Drugs online research references
Clin Exp Hypertens. 1999 Jan-Feb;21(1-2):51-9.
Effect of nifedipine and enalapril on insulin-induced glucose disposal in spontaneous hypertensive and diabetic rats.
Mehta AA, Patel S, Santani DD, Goyal RK.
Department of Pharmacology, L.M. College of Pharmacy, Ahmedabad, India.
Hypertension and diabetes mellitus are associated with hyperinsulinemia and insulin resistance. The present work was undertaken to study the effects of enalapril and nifedipine on insulin sensitivity in spontaneously hypertensive (SH) rats and diabetic rats. Insulin sensitivity was measured by insulin tolerance test using K(ITT) as an index of insulin mediated glucose metabolism. The time to produce 50% fall in initial blood sugar level (T1/2) was significantly higher in non-insulin dependent diabetes mellitus (NIDDM) and SH rats as compared to Wistar control. The mean K(ITT) values were significantly lower in NIDDM and SH rats as compared to Wistar control. Treatment with nifedipine (10 mg/kg) and enalapril (5 mg/kg) for 15 days produced a significant reduction in T1/2. Further, K(ITT) value was found to be significantly increased in SH rats treated with nifedipine or enalapril as compared to control. Our data indicate that NIDDM and SH rats are not only hyperinsulinemic but also insulin resistant. Nifedipine and enalapril treatment produced increase in insulin sensitivity in these animals.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10052641&dopt=Abstract
Zhongguo Yao Li Xue Bao. 1996 Mar;17(2):142-5.
Effects of captopril and enalapril on intracellular Ca2+ in vascular smooth muscle cell.
Qi JH, Zhang L, Wang J, Wei PJ, Gu PK, Jin ZJ, Huang MZ, Wang HY.
Department of Pharmacology, Shanghai Second Medical University, China.
AIM: To determine whether angiotensin-converting enzyme inhibitors can affect Ca2+ handling in cultured aortic smooth muscle cells (ASMC) directly. METHODS: Cultured ASMC derived from rat aorta were loaded with the intracellular Ca2+ ([Ca]2+i) fluorescent indicator Fura 2-AM and digital image processing technique was used. RESULTS: Resting [Ca2+]i was greater in ASMC from SHR vs WKY (P < 0.01). KCl-, norepinephrine (NE)-, and angiotensin II (Ang)-induced [Ca2+]i increases were enhanced in ASMC of SHR vs WKY (220 +/- 6, 212 +/- 8, and 215 +/- 14 vs 199 +/- 6, 202 +/- 7, and 195 +/- 7 nmol.L-1, respectively). Captopril (Cap) and enalapril (Ena) had no inhibitory effect on KCl-, NE-, and Ang-induced [Ca2+]i increases in ASMC of WKY. Cap and Ena inhibited KCl-, NE-, and Ang-increased [Ca2+]i in ASMC of SHR (210 +/- 7, 194 +/- 6, and 201 +/- 6 nmol.L-1, respectively). Ena and nifedipine similarly decreased KCl-, NE-, and Ang-increased [Ca2+]i. CONCLUSION: Cap blocked KCl-, NE-, and Ang-increased ([Ca2+]i) via a voltage-dependent Ca2+ channel of which function and specificity was altered in ASMC of SHR.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9772664&dopt=Abstract
Kidney Int. 1991 Jun;39(6):1112-7.
Effects of nifedipine and enalapril on glomerular structure and function in uninephrectomized SHR.
Dworkin LD, Feiner HD, Parker M, Tolbert E.
Department of Medicine, New York University Medical Center, New York, New York.
Spontaneously hypertensive rats (SHR) that underwent uninephrectomy (UNX) at six weeks of age were randomly assigned to receive no treatment, the calcium channel blocker, nifedipine, or the angiotensin converting enzyme inhibitor, enalapril. Both drugs reduced systemic blood pressure, however, blood pressure tended to be greater in rats given nifedipine than in those on enalapril. After six months, proteinuria and the relevance of glomerula sclerosis were significantly reduced in the two treated groups compared to values observed in untreated SHR. Kidney weight was also reduced by therapy, suggesting that both enalapril and nifedipine inhibited compensatory kidney growth. Micropuncture studies performed in similarly treated groups of rats, but at 11 weeks of age, revealed that PGC was elevated in untreated UNX SHR and reduced by both nifedipine and enalapril. These findings support the hypothesis that glomerular hypertension and renal hypertrophy are important risk factors for glomerular injury. They suggest that calcium blockers are as effective as angiotensin converting enzyme inhibitors in preventing progressive kidney damage.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1895665&dopt=Abstract
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