Published Online
on August 23, 2004

A more recent version of this article appeared on October 1, 2004

This Article Full Text (PDF) All Versions of this Article: 44/4/454    most recent 01.HYP.0000141411.94596.0fv1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Burns, J. Articles by Greenwood, J. P. Search for Related Content PubMed PubMed Citation Articles by Burns, J. Articles by Greenwood, J. P. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB ATENOLOL Medline Plus Health Information Blood Pressure Medicines High Blood Pressure Related Collections Cardiovascular Pharmacology

Submitted on June 23, 2004
Revised on July 5, 2004

Arterial Pressure Lowering Effect of Chronic Atenolol Therapy in Hypertension and Vasoconstrictor Sympathetic Drive

Joanna Burns^*; David A.S.G. Mary; Alan F. Mackintosh; Stephen G. Ball; and John P. Greenwood

From the Department of Cardiology, Leeds Teaching Hospitals NHS Trust, Leeds, UK.

^* To whom correspondence should be addressed. E-mail: burnsjoanna1{at}hotmail.com.

Abstract--Although the ₁-adrenergic blocking agent atenolol is an established antihypertensive therapy, its effect on peripheral sympathetic vasoconstrictor drive has remained controversial. In patients with hypertension, atenolol therapy has been reported to either increase or have no effect on peripheral vascular resistance, despite other reports showing no change or a decrease in peripheral sympathetic drive. This study was designed, in patients with untreated essential hypertension (EHT), to quantify changes in simultaneously measured peroneal muscle sympathetic nerve activity (MSNA) and calf vascular resistance (CVR) accompanying atenolol therapy. MSNA was quantified as the mean frequency of single units (s-MSNA) and as multiunit bursts (MSNA bursts) using the technique of microneurography, and CVR was measured using a standard plethysmographic technique. Firstly, by comparing two age- and body weight- matched groups, each of 14 patients with hypertension, we found that the group on atenolol therapy (treated-HT) had similar MSNA values counted over the same number of cardiac beats and similar CVR levels (at least P>0.40) to the group without therapy (untreated-HT). Secondly, we examined 10 EHT patients before and after 8±0.4 weeks of oral atenolol therapy (HT-A) in comparison to seven control patients with hypertension and no treatment (HT-C) who were examined over a similar period of time. We found that the measures of MSNA and CVR did not significantly change in both groups. We conclude that the arterial pressure lowering effect of atenolol was not related to significant changes in central vasoconstrictor sympathetic drive to the periphery.

Key words: antihypertensive therapy • sympathetic nervous system • hypertension, essential • vascular resistance

This article has been cited by other articles:

				S.P. Beloka, S. Gouveia, M. Gujic, R. Naeije, A.P. Rocha, and P. van de Borne Differential Effects of Oral {beta} Blockade on Cardiovascular and Sympathetic Regulation Journal of Cardiovascular Pharmacology and Therapeutics, December 1, 2009; 14(4): 323 - 331. [Abstract] [PDF]

				N. Charkoudian and J. A. Rabbitts Sympathetic Neural Mechanisms in Human Cardiovascular Health and Disease Mayo Clin. Proc., September 1, 2009; 84(9): 822 - 830. [Abstract] [Full Text] [PDF]

				S. Laurent, M. Briet, and P. Boutouyrie Large and Small Artery Cross-Talk and Recent Morbidity-Mortality Trials in Hypertension Hypertension, August 1, 2009; 54(2): 388 - 392. [Full Text] [PDF]

				A. J. Hogarth, L. N. Graham, D. A.S.G. Mary, and J. P. Greenwood Gender differences in sympathetic neural activation following uncomplicated acute myocardial infarction Eur. Heart J., July 2, 2009; 30(14): 1764 - 1770. [Abstract] [Full Text] [PDF]

				M. Yoshimoto, E. A. Wehrwein, M. Novotny, G. M. Swain, D. L. Kreulen, and J. W. Osborn Effect of stellate ganglionectomy on basal cardiovascular function and responses to {beta}1-adrenoceptor blockade in the rat Am J Physiol Heart Circ Physiol, December 1, 2008; 295(6): H2447 - H2454. [Abstract] [Full Text] [PDF]

				J. Burns, M. U. Sivananthan, S. G. Ball, A. F. Mackintosh, D. A.S.G. Mary, and J. P. Greenwood Relationship Between Central Sympathetic Drive and Magnetic Resonance Imaging-Determined Left Ventricular Mass in Essential Hypertension Circulation, April 17, 2007; 115(15): 1999 - 2005. [Abstract] [Full Text] [PDF]

				M. J. Joyner Treating Hypertension: When to Say Win Hypertension, April 1, 2005; 45(4): 487 - 488. [Full Text] [PDF]

				Q. Fu, R. Zhang, S. Witkowski, A. Arbab-Zadeh, A. Prasad, K. Okazaki, and B. D. Levine Persistent Sympathetic Activation During Chronic Antihypertensive Therapy: A Potential Mechanism for Long Term Morbidity? Hypertension, April 1, 2005; 45(4): 513 - 521. [Abstract] [Full Text] [PDF]