Increased plasma adrenaline concentrations in benign essential hypertension.

Franco-Morselli, R; Elghozi, Jean‐Luc; Joly, Emma; Giuilio, S Di; Meyer, Philippe

doi:10.1136/bmj.2.6097.1251

Cited by 193 publications

(62 citation statements)

References 14 publications

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“…Overall these results reflect a reversal of the state of catecholamine secretion encountered in early hypertension (i.e., increased plasma NE 4 ' ' Oi 23 and E 54 ' 55 levels in some young hypertensive persons). In fact, plasma NE levels appear to be particularly elevated during VOL.…”

Section: Discussionmentioning

confidence: 77%

Dissociation of 24-hour catecholamine levels from blood pressure in older men.

Stern¹,

Beahm²,

McGinty³

et al. 1985

Hypertension

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SUMMARY Increased plasma norepinephrine levels have been observed in some persons with early essential hypertension. Although both plasma norepinephrine level and mean arterial blood pressure rise with age, little is known about the state of catecholamine secretion in elderly patients with essential hypertension. We studied the 24-hour cycle levels of plasma norepinephrine, epinephrine, and dopamine in 12 elderly hypertensive subjects and 13 age-matched normotensive controls (mean ages, 63.8 ± 1.2 yr and 64.8 ± 1.8 yr [SEM] respectively). Blood samples were obtained at bihourly intervals from 0900 to 2100 hours and every 30 minutes from 2100 to 0900 hours, during which time sleep and breathing were continuously monitored. A circadian rhythm was displayed in both groups by plasma epinephrine levels (mesor, 49 ± 2 pg/ml and 38 ± 1 pg/ml; amplitude, 15 ± 2 pg/ml and 11 ± 1 pg/ml; acrophase, 12.20 ± 0.40 hr and 14.41 ± 0.34 hr in the normotensive and hypertensive groups respectively) but not by plasma norepinephrine or dopamine levels. During the 24-hour cycle plasma epinephrine, but not norepinephrine or dopamine, levels were positively related to mean arterial blood pressure (r = 0.60 for the normotensive subjects, r = 0.57 for the hypertensive subjects, p < 0.01 for both). Mean 24-hour plasma norepinephrine (377 ± 9 pg/ml vs 455 ± 9 pg/ml; p < 0.001), epinephrine (34 ± 2 pg/ml vs 45 ± 2 pg/ml; p < 0.01), and dopamine (40 ± 2 pg/ml vs 62 ± 3 pg/ml; p < 0.01) levels were lower in the hypertensive group, although groups did not differ in parameters known to affect catecholamine secretion such as body weight, sodium intake, sleep efficiency, or sleeprelated breathing disorders. Mean 24-hour plasma norepinephrine level was inversely related to the 24-hour mean arterial blood pressure (r = -0.48, p < 0.05). High norepinephrine levels in the elderly may reflect decreased baroreceptor sensitivity as well as compensatory response to decreased /3-adrenergic receptor sensitivity. It is unclear why elderly hypertensive persons, unlike younger hypertensive persons, have lower plasma catecholamine levels than do elderly normotensive persons. Whereas increased sympathetic outflow has been implicated in the induction of early "neurogenic" essential hypertension, 4 the age-dependent increase in NE is observed in normotensive subjects. Whether the ob- served increment in circulating NE is related to the age-associated rise in blood pressure or to the increased incidence of hypertension in aging humans is unclear. 5 The increase in NE with advancing age instead could reflect a compensatory mechanism to a declining peripheral response to adrenergic stimuli 6 -7 or an age-related decrease in clearance of NE. 8 Moreover, a recent study based on single NE samples obtained from a large number of subjects with a wide age range concluded that NE increases with age in normotensive subjects but not in subjects with essential hypertension. 9 However, there is relatively little direct information about the state of plasma catecholamines in...

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Section: Discussionmentioning

confidence: 77%

Dissociation of 24-hour catecholamine levels from blood pressure in older men.

