Adrenaline and Noradrenaline output in Urine After Unilateral and Bilateral Adrenalectomy in Man

Euler, U. S. v.; Franksson, C; Hellström, J

doi:10.1111/j.1748-1716.1954.tb01107.x

Cited by 134 publications

(21 citation statements)

References 3 publications

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“…Plasma NA is derived from the peripheral sympathetic nervous system (von Euler et al, 1954;Glowinski et al, 1965;Cryer, 1976) and reflects the activity of the system (Lake et al, 1976;Kopin et al, 1978;Saar & Gordon, 1979;Watson et al, 1979;Kiowski et al, 1981), although some care may be necessary in interpretation of the results due to different patterns of organ release and extraction (Brown et al, 1981). Secretion of renin is partly under the control of the sympathetic nervous system (Gordon et al, 1967;Winer et al, 1969) so that PRA is also a marker of sympathetic activity (Kotchen et al, 1971), but other factors such as local renal haemodynamics (Pettinger et al, 1973;Mathias et al, 1975) and sodium intake (Watson et al, 1980) may also influence PRA.…”

Section: Discussionmentioning

confidence: 99%

Differential blockade of alpha‐adrenoceptors by indoramin.

Nicholls¹,

O'Connor²,

Harron³

et al. 1984

Brit J Clinical Pharma

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1 The effect of equihypotensive single oral doses of indoramin (mean dose 67 mg), phenoxybenzamine (mean dose 50 mg), hydralazine (mean dose 133 mg) and placebo on arterial pressure and heart rate in the supine and standing position was studied in six normal volunteers. Observations were made before and at 2 and 4 h after drug administration.2 Plasma noradrenaline (NA) was measured at each time interval in the supine position, and after 4 min of standing. Plasma renin activity (PRA) was measured at each time interval after 30 min in the standing position. 3 The three active drugs reduced systolic arterial pressure in the standing position to a similar extent (indoramin, -24 mm Hg; phenoxybenzamine, -23.4 mm Hg; hydralazine, -30.4 mm Hg). The maximum effect of indoramin and phenoxybenzamine was observed at 4 h, and of hydralazine at 2 h after drug administration. 4 The reductions of arterial pressure in the standing position were accompanied by increases in heart rate, plasma NA and PRA. Small increases were observed after indoramin (heart rate, + 9.2 beats min-'; plasma NA, + 126 pg/ml; PRA, + 0.33 ng angiotensin 1 ml-' h-1), greater increases after phenoxybenzamine (heart rate, + 20; plasma NA, + 210; PRA, + 0.47), and the greatest increases after hydralazine (heart rate, + 26; plasma NA, + 250; PRA, + 1.16). 5 In the supine position, indoramin and phenoxybenzamine produced no effect on arterial pressure, heart rate or plasma NA. Hydralazine produced small reductions in diastolic pressure, which were accompanied by an increase in heart rate of 25.5 beats min (P < 0.01 when compared to placebo) and in plasma NA of 223 pg ml-'(P < 0.05). 6 Plasma NA, PRA and heart rate increased together and may be regarded as three interdependent indices of sympathetic activity. 7 Indoramin reduced the degree of increase of plasma NA, PRA and heart rate per unit fall in pressure, when compared to phenoxybenzamine and hydralazine. The effect of phenoxybenzamine and hydralazine on the degree of increase was similar. 8 The results are consistent with the hypothesis that indoramin produces selective postsynaptic al-adrenoceptor blockade in man, and therefore produces relatively less tachycardia and NA increase than does a non-selective a-adrenoceptor antagonist (phenoxybenzamine) or an arteriolar vasodilator (hydralazine).Keywords indoramin phenoxybenzamine hydralazine a-adrenoceptors 719 720 D. P. Nicholls et al.

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Section: Discussionmentioning

confidence: 99%

Differential blockade of alpha‐adrenoceptors by indoramin.

