Mechanisms of β‐adrenergic Receptor–mediated Venodilation in Humans

  title={Mechanisms of $\beta$‐adrenergic Receptor–mediated Venodilation in Humans},
  author={Christoph Schindler and Dobromir Petkov Dobrev and Matthias Grossmann and Klaus Francke and David Pittrow and Wilhelm Kirch},
  journal={Clinical Pharmacology \& Therapeutics},

Predictors of inotropic and chronotropic effects of N G‐monomethyl‐l‐arginine

Background  The haemodynamic effects of intravenous infusion of the non‐selective nitric oxide synthase (NOS) l‐omega monomethyl arginine (l‐NMMA) have previously been characterized in humans. Its

The Role of NO and cGMP in vasodilatory effect of β2-adrenoceptors in rat skin

Investigation of the role of nitric oxide and cyclic guanosine monophosphate in β2-adrenoceptors (β2-AR) mediated vasodilation in rat skin vessels indicated that, salbutamol dilates rat skin Vessels via β 2- ARs.

Hemodynamics Changes after Tilting and the Efficacy of Preventive Drugs

Whether hemodynamics changes during head‐up tilt test (HUT) predict the efficacy of preventive drugs in neurally mediated syncope (NMS) patients is investigated to clarify the differences between drug responders and nonresponders.

Characterization of Local Vascular Effects of the Nitric Oxide Inhibitor NG‐Monomethyl‐L‐Arginine on Dorsal Hand Veins

Results suggest that endothelial nitrics oxide synthase‐mediated formation of nitric oxide (NO) from L‐NMMA in doses >3.2 μmol/min and continuous PE‐induced α‐adrenergic stimulation resulting in release of very small amounts of NO from L-NMMA contribute to the observed L‐ NMMA‐induced increase in vein size.

Comparison of Inhibitory Effects of Irbesartan and Atorvastatin Treatment on the Renin Angiotensin System (RAS) in Veins: A Randomized Double‐Blind Crossover Trial in Healthy Subjects

The data indicate that atorvastatin does not inhibit Ang II–induced venoconstriction in vivo and point toward a supportive role of Ang‐(1–7) in contributing to the antihypertensive and beneficial vascular effects of irbesartan.

Effect of an inhaled glucocorticoid on endothelial function in healthy smokers.

Endothelial dysfunction, as assessed by vascular reactivity, can be corrected with an inhaled corticosteroid in the airway of lung-healthy current smokers and can serve as the basis for future clinical investigations on the effect of glucocorticoids on endothelial function in smokers.

Airway blood flow reactivity in smokers.



Decreased vasodilator response to isoproterenol during nitric oxide inhibition in humans.

It is indicated that NO inhibition blunts the vasodilator effect of beta-adrenergic agonists in the human forearm and suggest that an abnormal response to adrenergic stimulation may occur in conditions associated with impaired NO activity.

Endothelial adrenoceptors.

  • P. Vanhoutte
  • Biology, Medicine
    Journal of cardiovascular pharmacology
  • 2001
The relaxation of isolated arteries caused by beta-adrenergic agonists is reduced by removal of the endothelium and, in most cases, by inhibitors of the l -arginine nitric oxide pathway.

Venous neuropeptide Y receptor responsiveness in patients with chronic heart failure

This study investigated whether increased neuropeptide Y release altered vascular neuropeptic Y responses in the dorsal hand veins in patients with chronic heart failure to find out if this results in increased sympathetic nerve activity and elevated plasma neuropePTide Y levels.

Activation of nitric oxide synthase by β2‐adrenoceptors in human umbilical vein endothelium in vitro

Results indicate that endothelial β2‐adrenergic stimulation and cyclic AMP elevation activate the L‐arginine/NO system, and give rise to vasorelaxation, in human umbilical vein.

Effects of inhibition of the L-arginine/nitric oxide pathway on vasodilation caused by beta-adrenergic agonists in human forearm.

Results suggest that beta-adrenergic vasodilator responses in human forearm vasculature are mediated predominantly through beta 2- adrenergic receptors and are dependent on nitric oxide synthesis.

Thiazide-induced vasodilation in humans is mediated by potassium channel activation.

The vasodilator effect of hydrochlorothiazide in the human forearm is small and only occurs at high concentrations, and the mechanism of action is not mediated by inhibition of vascular Na-Cl cotransport but involves vascular potassium channel activation.

Role of nitric oxide in isoprenaline and sodium nitroprusside-induced relaxation in human hand veins.

It is concluded that in human veins, spontaneously released NO does not play a major role in isoprenaline-induced relaxation and the effects of sodium nitroprusside in this vascular bed may be attenuated by endothelium-derived NO.

Comparison of the effects of nadolol and bisoprolol on the isoprenaline-evoked dilatation of the dorsal hand vein in man.

The failure of bisoprolol to attenuate isoprenaline-evoked venodilatation in the human dorsal hand vein argues against the involvement of a beta1-adrenoceptor-mediated component in the isoprelatory responses.

Local venous response to N‐desethylamiodarone in humans

The aim of this study was to explore the mechanism of action of N‐desethylamiodarone in human hand veins by infused after oral treatment with hydrocortisone or coinfused with α‐tocopherol.