scholarly journals Therapeutic Effects of a Calcium Antagonist, Lacidipine, on Stroke-Prone Spontaneously Hypertensive Rats With Cerebrovascular Lesions

1999 ◽  
Vol 80 (3) ◽  
pp. 199-208 ◽  
Author(s):  
Hideyuki Funato ◽  
Mitsutoshi Watanabe ◽  
Akio Uemura
Keyword(s):  
Calcium Antagonist ◽  
Spontaneously Hypertensive Rats ◽  
Therapeutic Effects ◽  
Hypertensive Rats ◽  
Cerebrovascular Lesions ◽  
Spontaneously Hypertensive

Therapeutic effects of losartan on prostatic hyperplasia in spontaneously hypertensive rats

Life Sciences ◽  
2021 ◽  
Vol 266 ◽  
pp. 118924
Author(s):  
Shogo Shimizu ◽  
Yoshiki Nagao ◽  
Takahiro Shimizu ◽  
Youichirou Higashi ◽  
Takashi Karashima ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Prostatic Hyperplasia ◽  
Therapeutic Effects ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Studies on Hypertension in Spontaneously Hypertensive Rats

1973 ◽  
Vol 45 (s1) ◽  
pp. 11s-14s
Author(s):  
Kozo Okamoto ◽  
Yukio Yamori ◽  
Shoichiro Nosaka ◽  
Akira Ooshima ◽  
Fumitada Hazama
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Genetic Factors ◽  
Vascular Lesions ◽  
Hypertensive Rats ◽  
Cerebrovascular Lesions ◽  
Spontaneously Hypertensive

1. The pathogenesis and complications occurring in spontaneously hypertensive rats (SHR) have been studied. 2. Genetic factors are important both in the development of hypertension and in determining susceptibility to vascular lesions. 3. Selective substrains of SHR may be particularly prone to develop cerebrovascular lesions.

Implication of renal perfusion pressure in stroke of spontaneously hypertensive rats

1980 ◽  
Vol 238 (3) ◽  
pp. H317-H324 ◽  
Author(s):  
A. Nagaoka ◽  
A. Shino ◽  
M. Shibota
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renal Cortex ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Hypertensive Rats ◽  
Cerebrovascular Lesions ◽  
Spontaneously Hypertensive ◽  
Renal Perfusion Pressure ◽  
Renal Changes ◽  
Renal Cortical Blood Flow

To elucidate the significance of hypertension associated with cerebrovascular lesions (CVL), renal perfusion pressure (RPP) was controlled by aortic clips of two different sizes in stroke-prone spontaneously hypertensive rats kept under normal or salt-loaded conditions. Tail and femoral arterial pressures (RPPs) in the mildly and severely clamped animals were reduced in proportion to the severity of the clamping. In contrast, carotid pressures in both clamped groups were significantly higher than that in the controls. Proteinuria and hyperreninemia accompanied by arteriolar changes in the renal cortex were observed in the controls prior to the onset of CVL. The renal changes were inhibited by both types of clamping. The onset of CVL was delayed by the mild clamping in salt-loaded animals, but accelerated by the severe clamping in both the normal and salt-loaded animals. Renal cortical blood flow was decreased only by the severe clamping. The results suggest that reduction in RPP and/or renal ischemia, which seems to be due to the hypertensive arteriolar changes in the renal cortex, may be related to the pathogenesis of CVL in the stroke-prone rats with or without hyperreninemia.

Exercise training and incidence of cerebrovascular lesions in stroke-prone spontaneously hypertensive rats

1990 ◽  
Vol 68 (3) ◽  
pp. 1080-1085 ◽  
Author(s):  
C. M. Tipton ◽  
S. McMahon ◽  
J. R. Leininger ◽  
E. L. Pauli ◽  
C. Lauber
Keyword(s):  
Exercise Training ◽  
Spontaneously Hypertensive Rats ◽  
Female Rats ◽  
Moderate Exercise ◽  
Hypertensive Rats ◽  
Cerebrovascular Lesions ◽  
Spontaneously Hypertensive ◽  
Male And Female Rats ◽  
Blood Pressures ◽  
Subjective Evidence

To assess the effects of moderate exercise [40-70% maximal oxygen uptake (VO2max)] on resting blood pressures, the presence of cerebrovascular lesions, and the life spans of stroke-prone hypertensive rats, nontrained and trained male and female rats were assigned to two experimental groups. The first (n = 48) were exercise trained after 38 days of age, whereas the second (n = 44) initiated exercise training when the animals were 134 days of age. To facilitate cerebrovascular lesions, the sodium concentrations in the rat chow and in the drinking solutions were increased. Symptoms utilized to denote the presence of cerebrovascular lesions were irritability, hyperresponsiveness, ataxia, lethargy, unwillingness to run, and combinations thereof. All brains were removed immediately after death, fixed, and evaluated grossly and microscopically for lesions. In the study with the younger animals, training was associated with a 7-9% increase in VO2max that was statistically significant only in animals with no histological evidence of cerebrovascular lesions. For the older animals, a significant 5-8% increase in VO2max was noted for animals with or without lesions. After 42 days of training for both groups, resting blood pressures for the trained groups with histological lesions were significantly lower. However, this trend did not continue, and the older trained rats appeared to have strokes earlier and to die sooner than their nontrained controls. Although 83% of the older animals had subjective evidence for a stroke before they died, the percentage of animals with lesions ranged from 42 to 58%, with the trained groups having higher percentages.(ABSTRACT TRUNCATED AT 250 WORDS)

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