Nicholls¹,

O'Connor²,

Harron³

et al. 1984

Brit J Clinical Pharma

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“…Alterations in urinary output of adrenaline and noradrenaline following bilateral adrenalectomy or medullo-adrenalectomy have been reported in a variety of animal species (von Euler, Franksson & Hellstrom, 1954;Carpi & Oliverio, 1964). It has been proposed that bilateral adrenalectomy results in a compensatory increase in sympathetic nerve activity secondary to the decrease in blood pressure (Imms & Jones, 1968).…”

Section: Introductionmentioning

confidence: 99%

Evidence for the Role of Adrenocortical Hormones in the Regulation of Noradrenaline and Dopamine Metabolism in Certain Brain Areas

Rastogi

Singhal

1978

British J Pharmacology

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1 Bilateral adrenalectomy suppressed body growth and increased the activity of tyrosine hydroxylase in rat striatum in a time-dependent manner. Fifteen days after adrenalectomy, the concentrations of noradrenaline were decreased significantly in hypothalamus and striatum, as were those of dopamine in brain stem and striatum. 2 Catechol-O-methyltransferase failed to change in response to adrenalectomy, but the activity of monoamine oxidase in cortex was significantly increased 7 days after surgery. These changes in various neurochemical parameters were even more pronounced 15 days after adrenal ablation. 3 Administration of corticosterone (10 mg/kg i.p.) to adrenalectomized rats effectively reversed the observed effects on brain amine metabolism. Corticosterone treatment for 7 days beginning from the 8th day of adrenalectomy virtually restored the concentrations of noradrenaline and dopamine as well as the activities of striatal tyrosine hydroxylase and cerebrocortical monoamine oxidase to the values seen for sham-operated controls. 4 Our data suggest that changes seen in brain noradrenaline and dopamine of adrenalectomized rats are specific to adrenocortical steroids and that these hormones play a role in the regulation of catecholamine formation.

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“…norepinephrine per L. or (8,9) which do not secrete directly into the general circulation; hence, only that portion escaping metabolic destruction or binding between the sites of secretion and subsequent entry into the blood circulatory system is reflected in the plasma concentration. Therefore the average endogenous -self-infusion rate calculated for norepinephrine should be distinguished from the average endogenous secretion rate, for which the self-infusion rate represents a lower limit.…”

Section: Estimation Of Resting Secretion Ratesmentioning

confidence: 99%

Plasma Concentrations of Epinephrine and Norepinephrine During Intravenous Infusions in Man *†

Cohen¹,

Holland²,

Sha³

et al. 1959

J. Clin. Invest.

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Although numerous clinical studies have centered about the infusion of epinephrine and norepinephrine (1-3), the plasma concentrations attained by the infused catecholamines during such investigations have never been delineated. Recently a highly specific and sensitive procedure for the simultaneous fluorometric determination of epinephrine and norepinephrine in plasma was described (4, 5 while they were lying on a bed. Blood pressure and pulse were noted at various intervals. Routinely, 30 ml. blood specimens were drawn from the right antecubital vein into syringes wetted with heparin solution (sterile Liquaemin® Sodium, Organon Inc., Orange, N. J.), and then transferred immediately to cold 40 ml. centrifuge tubes equipped with ground glass stoppers. Specimens were chilled in an ice-water bath until the complete set for the particular experiment had been collected. They were then centrifuged at 700 G for 15 minutes following which the supernatant plasmas were removed and analyzed for epinephrine and norepinephrine as described elsewhere (4, 5). The plasma concentrations of catecholamine reported in this communication are uncorrected for recoveries which had been demonstrated previously to range from 70 to 90 per cent (5).Infusions were automatically terminated after infusion speeds of 30 ,ug. catecholamine per minute had been reached, or if a pulse pressure of 100 mm. Hg or a basal pressure increase of 100 mm. Hg were attained. Cessation of infusions also followed upon request of the subject, report of a persistent headache, or if the subject appeared extremely uncomfortable although willing to continue. RESULTSConstant rate infusions of epinephrine or norepinephrine were characterized by the attainment of steady state plasma concentrations as demonstrated in Figure 1. Although at times fluctuations in the steady state concentrations were observed, particularly for norepinephrine (cf. Curves B, C and E), the data in general were indicative of the maintenance of a dynamic balance between the rate at which the particular catecholamine was added to plasma and the rate at which it was simultaneously removed. Steady states were maintained for up to 65 minutes, the longest period tested. For epinephrine infusions, steady 1935

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Adrenaline and Noradrenaline output in Urine After Unilateral and Bilateral Adrenalectomy in Man

Cited by 134 publications

References 3 publications

Differential blockade of alpha‐adrenoceptors by indoramin.

Differential blockade of alpha‐adrenoceptors by indoramin.

Evidence for the Role of Adrenocortical Hormones in the Regulation of Noradrenaline and Dopamine Metabolism in Certain Brain Areas

Plasma Concentrations of Epinephrine and Norepinephrine During Intravenous Infusions in Man *†

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