Hormonal and Renal Responses to Oral Once-Daily Calcium Entry Blocker in Normotensive and Hypertensive Persons

Fuji, Yoshiaki; Suzuki, Hiromichi; Katsumata, H.; Nakajima, Sadao; Saruta, Takao

doi:10.1097/00005344-198804000-00009

Cited by 37 publications

(22 citation statements)

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“…Hyper cholesterolemia neutralizes anionic charges in the glomerulus, inducing the increase in urinary excretion of albumin (35). Recently, antihyperlipidemic agents like lovastatin were shown to be beneficial for glomeru losclerosis (14). In the present study, vehicle-treated rats showed a marked increase in sTC, which is likely to exacerbate the nephrotic syndrome.…”

Section: Methodsmentioning

confidence: 46%

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Protective Effect of Benidipine against the Development of Glomerular Sclerosis in Experimental Nephrotic Syndrome

Shirakura

Sano

Karasawa

et al. 1992

Japanese Journal of Pharmacology

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ABSTRACT-An experimental focal segmental glomerular sclerosis (FSGS) was induced by the com bined administration of puromycin aminonucleoside (PAN) and protamine sulfate (PS). Blood collec tions were made on days 0, 37, 70 and 94. Urine collections were made on days 0, 24, 80 and 94. Vehicle-treated rats showed severe proteinuria and an increase in serum total cholesterol (sTC). Benidi pine (1 or 3 mg/kg, p.o.)-treated rats exhibited less proteinuria and lower sTC than the vehicle-treated rats. On days 70 and 94, both blood urea nitrogen (BUN) and serum creatinine (sCR) values in the vehicle-treated rats were significantly higher than those in normal rats (without treatment with PAN and PS). On the other hand, the treatment with benidipine (1 or 3 mg/kg, p.o.) attenuated the in creases in BUN and sCR. On day 94, vehicle-treated rats showed a significant decrease in creatinine clearance as compared with normal rats, but benidipine (1 or 3 mg/kg, p.o.)-treated rats did not. The histology was examined on day 94. Vehicle-treated rats demonstrated a significantly greater percentage of glomeruli with segmental areas of glomerulosclerosis/hyalinosis, mesangial cell proliferation, and mesangial foam cell. Benidipine (3 mg/kg, p.o.) ameliorated the development of renal regeneration as estimated by histological examination. These results suggest that the Ca-channel blocker benidipine is a favorable drug for preventing the progression of glomerular sclerosis.

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Section: Methodsmentioning

confidence: 46%

“…Benidipine is a potent Ca-channel blocker with long lasting antihypertensive and antianginal activities (13,14). The present study was conducted to determine whether the Ca-channel blocker benidipine could pre vent nephrotic syndrome in a rat model of FSGS in duced by PAN and PS.…”

mentioning

confidence: 98%

Protective Effect of Benidipine against the Development of Glomerular Sclerosis in Experimental Nephrotic Syndrome

Shirakura

Sano

Karasawa

et al. 1992

Japanese Journal of Pharmacology

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“…The effect of combined administration of benidipine (Kubo et al 1985;Fujii et al 1988) or nilvadipine (Ohtsuka et al 1983) with endothelin was assessed in rats on a regular diet. Following a 7 day control period, the rats were administered either with benidipine at a rate of 6 mg/kg/day or with nilvadipine at a rate of 10 mg/kg/day dissolved in polyethylene glycol by oral gavage once a day in combination with endothelin infused intravenously at a rate of 60pg/kg/day for up to 6 days.…”

Section: Methodsmentioning

confidence: 99%

Calcium channel blockers reverse the sustained elevation of blood pressure induced by chronic infusion of endothelin in conscious rats.

Yasujima¹,

Abe²,

Kanazawa

et al. 1990

Tohoku J. Exp. Med.

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To determine whether endothelin could act as a circulating hormone in the regulation of blood pressure and sodiumwater excretion, we assessed the chronic effects of synthetic endothelin on systolic blood pressure, urine volume and urinary sodium excretion in conscious rats, and also evaluated the effects of benidipine or nilvadipine, newly developed calcium channel blockers, in rats infused chronically with synthetic endothelin. Continuous infusion of endothelin at a rate of 60,ug/kg/day into the jugular vein via osmotic minipumps induced a significant increase in systolic blood pressure, but did not induce any significant changes in urine volume and urinary sodium excretion, compared to those in vehicle-infused rats. On the contrary, the infusion of endothelin at a rate of 6 jig/kg/day did not induce any significant changes in systolic blood pressure, urine volume and urinary sodium excretion, compared to those in vehicle-infused rats. When 6 mg/kg/day of benidipine or 10 mg/kg/day of nilvadipine was administered simultaneously with 60 ,u g/kg/day of endothelin, the systolic blood pressure rose on Day I to only 137.0+2.4 mmHg (p <0.05) and 119.7 + 5.9 mmHg (p <0.05) compared to the rise to 163.8 + 4.7 mmHg when endothelin alone was infused. The antihypertensive effect of benidipine or nilvadipine was sustained for the entire experimental period and was not associated with any significant changes in urine volume and urinary sodium excretion. The present results suggest that endothelin can act as a circulating hormone and might be involved in the regulation of blood pressure. In addition, they clearly

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“…[12][13][14] Pharmacologic studies have shown that this drug differs from nifedipine in the very slow rate of onset and cessation of cardiovascular effects both in vitro and in vivo. 1,2,15) In the present study, the in vivo 1,4-DHP receptor binding of cilnidipine and nifedipine in the mesenteric artery of SHR was investigated and compared with that in the aorta, myocardium, and cerebral cortex.…”

Section: Specific Binding Of (ϩ)-[mentioning

confidence: 99%

In Vivo Measurement of 1,4-Dihydropyridine Receptors in Mesenteric Arteries of Spontaneously Hypertensive Rats and Effect of Nifedipine and Cilnidipine.

Nakajima

Yamada

Uchida

et al. 2002

Biological & Pharmaceutical Bulletin

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The present study was undertaken to measure 1,4-dihydropyridine (DHP) receptor binding sites in vivo in the mesenteric artery and other tissues of spontaneously hypertensive rats (SHR) and to examine the effect of nifedipine and cilnidipine. Specific in vivo binding of (؉)- 4 or 1.7) of the AUC mesenteric artery to AUC aorta or AUC myocardium after oral administration of cilnidipine was greater than the corresponding value (1.1) for nifedipine. In conclusion, the present study demonstrates that cilnidipine, but not nifedipine, may occupy 1,4-DHP receptors in the small artery in a more selective and sustained manner than in other tissues of SHR, and thus such receptor binding specificity may be responsible for the long-lasting hypotensive effect of this drug.

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Hormonal and Renal Responses to Oral Once-Daily Calcium Entry Blocker in Normotensive and Hypertensive Persons

Cited by 37 publications

References 0 publications

Protective Effect of Benidipine against the Development of Glomerular Sclerosis in Experimental Nephrotic Syndrome

Protective Effect of Benidipine against the Development of Glomerular Sclerosis in Experimental Nephrotic Syndrome

Calcium channel blockers reverse the sustained elevation of blood pressure induced by chronic infusion of endothelin in conscious rats.

In Vivo Measurement of 1,4-Dihydropyridine Receptors in Mesenteric Arteries of Spontaneously Hypertensive Rats and Effect of Nifedipine and Cilnidipine.

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