HALOTHANEINHIBITS PRESYNAPTIC Β2-Induced NOREPINEPHRINE (NE) RELEASE IN VIVO

Deegan, Robert; He, Huaibing; Krivoruk, Y.; Wood, Ajj; Wood, Margaret

doi:10.1097/00000542-199209001-00622

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“…Therefore enhanced presynaptic beta adrenoceptor-mediated NE release in the BHT group does not explain the attenuated postsynaptic beta adrenoceptor-mediated vasodilation observed in this group. Furthermore, isoproterenol-stimulated norepinephrine release was maintained despite the impaired vasodilatory response in borderline hypertension, suggesting a differential sensitivity of these two isoproterenol-mediated responses as we have previously shown occurs in response to anesthesia (27). The unaltered sensitivity of presynaptic beta adrenergic receptors in hypertension is supported by a study performed by Chang and colleagues (13) that found that the increase in forearm norepinephrine spillover occurring after the administration of epinephrine (a mixed a and ,3 receptor agonist) did not differ between subjects with longstanding hypertension and normal controls.…”

Section: Discussionsupporting

confidence: 60%

Forearm beta adrenergic receptor-mediated vasodilation is impaired, without alteration of forearm norepinephrine spillover, in borderline hypertension.

Stein¹,

Nelson²,

Deegan³

et al. 1995

J. Clin. Invest.

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Impaired beta adrenoceptor-mediated vasodilation associated with enhanced sympathetic activity has been reported in established hypertension. We examined whether altered beta adrenoceptor-mediated vasodilation occurs early in the disease process, when structural vascular changes are likely to be less marked, by measurement of forearm blood flow by strain gauge plethysmography after the intraarterial administration of increasing doses of a beta receptor agonist, isoproterenol, in eight subjects with borderline hypertension (BHT) and 13 normotensive (NT) controls. To determine the role of sympathetic activation in the regulation of responsiveness, we measured local sympathetic activity in the forearm by a radioisotope dilution technique. Vasodilation in response to isoproterenol, measured either as changes in forearm blood flow or forearm vascular resistance, was impaired in the BHT group so that flow at the highest dose of isoproterenol (400 ng/min) increased less (15.2±1.5 ml/ 100 ml per min) than in the NT group (24.4±2.4 ml/100 ml per minute) (P < 0.001). Although, systemic norepinephrine spillover was significantly greater in BHT, the difference in blood flow response to isoproterenol was not accounted for by increased local sympathetic activity since forearm norepinephrine spillover at baseline (BHT 1.0±0.4 ng/min vs. NT 0.64±0.13 ng/min) and after the administration of isoproterenol 60 ng/min (BHT 5.2±1.4 ng/min vs. NT 6.0±1.5 ng/min) and 400 ng/min (BHT 13.5±2.9 ng/ min vs. NT 16.5±2.7 ng/min) did not differ between the two groups. We therefore conclude that vasodilation in response to isoproterenol is impaired in subjects with BHT and that this impairment is not explained by locally increased basal, or stimulated, sympathetic activity. (J. Clin. Invest. 1995. 96:579-585.)

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Section: Discussionsupporting

confidence: 60%