BACKGROUND: In patients with congestive heart failure, the chronotropic and inotropic responses to beta-adrenergic agonists are reduced. It is not known whether desensitization of peripheral beta-adrenoceptors accounts for impaired limb vasodilation in these patients. Accordingly, we studied 14 normal subjects and 13 age-matched patients with congestive heart failure. METHODS AND RESULTS: To distinguish vasodilation mediated by beta-adrenoceptors and adenylate cyclase from that mediated by stimulation of guanylate cyclase, each subject received intrabrachial artery infusions of isoproterenol (1-100 ng/min) and sodium nitroprusside (0.3-10 micrograms/min), respectively. Forearm blood flow was determined by venous occlusion plethysmography. Maximal vasodilative potential, determined during reactive hyperemia, was reduced in the patients with congestive heart failure. The maximal forearm blood flow response to isoproterenol was comparable in patients with heart failure and in normal subjects (8.0 +/- 1.1 versus 9.2 +/- 1.2 ml/100 ml of tissue/min, respectively, p = NS). Furthermore, the dose-response relation to isoproterenol was similar in both groups. Likewise, the forearm vasodilative response to sodium nitroprusside was preserved in the heart failure group. Plasma concentration of norepinephrine was higher in the patients with heart failure (436 +/- 34 versus 201 +/- 74 pg/ml, p less than 0.01). When both groups were considered, there was no correlation between norepinephrine levels and the maximal forearm blood flow response to isoproterenol (r = 0.10, p = NS). CONCLUSIONS: We conclude that beta-adrenoceptor desensitization does not occur in the limb vessels of patients with congestive heart failure.
BACKGROUND: In patients with congestive heart failure, the chronotropic and inotropic responses to beta-adrenergic agonists are reduced. It is not known whether desensitization of peripheral beta-adrenoceptors accounts for impaired limb vasodilation in these patients. Accordingly, we studied 14 normal subjects and 13 age-matched patients with congestive heart failure. METHODS AND RESULTS: To distinguish vasodilation mediated by beta-adrenoceptors and adenylate cyclase from that mediated by stimulation of guanylate cyclase, each subject received intrabrachial artery infusions of isoproterenol (1-100 ng/min) and sodium nitroprusside (0.3-10 micrograms/min), respectively. Forearm blood flow was determined by venous occlusion plethysmography. Maximal vasodilative potential, determined during reactive hyperemia, was reduced in the patients with congestive heart failure. The maximal forearm blood flow response to isoproterenol was comparable in patients with heart failure and in normal subjects (8.0 +/- 1.1 versus 9.2 +/- 1.2 ml/100 ml of tissue/min, respectively, p = NS). Furthermore, the dose-response relation to isoproterenol was similar in both groups. Likewise, the forearm vasodilative response to sodium nitroprusside was preserved in the heart failure group. Plasma concentration of norepinephrine was higher in the patients with heart failure (436 +/- 34 versus 201 +/- 74 pg/ml, p less than 0.01). When both groups were considered, there was no correlation between norepinephrine levels and the maximal forearm blood flow response to isoproterenol (r = 0.10, p = NS). CONCLUSIONS: We conclude that beta-adrenoceptor desensitization does not occur in the limb vessels of patients with congestive heart failure.
Authors: Kanokwan Bunsawat; Stephen M Ratchford; Jeremy K Alpenglow; Soung Hun Park; Catherine L Jarrett; Josef Stehlik; Stavros G Drakos; Russell S Richardson; D Walter Wray Journal: Exp Physiol Date: 2020-06-18 Impact factor: 2.969