gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

Beta-adrenoceptor-mediated, nitric oxide dependent vasodilation is abnormal in early hypertension: restoration by L-arginine

Verminderte beta-Adrenoceptor vermittelte Vasodilatation bei essentieller Hypertonie: Normalisierung durch L-Arginin

Meeting Abstract (Hypertonie 2004)

Suche in Medline nach

  • presenting/speaker M.P. Schlaich - Universität Erlangen-Nürnberg (Erlangen, D)
  • B.A. Ahlers - Universität Erlangen-Nürnberg (Erlangen, D)
  • M.M. Parnell - Baker Heart Research Insitute (Melbourne, AUS)

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP110

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Veröffentlicht: 10. August 2005

© 2005 Schlaich et al.
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Background: Whether beta-adrenoceptor mediated vasodilation is altered in early hypertension and whether it can be modulated by L-arginine is unknown.

Methods and Design: We measured changes in forearm blood flow by plethysmography in response to acetylcholine (9 and 37µg/min), sodium-nitroprusside (200 and 800ng/min) and the beta-receptor agonist isoproterenol (ISP)(50 and 200ng/min) in 12 hypertensive patients (EH) and in healthy volunteers with (PFH; n=14) and without (NFH; n=14) a family history of hypertension before and during concomitant infusion of L-arginine (10µmol/min). In 5 subjects from each group infusion of acetylcholine and isoproterenol was repeated during the concurrent blockade of NO-synthesis by L-NMMA (4µmol/min).

Results: The response to acetylcholine was reduced in EH and PFH compared to NFH (both p<0.05), whereas the vasodilator effects of isoproterenol and sodium-nitroprusside were similar in all three groups. Acetylcholine- and isoproterenol-induced vasodilation did not change during infusion of the NO-precursor L-arginine in NFH, but were significantly enhanced by L-arginine in PFH and EH (ISP 200ng/min: PFH:11.8plusminus1.02 vs 13.3plusminus1.08ml/min;p<0.05; EH: 11.3plusminus1.57 vs 14.9plusminus1.91ml/min;p<0.01). Coinfusion of L-NMMA blunted the response to acetylcholine and isoproterenol in NFH (p<0.05) but did not significantly modify vasodilation in PFH and EH.

Conclusions: Although beta-adrenergic vasodilation seems unaltered in early hypertension, L-arginine enhances the response to isoproterenol, whereas concomitant NO-synthase inhibition by L-NMMA has no significant effect. These findings suggest that the NO component of isoproterenol mediated vasodilation is impaired in early hypertension and possibly compensated by increased â-adrenoceptor responsiveness of smooth muscle cells. In this setting, supplementation of the NO-precursor L-arginine enhances the vasodilator response to â-adrenergic stimulation.