LONG-TERM BETA(1)-ADRENERGIC BLOCKADE RESTORES ADRENOMEDULLARY ACTIVITY IN PRIMARY HYPERTENSION

Citation
Mc. Jacobs et al., LONG-TERM BETA(1)-ADRENERGIC BLOCKADE RESTORES ADRENOMEDULLARY ACTIVITY IN PRIMARY HYPERTENSION, Journal of cardiovascular pharmacology, 30(3), 1997, pp. 338-342
Citations number
16
Categorie Soggetti
Cardiac & Cardiovascular System","Pharmacology & Pharmacy
ISSN journal
01602446
Volume
30
Issue
3
Year of publication
1997
Pages
338 - 342
Database
ISI
SICI code
0160-2446(1997)30:3<338:LBBRAA>2.0.ZU;2-B
Abstract
In this study we examined the effects of long-term treatment of 19 pat ients with primary hypertension with the beta(1)-adrenoceptor antagoni st atenolol on norepinephrine and epinephrine kinetics, at rest and du ring sympathoadrenal stimulation by lower body negative pressure. Nore pinephrine and epinephrine kinetics were measured by using the radiois otope-dilution technique by steady-state infusion of tritiated norepin ephrine and epinephrine. The patients were studied before and at the e nd of 3 months of treatment with atenolol (50 or 100 mg daily). A cont rol group of four normotensive subjects was studied before and after 3 months without any drug treatment. In this group, only arterial blood samples were collected without infusion of the tritiated catecholamin es. Atenolol decreased blood pressure and heart rate, but forearm vasc ular resistance was not affected by atenolol. During atenolol, baselin e arterial plasma epinephrine decreased from 0.23 +/- 0.02 to 0.17 +/- 0.01 nM (p < 0.05), and this was accompanied by a decrease in total b ody epinephrine spillover from 0.50 +/- 0.05 to 0.35 +/- 0.04 nmol/min (p < 0.05). In the control group, arterial plasma epinephrine had not decreased after 3 months. In addition, the increment of arterial plas ma epinephrine during lower body negative pressure at -40 mm Hg was at tenuated during atenolol. Atenolol had no effect on total body and for earm norepinephrine spillover rates, either at rest or during lower bo dy negative pressure. Clearance rates of epinephrine and norepinephrin e were not significantly affected by atenolol. These results suggest t hat treatment of patients with primary hypertension with the beta(1)-a drenoceptor blocker atenolol inhibits the adrenomedullary secretion of epinephrine, but it does not affect the biochemical indices of sympat honeural activity. It remains speculative whether this selective effec t of atenolol on epinephrine secretion contributes to its hypotensive action and to its cardioprotective effects in the long term.