Chronic Effects of Enalapril on Blood Pressure, Stroke, Plasma Renin, Urinary Electrolytes and PGE2 Excretion in Stroke-Prone Spontaneously Hypertensive Rats

Watanabe, Takushi X.; Kawashima, Koichiro; Sokabe, Hirofumi

doi:10.1254/jjp.38.419

Cited by 21 publications

(7 citation statements)

References 16 publications

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“…The antihyper tensive potency of these CE inhibitors in SHRSP rats is compatible with that found in our previous study (10). Urinary excretion of kinins during treatment with CE inhibitors is shown in Fig.…”

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confidence: 90%

“…In a previous study in 14 to 15 -week old SH RSP rats, we found significant decreases in urinary excretion of kinins and urine volume (UV) in the 5th and 10th weeks of treatment with both enalapril and captopril (10). However, the data on urinary kinin excretion were not included in the paper because we collected acidified urine samples without pepstatin A, and the pos sibility of kinin formation during urine collection could not be excluded.…”

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confidence: 98%

“…To investigate the possible involvement of renal kinins in the antihypertensive effect of CE inhibitors, we determined the urinary excretion of kinins and electrolytes in stroke-prone spontaneously hypertensive (SHRSP) rats during treatment with enalapril and captopril. We have previously demonstrated that plasma renin activity in SHRSP rats is elevated during the late developmental and maintenance stage of hypertension (7,8) and that CE inhibitors produce a marked antihypertensive effect and prevent development of malignant hyper tensive cardiovascular diseases in this hyper tensive model (9,10).…”

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Effects of Enalapril and Captopril on Urinary Excretion of Kinins and Electrolytes in Stroke-Prone Spontaneously Hypertensive Rats

Kawashima¹,

Kimura²,

Watanabe

et al. 1985

Japanese Journal of Pharmacology

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Abstract-Urinary excretion of kinins in stroke-prone spontaneously hypertensive (SHRSP) rats was unchanged during oral enalapril (10 mg/kg) or captopril (30 mg/kg) treatment once a day for 8 days compared to vehicle treatment.However, a significant decrease in urinary kinin excretion was observed on the 5th and 7th day compared to the pretreatment value in rats treated with enalapril.Both enalapril and captopril produced a significant reduction in blood pressure when compared to the vehicle.These findings provide no positive evidence to support the hypothesis of possible involvement of renal kinins in the antihypertensive effect of converting enzyme inhibitors in SHRSP rats.

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Effects of Enalapril and Captopril on Urinary Excretion of Kinins and Electrolytes in Stroke-Prone Spontaneously Hypertensive Rats

Kawashima¹,

Kimura²,

Watanabe

et al. 1985

Japanese Journal of Pharmacology

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“…22 - 23 The renin-angiotensin system also participates in the pathophysiology of malignant hypertension in SHRSP, as shown by previous reports. 24 - 26 However, previous research done on the renin-angiotensin system of SHRSP has been limited to the circulating system. 22 -24 -26 -mating at Santen Pharmaceutical Co., Ltd., Osaka, Japan.…”

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Adrenal and circulating renin-angiotensin system in stroke-prone hypertensive rats.

