Abstract P314: Effect of Sex on Blood Pressure and Endothelial Dysfunction in the Novel BPH2 Mouse Model of Hypertension

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Sean P Didion
Keyword(s):  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Renin Angiotensin System ◽  
Similar Degree ◽  
The Novel ◽  
Angiotensin System ◽  
Male And Female ◽  
Renin Angiotensin

Very little is known regarding blood pressure and endothelial function between the sexes in the hypertensive BPH2 mouse. Thus, the first goal was determine whether blood pressure and endothelial function are significantly different between male and female BPH2 mice. Information regarding the role of the renin-angiotensin system in the BPH2 mouse is also limited; therefore the second goal was to determine the role of the renin-angiotensin system by treating BPH2 mice with captopril for 4 weeks. Systolic blood pressure (SBP) was significantly elevated (P<0.05) and yet comparable (P>0.05) in male and female BPH2 mice and averaged 140±3 and 136±3 mmHg, respectively, whereas, in control mice SBP averaged 112±4 mmHg. Endothelial responses to acetylcholine in carotid artery were markedly impaired (P<0.05) and to a similar degree in male and female BPH2 mice as compared to controls. Captopril treatment was associated with a significant (P<0.05) reduction in blood pressure of 35±7 and 43±4 mmHg in male and female BPH2 mice, respectively. Captopril also resulted in an improvement of endothelial responses in male and female BPH2 mice. These findings demonstrate that male and female BPH2 mice are equally hypertensive and both sexes are characterized by endothelial dysfunction. In addition, the renin-angiotensin system may contribute to both hypertension and endothelial dysfunction in this model. Taken together, our data define the BPH2 mouse as an important model to compare and contrast the effects of hypertension between the sexes. Supported by NIH HL-107632.

Role of renin-angiotensin system in glucocorticoid hypertension in rats

1982 ◽  
Vol 243 (1) ◽  
pp. E48-E51 ◽  
Author(s):  
H. Suzuki ◽  
M. Handa ◽  
K. Kondo ◽  
T. Saruta
Keyword(s):  
Blood Pressure ◽  
Intravenous Injection ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Dependent Manner ◽  
Concurrent Administration ◽  
Angiotensin System ◽  
Renin Angiotensin

The role of the renin-angiotensin system in the regulation of the blood pressure of dexamethasone-treated rats (Dex) was evaluated using saralasin, an angiotensin II antagonist, and SQ 14225 (SQ) (d-3-mercapto-2-methylpropranoyl-1-proline), an angiotensin-converting enzyme inhibitor. During a 7-day period blood pressure rose 65 +/- 10 mmHg (P less than 0.001) in Dex with no significant changes in plasma renin activity. Concurrent administration of dexamethasone and SQ attenuated the elevation of blood pressure (P less than 0.05). In the conscious, freely moving state, intravenous injection of SQ (10, 30, 100 micrograms/kg) reduced blood pressure of DEX in a dose-dependent manner (P less than 0.05). Also, intravenous injection of saralasin (10 micrograms.kg-1 . min-1) reduced blood pressure significantly (P less than 0.01). Bilateral nephrectomy abolished the effects of saralasin and SQ on blood pressure in Dex. These results indicate that the elevation of blood pressure in DEX depends partially on the renin-angiotensin system.

Is angiotensin essential in drinking induced by water deprivation and caval ligation?

1981 ◽  
Vol 240 (1) ◽  
pp. R75-R80 ◽  
Author(s):  
M. C. Lee ◽  
T. N. Thrasher ◽  
D. J. Ramsay
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Water Deprivation ◽  
Essential Role ◽  
Vena Cava ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

The role of the renin-angiotensin system in drinking induced by water deprivation and caval ligation was assessed by infusion of saralasin into the lateral ventricles of rats. This technique was first validated by demonstrating its capability to specifically antagonize drinking to both systemic and central angiotensin II. However, neither the latency to drink nor the amount of water consumed following 24- or 30-h water deprivation was affected by saralasin. Furthermore, saralasin had no significant effect on the recovery of blood pressure or on the water intake following ligation of the abdominal vena cava. These observations suggest that the renin-angiotensin system alone does not play an essential role in the control of drinking following water deprivation or caval ligation in rats.

Role of the Brain Renin-angiotensin System in Blood Pressure Regulation

2007 ◽  
Vol 31 (S1) ◽  
pp. 343-346
Author(s):  
M. V. Varoni ◽  
D. Palomba ◽  
M. P. Demontis ◽  
S. Gianorso ◽  
G. L. Pais ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renin Angiotensin System ◽  
Blood Pressure Regulation ◽  
Pressure Regulation ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain

Role of the renin-angiotensin system in the development of thyroxine-induced hypertension

1997 ◽  
Vol 136 (6) ◽  
pp. 656-660 ◽  
Author(s):  
Cipriano Garcia del Rio ◽  
María Rosario R Moreno ◽  
Antonio Osuna ◽  
Juan de Dios Luna ◽  
Joaquín García-Estañ ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Tap Water ◽  
Weight Ratio ◽  
Renin Angiotensin System ◽  
Control Group ◽  
Angiotensin System ◽  
Renin Angiotensin

Abstract Objective: We evaluated the influence of chronic blockade of the renin-angiotensin system on hypertension induced by long-term thyroxine (T4) administration. To this end, we determined the effects of chronic treatment with captopril on blood pressure, cardiac hypertrophy and other renal and metabolic variables of hypertensive hyperthyroid rats. Methods: T4 was administered s.c. at 0·38 μmol/kg per day and captopril was given in the drinking water (1·38 mmol/l). Both treatments were maintained for 6 weeks. Control rats received tap water. After the treatment period, the rats were placed in metabolic cages. Later, blood pressure was measured in conscious rats by intra-arterial determination. Results: T4-treated rats showed an increased mean arterial pressure (MAP) whereas, in rats treated with T4 plus captopril, MAP was similar to that of the control group. Captopril did not affect the increased heart rate or ventricular weight/body weight ratio of hyperthyroid rats, but it improved the reduced creatinine clearance of these animals. Conclusions: The elevation in blood pressure produced by long-term T4 administration was prevented by chronic blockade of the renin-angiotensin system. Captopril improved the renal function of hyperthyroid rats, but did not affect the relative cardiac hypertrophy of these animals. European Journal of Endocrinology 136 656–660

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