scholarly journals Influence of blood pressure on development of aortic medial smooth muscle hypertrophy in spontaneously hypertensive rats.

Hypertension ◽  
1987 ◽  
Vol 9 (2) ◽  
pp. 178-187 ◽  
Author(s):  
G K Owens
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Hypertrophy ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Baicalin relaxes vascular smooth muscle and lowers blood pressure in spontaneously hypertensive rats

2019 ◽  
Vol 111 ◽  
pp. 325-330 ◽  
Author(s):  
Liliqiang Ding ◽  
Chenglin Jia ◽  
Yong Zhang ◽  
Wenjian Wang ◽  
Weiliang Zhu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Expression of smooth muscle MyHC B in blood vessels of hypertrophied heart in experimentally hypertensive rats

2003 ◽  
Vol 284 (2) ◽  
pp. R607-R610 ◽  
Author(s):  
Katharina Wetzel ◽  
Ovidiu Baltatu ◽  
Benno Nafz ◽  
Pontus B. Persson ◽  
Hannelore Haase ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Adaptive Response ◽  
Spontaneously Hypertensive Rats ◽  
Expression Patterns ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Genetic Origin ◽  
Spontaneously Hypertensive ◽  
Muscle Myosin

We demonstrated recently a significantly lower fraction of cardiac precapillary arterioles that expressed smooth muscle myosin heavy chain (MyHC) B (SMB) in spontaneously hypertensive rats. To clarify whether this reduction of SMB expression is of genetic origin, we investigated SMB expression in cardiac precapillary arterioles of normotensive and experimentally hypertensive rats (one clip, one kidney or ANG II minipump). We observed similar SMB expression patterns in precapillary arterioles of experimentally hypertensive rats compared with normotensive controls. These observations suggest that the downregulation of SMB in spontaneously hypertensive rats is of genetic origin rather than an adaptive response to chronically enhanced blood pressure and cardiac hypertrophy.

Heparin suppresses endothelin-1 action and production in spontaneously hypertensive rats

1992 ◽  
Vol 263 (5) ◽  
pp. R1035-R1041
Author(s):  
K. Yokokawa ◽  
A. K. Mandal ◽  
M. Kohno ◽  
T. Horio ◽  
K. Murakawa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Spontaneously Hypertensive Rats ◽  
Antihypertensive Effect ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Endothelin 1

Previous studies have shown that chronic subcutaneous administration of heparin significantly reduces blood pressure in hypertensive rats. The intracellular mechanisms of how heparin prevents smooth muscle cell proliferation remain unclear. This study was designed to examine whether heparin affects endothelin-1 action and production, to further elucidate the mechanism of the antihypertensive effect of heparin. Four-week treatment with heparin (300 U/day sc) significantly decreased blood pressure in spontaneously hypertensive rats (SHR; 199 +/- 8 vs. 164 +/- 9 mmHg; P < 0.001) and completely blunted pressor response to endothelin-1 in SHR. Heparin treatment did not decrease blood pressure response nor did it attenuate blood pressure responses to endothelin-1 in Wistar-Kyoto rats (WKY). Heparin significantly suppressed endothelin-1-induced increase in intracellular calcium concentration and inositol 1,4,5-trisphosphate level in cultured vascular smooth muscle cells in a dose-dependent manner and endothelin-1 release from cultured endothelial cells. These inhibitions were significantly more pronounced in SHR than in WKY. In conclusion, our findings indicate that the antihypertensive effect of heparin is mediated, at least in part, by the inhibition of endothelin-1 action on vascular smooth muscle cells and endothelin-1 production from endothelial cells.

Membrane potential of vascular smooth muscle and hypertension in spontaneously hypertensive rats

1984 ◽  
Vol 62 (8) ◽  
pp. 957-960 ◽  
Author(s):  
D. W. Cheung
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Membrane Potential ◽  
Vascular Smooth Muscle ◽  
Spontaneously Hypertensive Rats ◽  
Chronic Treatment ◽  
Resting Membrane Potential ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

The resting membrane potential of tail arteries from spontaneously hypertensive rats (SHRs) and Wistar-Kyoto controls (WKYs) was compared. At 4–5 weeks old, the blood pressure and resting membrane potential of the SHRs was not significantly different from the WKYs. The blood pressure of 8- to 10-week-old SHRs increased significantly to 183 mmHg (1 mmHg = 133.322 Pa) from 127 mmHg at 4 weeks, and the membrane potential decreased from 60 to 51 mV. At 15 weeks of age, the blood pressure of the SHRs was 193 mmHg and the membrane potential was 49 mV. In WKYs, there was no significant change in membrane potential with age. The decrease in membrane potential in the SHRs is due to a decrease in the ouabain-sensitive electrogenic pumping. Chronic treatment of the SHRs with captopril (100 mg∙kg−1∙day−1) prevented the increase in blood pressure and the decrease in membrane potential.

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.

Evidence for circulating factors as a cause of venous hypertrophy in spontaneously hypertensive rats

1981 ◽  
Vol 241 (3) ◽  
pp. H421-H430 ◽  
Author(s):  
S. Greenberg ◽  
K. Gaines ◽  
D. Sweatt
Keyword(s):  
Smooth Muscle ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Hypertrophy ◽  
Dry Weight ◽  
Hypertensive Rats ◽  
Humoral Factors ◽  
Spontaneously Hypertensive ◽  
Blood Flows ◽  
Portal Veins ◽  
Wistar Kyoto

Increased contractility, decreased extensibility, and hypertrophy occur in portal veins (PV) obtained from spontaneously hypertensive rats (SHR). This study evaluates the potential existence of circulating humoral factors as mediators of these changes. SHR were parabiosed with normotensive Wistar-Kyoto rats (WKY) matched for sex and age. Blood pressure increased over a 3-wk to 5-mo period in 2-mo-old WKY parabiosed with SHR. Similar changes were absent in WKY parabiosed with WKY (WKY-WKY) or in SHR parabiosed with SHR (SHR-SHR). The functional blood flows between the parabiosed pairs were 1.4 +/- 0.21%. PV obtained from WKY-WKY developed less spontaneous tension, less tension in response to norepinephrine, potassium chloride, angiotensin II, an 9 alpha, 11 alpha-epoxymethano-prostaglandin H2, and were more extensible than PV obtained from SHR-SHR. In contrast, PV obtained from the WKY member of the WKY-SHR, developed changes similar to PV obtained from the SHR. The wet and dry weight and protein content increased in the PV of WKY-SHR, when compared with these parameters in the PV obtained from WKY-WKY. Light microscopy of the blood vessels demonstrated that PV obtained from the wKY parabiosed to SHR exhibited medial smooth muscle hypertrophy. These data support the conclusion that a circulating humoral factor in the SHR may initiate the venous smooth muscle derangements during the development of spontaneous hypertension.

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