Stern¹,

Beahm²,

McGinty³

et al. 1985

Hypertension

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“…In essential hypertension in man, increased levels of circulating adrenaline have been observed (de Champlain, Farley, Cousineau & van Ameringen, 1974;Franco-Morselli, Elghozi, Joly, di Guilio & Meyer, 1977) and may, through enhancing transmitter release from sympathetic nerves, be important in the aetiology and maintenance of high blood pressure. Drugs which block fi-adrenoceptors prevent this action of adrenaline in vitro and it has been shown that they decrease sympathetic transmitter release in man (de Champlain, Cousineau, van Ameringen & Marc Aurele, 1977).…”

Section: Statistical Analysis Of Resultsmentioning

confidence: 99%

Adrenaline Activation of Prejunctional Β‐adrenoceptors in Guinea‐pig Atria

Majewski

McCulloch

Rand

et al. 1980

British J Pharmacology

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1 Adrenaline in a concentration of 1.0 tM depressed the stimulation-induced efflux of tritium from the guinea-pig atria incubated with [3H]-noradrenaline, whereas adrenaline in a concentration of 0.5 nm significantly enhanced the stimulation-induced efflux of tritium. This enhancement was blocked by metoprolol (0.1 tM) and thus appears to be mediated by P-adrenoceptors. 2 In guinea-pig atria incubated with unlabelled adrenaline and then with [3H]-noradrenaline, both catecholamines were released by field stimulation. In such atria metoprolol, practolol, oxprenolol or propranolol decreased the stimulation-induced efflux of tritium. These effects did not occur if the atria were incubated with unlabelled noradrenaline and then with [3H]-noradrenaline, suggesting that neuronally released adrenaline activates prejunctional f-adrenoceptors. 3 The effect of oxprenolol in decreasing the release of tritium from guinea-pig atria, incubated with unlabelled adrenaline and then with [3H]-noradrenaline was greater in the presence of phentolamine. This may reflect the a-adrenoceptor blocking activity of oxprenolol.

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“…Continuous infusion of a so-called subpressor dose of adrenaline causes hypertension in rats (Majewski et al, 1981). Increased plasma levels of adrenaline have been observed in patients with essential hypertension (De Champlain et al, 1976;Franco-Morselli et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

Elevated plasma noradrenaline in response to beta‐adrenoceptor stimulation in man.

Vincent¹,

Veld²,

Boomsma³

et al. 1982

Brit J Clinical Pharma

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I Dose-dependent increments of plasma noradrenaline were observed during graded infusions of (-+-)isoprenaline (3.5-35 ng kg-' min-' i.v.) in seven normal subjects and in ten subjects with borderline hypertension. At the highest dose of isoprenaline, noradrenaline rose by 166 + 16 pg/ml in normals and by 169 + 34 pg/ml in hypertensives (mean + s.e. mean). 2 In the subjects with borderline hypertension isoprenaline infusions were repeated after 7 days of treatment with (±)propranolol (320 mg/day, divided into 4 doses) and subsequently after 7 days of treatment with (+)atenolol (100 mg/day) 2-3 h after the morning dose of /3-adrenoceptor blocker. The dose-response curve for plasma noradrenaline was shifted to higher doses of isoprenaline by a factor of 4 by atenolol and the heart rate response was similarly shifted. The heart rate response was shifted by a factor of 16 by propranolol, but plasma noradrenaline did not change after isoprenaline under propranolol treatment, even when isoprenaline was given at doses high enough to induce increments of heart rate similar to those without,8-adrenoceptor blocker treatment.3 In the subjects with borderline hypertension mean and diastolic intra-arterial pressures fell at the highest dose of isoprenaline by 9 + 2 and 13 ± 2 mm Hg respectively. These effects were antagonized by propranolol and not by atenolol. 4 The observed rise in plasma noradrenaline after isoprenaline might have been caused by baroreflex-stimulation of central sympathetic outflow. The isoprenaline-induced decrease in mean arterial pressure, however, was small. Moreover pulse pressure rose and this tends to suppress rather than stimulate baroreflex-mediated sympathetic activity. Activation of presynaptic /8-adrenoceptors, allegedly of the /32-subtype, is known to facilitate noradrenaline release upon nerve stimulation of isolated tissues. Our results lend support to the hypothesis that such a facilitatory mechanism is also operative in intact man.

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Increased plasma adrenaline concentrations in benign essential hypertension.

Cited by 193 publications

References 14 publications

Dissociation of 24-hour catecholamine levels from blood pressure in older men.

Dissociation of 24-hour catecholamine levels from blood pressure in older men.

Adrenaline Activation of Prejunctional Β‐adrenoceptors in Guinea‐pig Atria

Elevated plasma noradrenaline in response to beta‐adrenoceptor stimulation in man.

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