Drugs online research references
J Cardiovasc Pharmacol. 1993 Aug;22(2):231-9.
Effects of blocking the angiotensin II receptor, converting enzyme, and renin activity on the renal hemodynamics of normotensive guinea pigs.
el Amrani AI, Menard J, Gonzales MF, Michel JB.
INSERM U367, Paris, France.
The effects of three renin-angiotensin system (RAS) antagonists, DuP 753, a nonpeptide angiotensin II (Ang II) receptor antagonist, MK 521, an inhibitor of converting enzyme, and Ro 42-5892, a human renin inhibitor, on renal function and hemodynamics were investigated in anesthetized, ventilated normotensive guinea pigs. This species was selected because this human renin inhibitor inhibits guinea pig renin. Glomerular filtration rate (GFR) and renal blood flow (RBF) were measured by [3H]inulinmethoxy and [14C]aminohippuric acid clearances. Animals were perfused with isotonic saline at 0.2 ml/min. After a stabilization period of 1 h, drugs were given as an intravenous (i.v.) bolus (DuP 753, 1; MK 521, 0.1; Ro 42-5892, 1 mg/kg), followed by continuous infusion (DuP 753, 3; MK 521, 0.3; Ro 42-5892, 3 mg/kg/h). These doses have been used to induce slight but significant and similar decreases in mean arterial blood pressure (MABP). The mean changes during 1-h treatment showed similar decreases in MABP: vehicle, -2 +/- 1% (n = 10); DuP 753, -13 +/- 2% (n = 10); MK 521, -15 +/- 2% (n = 10); Ro 42-5892, -13 +/- 3% (n = 10), p < 0.001. Diuresis was unchanged in the four groups. GFR (vehicle, -0.2 +/- 8.4%; DuP 753, +10.7 +/- 6.4%; MK 521, +13.2 +/- 8.6%; Ro 42-5892, +37.2 +/- 7.5%, p < 0.01) and RBF (vehicle, -0.7 +/- 6.6%; DuP 753, +10.5 +/- 6.8%; MK 521, +16.4 +/- 6.8%; Ro 42-5892, +37.9 +/- 7.8%, p < 0.01) increased in parallel with the three drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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Br J Pharmacol. 1995 Jan;114(1):6-7.
Potentiation by aminopeptidase P of blood pressure response to bradykinin.
Kitamura S, Carbini LA, Carretero OA, Simmons WH, Scicli AG.
Henry Ford Hospital, Detroit, MI.
We examined whether a specific aminopeptidase P (APP) inhibitor, apstatin, increases vasodepressor responses to bradykinin in anaesthetized rats, and whether it would augment blood pressure responses further after treatment with the angiotensin-converting enzyme inhibitor (ACEi), lisinopril. Apstatin doubled the maximum blood pressure response to bradykinin. The area under the curve (AUC), which incorporates both peak blood pressure changes and duration of response, was doubled in apstatin-treated rats vs controls and in the apstatin+lisinopril group vs lisinopril alone. These data demonstrate that APP is an important kinase in vivo.
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Hypertension. 1995 Apr;25(4 Pt 1):570-80.
Differential gene expression of renin and angiotensinogen in the TGR(mREN-2)27 transgenic rat.
Lee MA, Bohm M, Kim S, Bachmann S, Bachmann J, Bader M, Ganten D.
Max-Delbruck-Center for Molecular Medicine, Berlin-Buch, Germany.
Transgenic rats carrying the murine Ren-2 gene represent a monogenetic model of hypertension characterized by low plasma renin and high extrarenal expression of the transgene. The hypothesis has been raised that stimulated local reninangiotensin systems may be responsible for the development of hypertension in this model. This study analyzes the effects of the converting enzyme inhibitor lisinopril, which specifically interferes with the renin-angiotensin system, and the direct vasodilator dihydralazine on the renal and extrarenal expression of renin and angiotensinogen. A comparison of gene expression between heterozygous and homozygous transgenic and normal Sprague-Dawley rats was also performed. We demonstrate high sensitivity of blood pressure toward converting enzyme inhibition in transgenic TGR(mREN-2)27 rats. In the kidney, expression of the transgene and the endogenous renin gene increased, suggesting that both are modulated by lisinopril in a similar manner. On the other hand, blood pressure reduction by dihydralazine did not abolish renal renin suppression in transgenic rats, indicating that mechanisms different from direct effects of blood pressure account for renin suppression. Homozygosity for the transgene led to increased Ren-2 expression and higher blood pressure and had opposite effects on angiotensinogen expression compared with heterozygous rats. Cardiac hypertrophy was reduced by lisinopril but not dihydralazine and was positively correlated with cardiac angiotensinogen expression. Increased angiotensin II in the adrenal gland of TGR(mREN-2)27 rats, which overexpresses the transgene, provides evidence that this leads to enhanced generation of tissue angiotensin II. We conclude that expression of the mouse transgene, the endogenous rat renin gene, and the angiotensinogen gene is subject to differential tissue-specific regulation. Reversal of cardiovascular damage with the converting enzyme inhibitor but not dihydralazine suggests that angiotensin II generated locally may be involved in the pathogenesis of hypertension and structural changes in TGR(mREN-2)27 rats.
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