Angiotensin(1-7) in the spontaneously hypertensive rat. [Lisinopril in the monotherapy of patients with essential hypertension: the effect of therapy on glucose and lipid metabolism] Regulation of beta-adrenergic receptors on endothelial cells in culture. Rx drugs

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Peptides. 1993 Sep-Oct;14(5):883-91.
Angiotensin(1-7) in the spontaneously hypertensive rat.

Kohara K, Brosnihan KB, Ferrario CM.

Hypertension Center, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27157-1095.

We profiled the concentrations of angiotensin I (Ang I), angiotensin II (Ang II), and angiotensin(1-7) [Ang(1-7)] by the combination of radioimmunoassay and high performance liquid chromatography in the blood of 14-week-old male Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) drinking either tap water or a solution containing ceranapril (30 mg/kg) or lisinopril (20 mg/kg) for 14 days. Differences in the chemical and pharmacokinetic properties of the two converting enzyme inhibitors ruled out class-related effects. Plasma renin activity, angiotensin converting enzyme (ACE) activity, and plasma levels of Ang I and Ang II were the same in vehicle-treated WKY and SHR. In contrast, plasma levels of both Ang(1-7) and vasopressin in SHR were 3.7-fold and 2.6-fold higher, respectively (p < 0.05). Angiotensin converting enzyme inhibition reduced the blood pressure of WKY and SHR, and augmented their intake of water and output of urine. These changes were associated with increases in renin activity and plasma levels of Ang I and Ang(1-7). In both WKY and SHR, lisinopril had a greater effect in inhibiting plasma and cerebrospinal fluid ACE, reducing levels of plasma angiotensinogen, and increasing the concentrations of authentic Ang II. The principal finding of this study is that plasma Ang(1-7) is the sole component of the circulating angiotensin system that is elevated in the established phase of genetic hypertension. The finding that chronic inhibition of ACE augments circulating levels of Ang(1-7) evidenced the existence of functional pathways for the alternate processing of Ang I.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8284265&dopt=Abstract

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Cas Lek Cesk. 1993 Dec 6;132(23):709-14.
[Lisinopril in the monotherapy of patients with essential hypertension: the effect of therapy on glucose and lipid metabolism]

[Article in Slovak]

Gajdos M, Spustova V, Dzurik R.

Oddelenie Klinickej Farmakologie Ustavu Preventivnej a Klinickej Mediciny, Bratislava.

Twenty patients with mild or medium severe essential hypertension were treated with lisinopril (Prinivil), 20 or 40 mg resp. by the oral route per day. After six weeks of treatment the mean values of systolic pressure declined from 169 +/- 4.38 mm Hg to 149 +/- 3.96 mm Hg and the diastolic pressure from 108 +/- 0.99 mm Hg to 91 +/- 1.77 mm Hg. The differences were statistically significant. In 40% of the patients it was necessary to increase the daily dose of lisinopril to 40 mg. When this was used, the mean values of systolic pressure declined to 140 +/- 3.18 mm Hg and those of diastolic pressure declined to 85 +/- 1.43 mm Hg during the subsequent six weeks. The blood pressure of all investigated patients was within the range of reference values. The authors recorded a positive effect on the glucose metabolism in particular in patients with impaired glucose tolerance. The mean blood sugar levels during the second hour following glucose administration during the oGTT declined from 9.81 +/- 0.54 mmol/l before treatment to 7.28 +/- 0.79 mmol/l after 12 weeks of lisinopril treatment. The values of immunoreactive insulin after the mentioned intervals declined from 82.49 +/- 5.6 to 34.94 +/- 8.37 microM/ml. The investigated parameters of the lipid spectrum did not change after 12 weeks of treatment. The authors did not observe any marked side-effects of treatment.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8293440&dopt=Abstract

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Eur Heart J. 1993 Nov;14 Suppl I:173-6.
Regulation of beta-adrenergic receptors on endothelial cells in culture.

Graf K, Grafe M, Dummler U, O'Connor A, Regitz-Zagrosek V, Kunkel G, Auch-Schwelk W, Fleck E.

Department of Internal Medicine and Cardiology, German Heart Institute, Berlin.

This study aimed to determine the density of vascular beta-adrenergic receptors in cultured endothelial cells and to study the regulation of endothelial receptors after exposure to catecholamines and the ACE inhibitors, lisinopril and ramiprilat. Membranes from bovine aortic endothelial cells (BAEC) and bovine pulmonary artery endothelial cells (BPAEC) showed saturable binding of the radioligand [125I]iodocyanopindolol (ICYP). The beta-receptor density and binding affinity were comparable in both types of endothelial cells. Isoproterenol induced significant down-regulation of beta-receptors (-50%; P < 0.01). Incubation (24h) with the ACE inhibitors lisinopril 10(-5) M (+28.8%; P < 0.05) and ramiprilat 10(-5) M (+33.7%, P < 0.09) augmented the beta-receptor density in BAEC, but lower ACE inhibitor doses had no affect. Incubation with lisinopril 10(-5) M for 24 h resulted in significantly lower cAMP baseline levels, but did not affect cAMP concentrations after stimulation with isoproterenol. These results indicate that down-regulation of endothelial beta-receptors occurs during prolonged exposure to beta-stimulation, and that high concentrations of ACE inhibitors may affect the density of endothelial beta-receptors.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8293771&dopt=Abstract

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