The renin-angiotensin system in hybrid NG108-15 cells. Renin gene is from mouse neuroblastoma, angiotensinogen and angiotensin-converting enzyme genes are of rat glioma origin. Differential effects of antihypertensive drugs with differing pharmacological properties on the basal ambulatory blood pressure. Japanese Ambulatory Pressure-ANtihypertensive Effects SEarching study group. Effect of chronic angiotensin converting enzyme inhibition on sympathetic nerve traffic and baroreflex control of the circulation in essential hypertension. Rx drugs

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Regul Pept. 1998 Oct 16;77(1-3):9-15.
The renin-angiotensin system in hybrid NG108-15 cells. Renin gene is from mouse neuroblastoma, angiotensinogen and angiotensin-converting enzyme genes are of rat glioma origin.

Laflamme L, Brechler V, Reudelhuber TL, Gallo-Payet N, Deschepper CF.

Service of Endocrinology, Faculty of Medicine, University of Sherbrooke, Canada.

Angiotensin II (Ang II) increases the level of tyrosine phosphorylation of several proteins in nondifferentiated NG108-15 cells, a hybrid derived from the fusion of mouse neuroblastoma and rat glioma cells. Conversely, incubation of NG108-15 cells with an angiotensin-converting enzyme (ACE) inhibitor decreased the basal level of tyrosine phosphorylation of proteins, suggesting that locally secreted Ang II may act as an autocrine regulator. By RT-PCR, we found that nondifferentiated NG108-15 cells contained the mRNA transcript of the rat angiotensinogen, mouse renin and rat ACE genes, thus confirming that NG108-15 cells contain all the elements of a local renin-angiotensin system.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9809791&dopt=Abstract

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J Hum Hypertens. 1998 Oct;12(10):719-26.
Differential effects of antihypertensive drugs with differing pharmacological properties on the basal ambulatory blood pressure. Japanese Ambulatory Pressure-ANtihypertensive Effects SEarching study group.

Sekino M, Imai Y, Ohkubo T, Omae T.

Department of Medicine, Tohoku University School of Medicine, Sendai, Japan.

To investigate how antihypertensive drugs with different pharmacological properties affect ambulatory blood pressure (BP) the JAPANESE Study Group developed a database of clinic and ambulatory BPs before and after antihypertensive treatment of patients throughout Japan. Drugs evaluated were nilvadipine (n = 195; b.i.d, 4-8 mg/day), amlodipine (n = 75; q.d., 2.5-10 mg/day), lisinopril (n = 80; q.d., 10-20 mg/day) and bisoprolol (n = 49; q.d., 5-10 mg/day). The relationship between basal ambulatory BP and the hypotensive effect on ambulatory BP during treatment was examined. All antihypertensive drugs significantly decreased both clinic BP and ambulatory BP. The hypotensive effect determined by measurement of clinic BP was significantly greater than that determined by ambulatory BP. The hypotensive effect was positively correlated with basal ambulatory BP. However, there was a quantitative difference in this characteristic among the drugs. The critical daytime systolic ambulatory BP below which a hypotensive effect was not observed was extrapolated to 128, 127 and 124 mm Hg with nilvadipine, amlodipine and bisoprolol, respectively, while that with lisinopril was 97 mm Hg. The slope of the correlation coefficient between basal daytime ambulatory systolic BP and hypotensive effect with lisinopril was significantly smaller than those with the other drugs (P < 0.0001). The slope for the relationship between night-time ambulatory systolic BP and the hypotensive effect with bisoprolol was the steepest (P < 0.0001). Antihypertensive drugs with different pharmacological properties exhibited differing hypotensive effects on the basal ambulatory BP. Such differences in efficacy of the drugs on the basal ambulatory BP may reflect adverse effects of the drugs and the prognosis of hypertension.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9819021&dopt=Abstract

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J Hypertens. 1998 Dec;16(12 Pt 1):1789-96.
Effect of chronic angiotensin converting enzyme inhibition on sympathetic nerve traffic and baroreflex control of the circulation in essential hypertension.

Grassi G, Turri C, Dell'Oro R, Stella ML, Bolla GB, Mancia G.

Cattedra di Medicina Interna I, Ospedale S. Gerardo Monza, Universita di Milano, Milan, Italy.

BACKGROUND: Human studies have shown that the blood pressure lowering effects of angiotensin converting enzyme inhibitors are accompanied by a reduction in plasma norepinephrine levels. Whether this is due to central or peripheral mechanisms is unknown, however. OBJECTIVE: To evaluate the effects of chronic interference with the renin-angiotensin system on sympathetic nerve traffic and baroreflex control of vagal and adrenergic cardiovascular drive. PATIENTS AND METHODS: In 18 untreated mild to moderate essential hypertensive patients aged 48.5+/-1.9 years (mean+/-SEM), we measured mean arterial pressure (Finapres), heart rate (electrocardiogram), plasma renin activity (radioimmunoassay), plasma norepinephrine (high-performance liquid chromatography) and postganglionic muscle sympathetic nerve activity (microneurography at a peroneal nerve). In nine patients, measurements were performed before and after 2 months of oral administration of lisinopril (10 mg/day), while in the remaining nine patients they were performed before and after a 2 month observation period, without the drug administration. Measurements were performed at rest and during baroreflex stimulation and deactivation elicited by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. RESULTS: Lisinopril induced a marked increase in plasma renin activity (from 1.1+/-0.2 to 6.4+/-1.3 ng/ml per h, P< 0.01) and a reduction in mean arterial pressure (from 109.6+/-3.1 to 98.7+/-2.9 mmHg, P < 0.01) without affecting the heart rate. Plasma norepinephrine and muscle sympathetic nerve activity values were not significantly different before and after lisinopril treatment (plasma norepinephrine values changed from 290.4+/-39.2 to 308.1+/-67.1 pg/ml; muscle sympathetic nerve activity changed from 56.4+/-5.3 to 50.6+/-6.6 bursts/100 heart beats). Neither the sympathoinhibitory nor the sympathoexcitatory responses to phenylephrine and nitroprusside were affected by lisinopril, nor the concomitant bradycardia and tachycardia. The curves relating mean arterial pressure to heart rate and muscle sympathetic nerve activity values during baroreceptor manipulation were shifted to the left, indicating a resetting of the baroreflex to the lower blood pressure values achieved during treatment. CONCLUSIONS In essential hypertension, sympathetic nerve traffic is not affected by chronic angiotensin converting enzyme inhibitor treatment that effectively interferes with the renin-angiotensin system and lowers the elevated blood pressure. The baroreflex ability to modulate heart rate and central sympathetic outflow is also unaffected. These data argue against the existence of a central sympathoexcitatory effect of angiotensin II in this condition. They also indicate that antihypertensive treatment with an angiotensin converting enzyme inhibitor preserves autonomic reflex control, with favorable consequences for cardiovascular homeostasis.

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