679-686 ◽  
Author(s):  
Anne B. Gould ◽  
Susan Goodman ◽  
Charles Swartz
Keyword(s):  
Blood Pressure ◽  
Cell Volume ◽  
Blood Volume ◽  
Packed Cell Volume ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
Pressure Control ◽  
Peripheral Vascular ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

We compared some of our latest experiments on blood pressure control and erythrocytosis in spontaneously hypertensive rats with Gaar's computer-simulated studies, which suggest that erythrocytosis is a key to understanding the hemodynamic changes in hypertension. We tested two of Gaar's several predictions: (i) peripheral vascular resistance decreases when the feedback control of erythrocytosis is blocked and (ii) in primary hypertension, blood volume is increased slightly. We also studied the interrelation of systolic blood pressure and plasma renin substrate in spontaneously hypertensive rats, and the effect of diet on renin, blood pressure, and erythrocytosis. Our data showed that (i) on a percentage basis the renin system supports blood pressure essentially in the same manner in normal and hypertensive rats, (ii) peripheral vascular resistance decreased when erythrocytosis was partially blocked by feeding a low-iron diet, (iii) blood volume was similar in normal and hypertensive rats, and (iv) dextrin stimulates plasma renin, packed cell volume, and blood pressure in hypertensive rats. We conclude that blood pressure and erythrocytosis are interrelated, that the combined data of simulated and experimental studies support the notion that primary hypertension is a blood-vessel adaptation in response to a renal energy need that may require additional oxygen.Key words: angiotensinogen, renin, dextrin, packed cell volume.

Effects of the Prdx2 depletion on blood pressure and life span in spontaneously hypertensive rats

2019 ◽  
Vol 42 (5) ◽  
pp. 610-617 ◽  
Author(s):  
Zinat Mahal ◽  
Koichi Fujikawa ◽  
Hiroyuki Matsuo ◽  
Hasan M. Zahid ◽  
Masamichi Koike ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Life Span ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Influence of chronic nadolol treatment on blood pressure and vascular changes in spontaneously hypertensive rats

1992 ◽  
Vol 70 (9) ◽  
pp. 1261-1270 ◽  
Author(s):  
Robert M. K. W. Lee ◽  
Jim Tsoporis ◽  
Roger R. J. Wang
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Cells ◽  
Mesenteric Arteries ◽  
Control Group ◽  
Vascular Changes ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

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.

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