Sympathetic Activity and Presynaptic Adrenoceptor Function in Patients With Longstanding Essential Hypertension

Pc, Chang; Kriek, E; P, van Brummelen

doi:10.1097/00004872-199402000-00011

Cited by 11 publications

(9 citation statements)

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“…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. Local NE spillover increases with increased flow but the calculation of NE plasma appearance rate has been reported to be a flow-independent measure of NE release (21), and we therefore have presented data for both NE spillover and plasma appearance rate.…”

Section: Discussionsupporting

confidence: 73%

“…Thus our findings that systemic norepinephrine spillover was increased but that local norepinephrine spillover in the forearm was unaltered in subjects with borderline hypertension is in keeping with that observation. However, the relatively small sample size in this and other studies examining overall and regional sympathetic activity in hypertension suggest that the power of these studies to exclude differences between groups is low and may account for differences in the literature (11)(12)(13)(14).…”

Section: Discussionmentioning

confidence: 62%

“…Stimulation of presynaptic beta adrenoceptors by the administration of low doses of isoproterenol directly into the brachial artery in vivo in humans has been shown to increase the release of norepinephrine locally by ourselves (15) and confirmed recently by others (13). The overall effect of a beta agonist on forearm blood flow may therefore be influenced not only by postsynaptic beta adrenoceptors but also by presynaptic beta receptor response.…”

Section: Discussionmentioning

confidence: 70%

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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: 73%

Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 70%

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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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“…In subsequent work, it was found that the effective concentration of intra-arterial noradrenaline that increases forearm vascular resistance by 30 % is similar in hypertensive and normotensive subjects, whereas responses to higher doses of noradrenaline and other vasoconstrictors are non-specifically increased in hypertensive patients, probably because of structural changes in resistance arteries [15]. There is evidence of reduced sympathetic activity and neuronal re-uptake, and of structural changes, in forearm resistance vessels of patients with longstanding essential hypertension [16]. Small gluteal or omental arteries in hypertensive patients have increased reactivity to noradrenaline compared with arteries in normotensive controls in terms of wall tension, but not in terms of active media stress [17].…”

Section: Discussionmentioning

confidence: 97%

Forearm vasoconstriction in response to noradrenaline and NG-monomethyl-L-arginine in essential hypertension

et al. 1999

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A role for abnormal NO production in essential hypertension remains controversial. Blunted vasoconstriction of forearm resistance vasculature in response to N(G)-monomethyl-L-arginine (L-NMMA; an inhibitor of NO biosynthesis), relative to the response to noradrenaline, has been reported in hypertensive patients and interpreted as evidence of reduced basal NO biosynthesis. We sought to determine whether reduced sensitivity of forearm vasculature to the vasoconstrictor action of L-NMMA relative to that of noradrenaline is a consistent finding in essential hypertension. We studied a group of patients (n=32; blood pressure 176+/-4/102+/-2 mmHg; means+/-S.E.M.) and a group of healthy normotensive controls (n=32; blood pressure 130+/-2/75+/-1 mmHg). Noradrenaline (60-240 pmol.min(-1)) and L-NMMA (1-4 micromol.min(-1)) were infused into the brachial artery, and forearm blood flow was measured by venous occlusion plethysmography. The effects of each vasoconstrictor were similar in hypertensive and control subjects. The highest dose of L-NMMA reduced forearm blood flow by 0.75+/-0.12 ml.min(-1).dl(-1) in the control group and by 0.89+/-0.10 ml.min(-1).dl(-1) in the hypertensive group. The study had 90% power (with P=0.05) to detect a 10% difference in forearm blood flow response between the hypertensive and control groups. We conclude that reduced sensitivity of forearm resistance vasculature to the vasoconstrictor action of L-NMMA is not a universal feature of essential hypertension. This argues against a primary role for reduced basal NO biosynthesis in skeletal muscle resistance vessels in the pathogenesis of essential hypertension.

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“…(3) Lower body negative pressure (k10, k20 and k40 mmHg, each lasting 7 min). (4) Forearm ischaemic response [8]. Forearm ischaemia was induced by inflation of a BP cuff around the upper arm to at least 40 mmHg above the systolic BP for 10 min.…”

Section: Physiological Testsmentioning

confidence: 99%

Effects of arm dominance and brachial artery cannulation on forearm blood flow measured by strain-gauge plethysmography

Kamper

Chang

1999

Clinical Science

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The human forearm model is used extensively in physiological, pharmacological and clinical investigations. Effects of arm dominance or arterial cannulation on forearm flow measurements have never been tested formally. In the present study we tested the hypotheses that left or right arm dominance or cannulation of the brachial artery do not affect forearm haemodynamic responses to physiological or pharmacological stimuli. Results obtained in 16 volunteers showed that forearm blood flow responses to physiological stimuli are comparable before and after intra-arterial cannulation in either the dominant or the non-dominant forearm. Cannulation of a forearm brachial artery has a small effect on baseline blood flow. Responses to intra-arterially infused noradrenaline (norepinephrine) were not influenced by left or right arm dominance. Intravenous infusion of noradrenaline in eight subjects resulted in small responses in forearm blood flow that were slightly asymmetrical. During the intravenous infusion of noradrenaline, forearm blood flow or the forearm blood flow ratio did not reflect the marked increase in FVR that occurred. These results support our hypotheses (a) that either arm can be used as the control or intervention arm, and (b) that intra-arterial cannulation does not affect the results of intra-arterial infusion studies.

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Sympathetic Activity and Presynaptic Adrenoceptor Function in Patients With Longstanding Essential Hypertension

Cited by 11 publications

References 0 publications

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

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

Forearm vasoconstriction in response to noradrenaline and NG-monomethyl-L-arginine in essential hypertension

Effects of arm dominance and brachial artery cannulation on forearm blood flow measured by strain-gauge plethysmography

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