et al. 1992

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The plasma and adrenal renin-angiotensin system in stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats were examined in animals at 5, 11, 18, and 25 weeks of age. Plasma active renin was significantly increased in 18-and 25-week-old SHRSP with impaired renal function, whereas there was no difference in the plasma prorenin level or renal renin content between the two strains at all ages examined. Thus, the rate of activation of prorenin seems to be enhanced in the kidney of SHRSP with malignant hypertension. Adrenal renin contents were severalfold higher in SHRSP than WKY rats at all ages. However, adrenal angiotensin peptides were not increased in SHRSP aged 5 and 11 weeks. In 18-week-old SHRSP, adrenal angiotensin II (Ang II) and HI (Ang III) levels were fourfold and 1.8-fold higher, respectively, than in WKY rats, accompanied by 1.5-fold higher plasma aldosterone. Increased adrenal angiotensin and plasma aldosterone were also found in 25-week-old SHRSP. Zonal distribution studies indicated that the elevated Ang H and DI in SHRSP were derived mainly from the capsular tissue (the zona glomerulosa). To examine the contribution of circulating angiotensin to the adrenal angiotensin content, effects of bilateral nephrectomy on adrenal angiotensin and renin were examined in 18-week-old rats. At 24 hours after nephrectomy, plasma angiotensin, prorenin, and active renin were decreased to almost negligible concentrations. Conversely, in both adrenal capsular and decapsular tissues of SHRSP and WKY rats, neither angiotensin nor renin was significantly decreased after nephrectomy. These results suggest that the increase in adrenal capsular Ang II contents in SHRSP may be partly due to an enhanced local production or Ang II. The renin-angiotensin system also participates in the pathophysiology of malignant hypertension in SHRSP, as shown by previous reports.24 -26 However, previous research done on the renin-angiotensin system of SHRSP has been limited to the circulating system.

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“…Consecutive dosing of enalapril at 10 mg/kg, p.o. produced a sustained antihypertensive effect in SHRSP rats (11).…”

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confidence: 89%

Antihypertensive Effect of Chronic KT3-671, a Structurally New Nonpeptide Angiotensin AT1-Receptor Antagonist, in Stroke-Prone Spontaneously Hypertensive Rats

Amano¹,

Fujimoto²,

Suzuki³

et al. 1995

Japanese Journal of Pharmacology

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ABSTRACT-KT3-671(2-propyl-8-oxo-1-[(2'-(1H-tetrazole-5-yl)biphenyl-4-yl)methyl]-4,5,6,7-tetrahydrocycloheptimidazole), a structurally new nonpeptide angiotensin AT,-receptor antagonist, was administered orally and repeatedly to 15-week-old stroke-prone spontaneously hypertensive rats for 7 weeks; and its effects on blood pressure, heart rate, renal function, plasma renin concentration (PRC), plasma aldosterone concentration (PAC) and hypertension-related tissue damage in the brain, heart, kidney and mesenteric artery were investigated. KT3-671 at a dose of 3 or 10 mg/kg, p.o. per day prevented development of hypertension and produced a significant and consistent reduction of blood pressure in a dose-dependent manner. Enalapril at a dose of 10 mg/kg per day produced cardiovascular effects similar to those of KT3-671 at 10 mg/kg. Despite marked reduction in blood pressure, neither KT3-671 nor enalapril affected the heart rate. KT3-671 at 10 mg/kg produced a transient and significant reduction of urinary sodium excretion in the second week, but did not affect renal function at any other time during the experimental period. Both KT3-671 at 10 mg/kg and enalapril at 10 mg/kg produced a significant increase in PRC and showed a tendency to decrease PAC. Repeated administration of KT3-671 reduced the severity of the pathological changes in the kidney. These results suggest that KT3-671 is a potentially useful antihypertensive drug.

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Chronic Effects of Enalapril on Blood Pressure, Stroke, Plasma Renin, Urinary Electrolytes and PGE2 Excretion in Stroke-Prone Spontaneously Hypertensive Rats

Abstract: Abstract-Antihypertensive effect of enalapril (MK-421

Cited by 21 publications

References 16 publications

Effects of Enalapril and Captopril on Urinary Excretion of Kinins and Electrolytes in Stroke-Prone Spontaneously Hypertensive Rats

Effects of Enalapril and Captopril on Urinary Excretion of Kinins and Electrolytes in Stroke-Prone Spontaneously Hypertensive Rats

Adrenal and circulating renin-angiotensin system in stroke-prone hypertensive rats.

Antihypertensive Effect of Chronic KT3-671, a Structurally New Nonpeptide Angiotensin AT1-Receptor Antagonist, in Stroke-Prone Spontaneously Hypertensive Rats

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