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Crit Rev Oral Biol Med. 1993;4(3-4):565-71.
The effect of adrenergic agonists and antagonists on the expression of proteins in rat submandibular and parotid glands.

Bedi GS.

Department of Oral Biology, School of Medicine, State University of New York, Buffalo 14214.

The present investigation was undertaken to study the effect of adrenoreceptor modulators on the expression of salivary proteins. Sprague-Dawley rats were treated for 10 consecutive days with adrenergic agonists isoproterenol, dobutamine, terbutaline, salbutamol, methoxyphenamine, or methoxamine. Antiserum to selected salivary proteins was used to compare the concentration of these proteins in the submandibular and parotid glands of treated animals. Chronic treatments of rats (50 mumol/kg body weight for 10 d) with either isoproterenol or dobutamine induced synthesis of a cysteine-proteinase inhibitor (cystatin) in the submandibular glands. When isoproterenol was injected concomitantly with the mixed beta-antagonist propranolol or the beta 1-adrenergic antagonists metaprolol, protocol, or atenolol, the induction of cystatin was totally suppressed. However, the beta 2-antagonist, ICI-118551, produced only partial reduction in cystatin induction elicited by isoproterenol. On the contrary, rats treated with either isoproterenol or beta 1-agonists demonstrated a significantly reduced concentration of serine-proteinase kallikrein in submandibular glands. The decrease observed in submandibular kallikrein of rats treated with isoproterenol was prevented by concomitant treatment with beta 1-antagonists but not with beta 2-antagonists. Because kallikreins are produced by ductal cells and cystatins are produced by acinar cells of submandibular glands, these observations suggest that there may be differential control of expression of proteins synthesized by ductal and acinar cells. Chronic treatment of rats with nonselective beta-agonist isoproterenol or beta 1-selective agonists increased markedly the proline-rich proteins (PRP) in parotid glands, but the parotid amylase concentration was not significantly affected by beta-adrenergic agonists.(ABSTRACT TRUNCATED AT 250 WORDS)

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Eur J Clin Pharmacol. 1981;20(5):335-8.
Serum lipoprotein changes during atenolol treatment of essential hypertension.

Eliasson K, Lins LE, Rossner S.

Serum lipoproteins were determined in 15 patients before and during antihypertensive treatment with atenolol (0.1-0.2 g/day for a mean of 8 months. The mean blood pressure fell from 171/103 to 154/93 mm Hg (p less than 0.05). Significant lipoprotein changes were an increase in very low density triglycerides (VLDL-TG) from 1.21 +/- 0.95 (SD) to 1.62 +/- 1.24 mmol/l (p less than 0.01) and in low density (LDL) TG from 0.46 +/- 0.12 to 0.51 +/- 0.12 mmol/l (p less than 0.05). Together, these TG increases resulted in development of hypertriglyceridaemia in 7/15 patients during atenolol treatment. No effect on whole serum cholesterol or on the high density lipoprotein cholesterol concentrations were found. Thus, some patients on long term treatment with atenolol seem to received the benefit of normotension at the cost of hypertriglyceridaemia. This may have practical implications, since hypertriglyceridaemia, constitutes an important risk factor for atherosclerosis.

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Rev Port Cardiol. 1991 Jun;10(6):503-9.
[Pressure response to dynamic exercise and antihypertensive therapy]

[Article in Portuguese]

da Silva JD, Mota E, Gomes A.

Servico de Carciologia do Hospital Militar Principal, Lisboa.

OBJECTIVES: To study the exercise systolic pressure (SP) in hypertensive patients, its relation with left ventricular (LV) mass and the efficacy of its control by some antihypertensive drugs. DESIGN: To study the echocardiogram (ECHO) and exercise test (ET) in hypertensives (HT), before and after rest blood pressure (BP) control. SETTING: Out-patient cardiology clinic in a military hospital. METHODS: 53 male moderate HT, 30 to 60 years old, without other pathology, were studied with ECHO and ET. 28 HT repeated ET after rest BP control: Group A--Diuretic (Hchlt/Triam), n: 7; Group B--Atenolol, n: 10; Group C--Nifedipine, n: 11. RESULTS: 1. There was a positive correlation between LV mass index and exercise SP (r: 0.37; p less than 0.01), but not rest blood pressure. 2. Exercise test duration was increased only in group C. 3. Hypertensives with rest BP control had also normal exercise SP in group B, but not in groups A or C (Qui2: 11 735; p less than 0.001). CONCLUSIONS: 1. Exercise systolic blood pressure seems to be more important than rest blood pressure to the development of LVH in hypertensive patients. 2. The observed increase of exercise capacity in Nifedipine group must be considered in the treatment of physically active hypertensives. 3. Hypertensives with rest BP controlled by Atenolol have also, very probably, a normal exercise systolic pressure. 4. In physically active HT with rest BP controlled by Diuretic or Nifedipine may be useful an exercise test to evaluate exercise systolic pressure.

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