Protein synthesis in the hypertrophied heart of spontaneously hypertensive rats and a comparison of the effects of an ACE-inhibitor and a calcium channel antagonist. Tissue- and subtype-specific modulation of angiotensin II receptors by chronic treatment with cyclosporin A, angiotensin-converting enzyme inhibitors and AT1 antagonists. Antihypertensive properties of a new long-acting angiotensin converting enzyme inhibitor in renin-dependent and independent hypertensive models. Rx drugs

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Cell Biochem Funct. 1995 Jun;13(2):111-24.
Protein synthesis in the hypertrophied heart of spontaneously hypertensive rats and a comparison of the effects of an ACE-inhibitor and a calcium channel antagonist.

Patel VB, Siddiq T, Richardson PJ, Preedy VR.

Department of Clinical Biochemistry, King's College School of Medicine & Dentistry, London, U.K.

The aim of the investigation was to assess and compare the effects of a calcium channel antagonist, (i.e. amlodipine) and an ACE-inhibitor (i.e. lisinopril) in reducing chronic left ventricular hypertrophy in 15-week old spontaneously hypertensive rats (SHR). Changes in cardiac hypertrophy were assessed after 8 weeks by measuring the fractional rates of protein synthesis using a 'flooding dose' of [3H]-phenylalanine for 10 min. Blood pressure was monitored throughout the treatment period in both SHR and Wistar-Kyoto control rats (WKY). The results showed a decrease in blood pressure by amlodipine after 1 week of treatment which was further reduced at 4 to 8 weeks. Lisinopril caused immediate and sustained reductions in blood pressure (190 mmHg to 130 mmHg, P < 0.001). After 8 weeks of treatment in SHR rats, amlodipine had no significant effect on left ventricular weight (P > 0.05), whereas lisinopril caused a marked reduction. The protein content and RNA were also not changed by amlodipine. In contrast, lisinopril significantly lowered the tissue protein, RNA and DNA content (P < 0.001). The changes in the left ventricles of lisinopril-treated SHR rats were accompanied by an increase in the fractional synthesis rate of left ventricular myofibrillar proteins (+12 per cent, P < 0.025). The synthesis rate per unit RNA was also increased in right ventricular tissue of lisinopril-treated SHR rats. However, amlodipine had no effect on the fractional synthesis rates of any of the left-ventricular fractions of SHR rats (P > 0.05). The cellular efficiency in the right ventricle was also increased in amlodipine-treated SHR rats, indicating a moderate effect on protein metabolism. In conclusion, amlodipine had minimal effects in the reduction of established left ventricular hypertrophy (LVH), despite reducing the blood pressure, whereas lisinopril caused regression of LVH. These events were associated with small changes in protein synthesis rates, with the contractile protein showing an increase.

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J Cardiovasc Pharmacol. 1995 Jul;26(1):66-72.
Tissue- and subtype-specific modulation of angiotensin II receptors by chronic treatment with cyclosporin A, angiotensin-converting enzyme inhibitors and AT1 antagonists.

Regitz-Zagrosek V, Auch-Schwelk W, Hess B, Klein U, Duske E, Steffen C, Hildebrandt AG, Fleck E.

Department of Internal Medicine/Cardiology and Angiology, Free University Berlin, University Hospital Rudolf Virchow, Germany.

We wished to determine whether chronic treatment of rats with cyclosporin A (CSA), an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor antagonists modulates the angiotensin receptor density. In rats treated chronically with CSA, the vasoconstrictor response to angiotensin II (AII) is increased and this increase is modulated by ACEI and angiotensin receptor antagonists. Rats were treated for 6 weeks orally with CSA (15 mg/kg/day), the ACE inhibitor lisinopril (10 mg/kg/day), the angiotensin receptor antagonists DUP 753 (10 mg/kg/day), and D 8731 (10 mg/kg/day) and the combinations CSA + lisinopril, CSA + DUP 753, and CSA + D 8731. Olive oil was used as a control. The number of total AII receptors (Bmax) was determined by Scatchard analysis of [125I]Sar1 Ile8 AII binding in kidney, liver, adrenal cortex, and adrenal medulla. The receptor subtypes were analyzed with the specific antagonists DUP 753 (subtype 1) and PD 123319 (subtype 2). CSA upregulated angiotensin receptors in all organs studied. Lisinopril alone downregulated angiotensin receptors and abolished the effect of CSA in liver and adrenal cortex and medulla, but not in the kidney, where it had no effect. DUP 753 alone downregulated the angiotensin receptor subtype 1 in kidney, liver and adrenal cortex; its effect on the adrenal medulla in which 89% of angiotensin receptors are subtype 2, did not quite reach significance. The combination of DUP 753 and cyclosporin CSA abolished the CSA-induced increase in angiotensin receptor density in all four organs. The angiotensin receptor antagonists D 8731 downregulated the angiotensin receptors (subtype 1) in liver and kidney and upregulated angiotensin receptors (subtype 2) in the adrenal medulla.(ABSTRACT TRUNCATED AT 250 WORDS)

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7564368&dopt=Abstract

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Arzneimittelforschung. 1995 Aug;45(8):853-8.
Antihypertensive properties of a new long-acting angiotensin converting enzyme inhibitor in renin-dependent and independent hypertensive models.

Nagata S, Takeyama K, Fukuya F, Nagai R, Hosoki K, Nishimura K, Deguchi T, Karasawa T.

Department of Pharmacology I, Dainippon Pharmaceutical Co., Ltd., Suita, Osaka, Japan.

The antihypertensive properties of a new long-acting, angiotensin-I-converting enzyme (ACE) inhibiting agent, (2S,3aS,7aS)-1-(N2-nicotinoyl-L-lysyl-gamma-D-glutamyl) octahydro-1H-indole-2-carboxylic acid (CAS 116662-73-8, DU-1777), were investigated orally in various experimental models of hypertension in comparison to a standard ACE inhibitor, lisinopril. The hypotensive potency of DU-1777 was not as marked as that of lisinopril in renin-dependent hypertensive models, i.e., two-kidney one-clip renal hypertensive rats (2K-1C RHR) (ED-20mmHg: 3.1 versus 1.0 mg/kg) or two-kidney two-clip renal hypertensive dogs (2K-2C RHD) (ED-20 mmHg: 2.5 versus 1.0 mg/kg), though the actions of the two drugs were both long-lasting and dose-related. When spontaneously hypertensive rats (SHR) were used, however, DU-1777 was as active as lisinopril (ED-20 mmHg: 17.9 versus 13.6 mg/kg). The most distinguishing results with DU-1777 were its hypotensive effects in renin-independent hypertensive models. In contrast to lisinopril, the drug produced a sustained and dose-related hypotensive effect in DOCA salt hypertensive rats (DOCA-HR) and one-kidney one-clip renal hypertensive rats (1K-1C RHR). There exists an inconsistency between the long duration of the agent's hypotensive action in all tested hypertensive models and its short duration of ACE inhibiting activity as demonstrated both in vivo and ex vivo. The sustained antihypertensive action of DU-1777 cannot be reasoned solely with respect to ACE inhibition, suggesting some additional mechanisms of action yet to be defined.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7575746&dopt=Abstract

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