Drugs online research references
Jpn Circ J. 1995 Sep;59(9):624-30.
Comparable effects of angiotensin II and converting enzyme blockade on hemodynamics and cardiac hypertrophy in spontaneously hypertensive rats.
Mori T, Nishimura H, Ueyama M, Kubota J, Kawamura K.
Third Department of Internal Medicine, Osaka Medical College, Japan.
Angiotensin-converting enzyme inhibitors may regress left ventricular hypertrophy (LVH) without decreasing blood pressure (BP). The aim of the present study was to compare the effects of low and high doses of lisinopril and the angiotensin II receptor antagonist TCV116 (TCV) on LVH and hemodynamics in spontaneously hypertensive rats (SHR). Lisinopril (0.5 and 3 mg/kg per day) and TCV (0.3 mg/kg per day) were given to 8-week-old male SHR daily for 2 weeks. Untreated SHR and Wistar-Kyoto rats (WKY) served as controls. Untreated SHR had a greater left ventricular (LV) weight than WKY (p < 0.01). Lisinopril (3 mg/kg per day) decreased both LV weight and BP. Lisinopril (0.5 mg/kg per day) significantly decreased LV weight, but not BP. In contrast, although TCV significantly decreased BP, LVH was not suppressed. Renal blood flow (RBF) in untreated SHR was less than that in WKY (p < 0.05), but was increased with either lisinopril (3 mg/kg per day)-treated rats (p< 0.05). These findings suggest that factors other than afterload reduction play a role in the regression of LVH with lisinopril, whereas a longer duration of treatment and/or a higher dose may be necessary with TCV. Despite the decrease in BP, TCV normalized RBF in SHR, perhaps due to the blockade of renal angiotensin II.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7500546&dopt=Abstract
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Urology. 1995 Dec;46(6):785-9.
Effect of angiotensin-converting enzyme inhibition on nephropathy in patients with a remnant kidney.
Novick AC, Schreiber MJ Jr.
Department of Urology, Cleveland Clinic Foundation, OH 44195, USA.
OBJECTIVES. This study was performed to evaluate the effect of angiotensin-converting enzyme inhibitor (ACEI) therapy and dietary protein restriction on nephropathy involving a remnant kidney. METHODS. Five patients with proteinuria > or = 5 years following partial removal of a solitary kidney were treated with a low-protein diet and an ACEI agent. Four patients had biopsy-proven focal segmental glomerulosclerosis. The daily urinary protein excretion ranged from 1240 to 10,032 mg. The serum creatinine levels ranged from 1.2 to 3.1 mg/dL. RESULTS. The post-treatment follow-up interval ranged from 18 to 30 months. The treatment regimen was well tolerated in all patients. Four patients experienced a reduction in the urinary protein level while maintaining stable overall renal function. In 1 patient, the urinary protein level increased and renal function gradually deteriorated following ACEI therapy. CONCLUSIONS. These preliminary data suggest that ACEI therapy and a low-protein diet may mitigate nephropathy associated with a remnant kidney.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7502416&dopt=Abstract
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J Cardiovasc Pharmacol. 1994 Jan;23(1):149-54.
Converting enzyme inhibition improves congestion and survival in hypertensive rats with high-output heart failure.
Nishimura H, Oka T, Ueyama M, Kubota J, Kawamura K.
Third Department of Internal Medicine, Osaka Medical College, Japan.
The effects of angiotensin-converting enzyme (ACE) inhibitors in high-output heart failure have not yet been well established. We evaluated the effects of lisinopril (3 mg/kg/day) on hemodynamics, neurohormones, and survival in 10-week-old spontaneously hypertensive rats (SHR) with aortocaval fistula. Sham-operated treated and untreated SHR served as controls. Cardiac output (CO) was determined by thermodilution method, and renal blood flow (RBF) was assessed by laser-Doppler flowmetry. In sham-operated SHR, 2-week treatment with lisinopril decreased blood pressure (BP), left ventricular (LV) weight, and total peripheral resistance (TPR) (p < 0.01 each) and increased RBF and plasma renin activity (PRA) (both p < 0.05); CO and LV end-diastolic pressure (LVEDP) were unchanged. Fistula creation induced biventricular hypertrophy and high-output heart failure [increased LVEDP, CO, pulse pressure, and plasma norepinephrine (NE) and decreased RBF] with congestive signs (ascites, tachypnea). Lisinopril decreased LVEDP (p < 0.01), increased RBF, prolonged survival (both p < 0.05), and prevented ascites (0 vs. 46%) and increased PRA (p < 0.05) and attenuated the increase in plasma NE. Heart weight, BP, and CO were not affected by lisinopril. Thus, lisinopril ameliorated congestion and improved survival in SHR with fistula without compromising cardiorenal hemodynamics. Venous and renal dilatation and attenuation of vasoconstrictive systems may have contributed to the beneficial effects.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7511728&dopt=Abstract
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