Gonadectomy and hormonal replacement changes systolic blood pressure and ventricular myosin isoenzyme pattern of spontaneously hypertensive rats.

Cardiac muscle can adapt to different functional demands, as evidenced by polymorphism of myosin. Pressure load in spontaneously hypertensive rats induced a shift of the myosin isoenzymes towards myosin V3 (18% V1, 27% V2, 55% V3) relative to normotensive Wistar rats (49% V1, 29% V2, 22% V3). A swimming routine with Wistar rats resulted in a shift towards myosin V1 (72% V1, 18% V2, 10% V3). The training effect is not restricted to normotensive rats, since spontaneously hypertensive rats subjected to the same swimming routine exhibited a myosin isoenzyme pattern (38% V1, 31% V2, 31% V3) approaching that of the sedentary Wistar rats. Swimming training can, therefore, prevent the myosin isoenzyme redistribution towards myosin V3 found in sedentary spontaneously hypertensive rats. Furthermore, systolic blood pressure was significantly reduced (130 ± 8 mmHg (1 mmHg = 133.322 Pa)) in the swim-trained compared with the sedentary spontaneously hypertensive rats (157 ± 12 mmHg). The training-induced changes in myosin polymorphism and systolic blood pressure are, at least partially, attributed to substantially normalized sympathetic activity. The functional relevance of swimming training in the spontaneously hypertensive rat is seen in the increased potential of coping with situations requiring fast contraction which may occur during sudden physical exertion or emotional stress.

Download Full-text

Effect oftrans fatty acids on plasma lipids, platelet function and systolic blood pressure in stroke-prone spontaneously hypertensive rats

Lipids ◽

10.1007/bf02544023 ◽

1991 ◽

Vol 26 (1) ◽

pp. 46-52 ◽

Cited By ~ 6

Author(s):

M. T. Chiang ◽

M. I. Otomo ◽

H. Itoh ◽

Y. Furukawa ◽

S. Kimura ◽

...

Keyword(s):

Blood Pressure ◽

Fatty Acids ◽

Systolic Blood Pressure ◽

Platelet Function ◽

Spontaneously Hypertensive Rats ◽

Plasma Lipids ◽

Hypertensive Rats ◽

Spontaneously Hypertensive

Download Full-text

Metformin decreases plasma insulin levels and systolic blood pressure in spontaneously hypertensive rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.4.h1250 ◽

1994 ◽

Vol 267 (4) ◽

pp. H1250-H1253 ◽

Cited By ~ 5

Author(s):

S. Verma ◽

S. Bhanot ◽

J. H. McNeill

Keyword(s):

Blood Pressure ◽

Systolic Blood Pressure ◽

Spontaneously Hypertensive Rats ◽

Plasma Insulin ◽

Metformin Treatment ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Insulin Levels ◽

Plasma Insulin Levels ◽

Wistar Kyoto

To determine the relationship between hyperinsulinemia and hypertension in spontaneously hypertensive rats (SHR), the antihyperglycemic agent metformin was administered to SHR and their Wistar-Kyoto (WKY) controls, and its effects on plasma insulin levels and blood pressure were examined. Five-week-old rats were started on oral metformin treatment (350 mg.kg-1.day-1, which was gradually increased to 500 mg.kg-1.day-1 over a 2-wk period). Metformin treatment caused sustained decreases in plasma insulin levels in the SHR (27.1 +/- 2.3 vs. untreated SHR 53.5 +/- 2.7 microU/ml, P < 0.001) without having any effect in the WKY (30.7 +/- 2.2 vs. untreated WKY 37.8 +/- 1.6 microU/ml, P > 0.05). The treatment did not affect the plasma glucose levels in any group. Metformin treatment also attenuated the increase in systolic blood pressure in the SHR (157 +/- 6.0 vs. untreated SHR 196 +/- 9.0 mmHg, P < 0.001) but had no effect in the WKY (134 +/- 3 vs. untreated WKY 136 +/- 4 mmHg, P > 0.05). Furthermore, raising plasma insulin levels in the metformin-treated SHR to levels that existed in the untreated SHR reversed the effect of metformin on blood pressure (189 +/- 3 vs. untreated SHR 208 +/- 5.0 mmHg, P > 0.05). These findings suggest that either hyperinsulinemia may contribute toward the increase in blood pressure in the SHR or that the underlying mechanism is closely associated with the expression of both these disorders.

Download Full-text