Drug-induced changes of urinary catecholamines in the rat: Role of the adrenal medulla

Basso, P. del; Rusca, Graziella; Carpi, A

doi:10.1016/0014-2999(70)90186-x

Cited by 4 publications

(4 citation statements)

References 12 publications

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“…Numerous small pieces of the cortical tissue were transplanted under the renal capsule, as described by Basso et ul. (1). In agreement with previous findings (6), the transplants were well vascularized at the time of sacrifice.…”

Section: Experiments In Ratssupporting

confidence: 92%

Development of Tolerance to the Metabolic Actions of β²‐Adrenoceptor Stimulating Drugs

Fredholm

Lunell

Persson

et al. 1982

Acta Obstet Gynecol Scand

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Abstract. Considerable evidence exists that treatment with β‐receptor stimulating drugs causes desensitization in several different tissues in vitro. There is also evidence that the administration of β‐receptor stimulating drugs during asthma therapy leads to the development of tolerance of at least some actions of β‐stimulating drugs. The present communication presents data from experiments in animals, including humans, suggesting that treatment with an oral salbutamol leads to the development of tolerance of metabolic actions of β‐adrenergic stimulating drugs. Rats given salbutamol, 20 mg/kg/day, showed a decreased lipolytic response to salbutamol and to noradrenaline. By contrast, rats subjected to adrenal demedullation showed an increased lipolytic response. These results suggested that β2‐adrenoceptor‐stimulating drugs may cause desensitization and also that the normal circulating levels of catecholamines may be sufficient to regulate the responsiveness of the adipose tissue. The effect of a single oral dose of salbutamol was compared in 10 women not previously given salbutamol and in 13 women treated with oral salbutamol in a dose of 4 mg 4 times/day for 12–33 days preceding study. The salbutamol‐induced increase in the levels of insulin, C‐peptide, glucose, and glycerol were significantly reduced in those exposed to salbutamol before the test. The rise in cyclic AMP and non‐esterified fatty acids was not significantly affected. There were also differences in the salbutamol‐induced fall in diastolic blood pressure and in heart rate. These differences in cardiovascular responsiveness could be accounted for by a difference in the values of these parameters before the test. Our results suggest that women receiving 16 mg/day of salbutamol, i.e. a normal clinical dose of the drug sufficient to achieve relaxation of the uterus, develop tolerance to some metabolic side effects. This, and the development of tolerance to the tremorogenic effect of β‐adrenoceptor‐stimulating drugs, may be clinically advantageous, but the possibility exists that tolerance may develop also to some of the therapeutic actions. The literature concerning the development of tolerance to β2adrenoceptor‐stimulating drugs is briefly reviewed, and some possible explanations for what appears to be an organ‐selective development of tolerance is discussed.

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Section: Experiments In Ratssupporting

confidence: 92%

Development of Tolerance to the Metabolic Actions of β²‐Adrenoceptor Stimulating Drugs

Fredholm

Lunell

Persson

et al. 1982

Acta Obstet Gynecol Scand

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“…An increase in the urinary excretion of NA and adrenaline in the rat after acute amphetamine administration has been demonstrated (BISCARDI et al, 1964;BEAU-VALLETet al, 1966b;GUNNE and LEWANDER, 1967;LEWANDER, 1968a, b;BEAUVAL-LET, 1968;BASSO et al, 1970). The ganglion blocking agent, mecamylamine, blocked the effect of amphetamine on the NA excretion but not on the A excretion; adrenal demedullation (by expression) did not completely block the increase in the A excretion after amphetamine (BISCARDI et al, 1964).…”

Section: Adrenergic Transmissionmentioning

confidence: 94%

“…The increase in the urinary A excretion was, however, absent after bilateral cutting ofthe splenchnic nerves (GUN NE and LEWANDER, 1967;LEWANDER, 1968b). Later BASSO et al (1970) could show that the adrenal demedullation could be performed more efficiently if the whole gland was removed and pieces of its cortex were grafted under the capsule of the kidney. Amphetamine administered to rats demedullated in this manner did not cause an increase in the urinary excretion of A.…”

Section: Adrenergic Transmissionmentioning

confidence: 99%

“…Later BASSO et al (1970) could show that the adrenal demedullation could be performed more efficiently if the whole gland was removed and pieces of its cortex were grafted under the capsule of the kidney. It was also found (LEWANDER, 1968 b;BASSO et al, 1970) that the amphetamine-induced increase in the urinary excretion of NA was more pronounced in rats with denervated or demedullated glands than in intact rats. It was also found (LEWANDER, 1968 b;BASSO et al, 1970) that the amphetamine-induced increase in the urinary excretion of NA was more pronounced in rats with denervated or demedullated glands than in intact rats.…”

Section: Adrenergic Transmissionmentioning

confidence: 99%

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General Pharmacology of Amphetamine-Like Drugs

Änggård¹,

Lewander²,

Gunne³

1973

Drug Addiction II

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Amphetamine and related central stimulant drugs are derivatives of ß-phenylethylamine (Table 1) and are thus relatively simple organic bases. The general ßphenylethylamine skeleton is one which amphetamine shares with the neurotransmitters noradrenaline, adrenaline, and dopamine. Phenylethylamine itselfhas central stimulant properties, but has an extremely short half-life in the body due to rapid metabolism by monoamine oxidase (MAO). Amphetamine has, due to steric hindrance by the ex-methyl group, much less affinity for MAO and therefore has a longer half-Iife.Most amphetamines have cardiovascular, psychomotor stimulant, hyperthermic, and anorexigenic actions. All of the structural features of amphetamine are important far its spectrum of pharmacologic activity. Any alteration may enhance, diminish, or attenuate one or several components in the actions of the parent drug. (1) Substitution of the phenyl ring, (2) alteration of the length of the side chain, (3) substitution on the primary nitrogen group, (4) substitution of the ex-and ß-carbon atoms, and (5) their absolute configuration have been studied and will be briefly discussed here. For a more thorough review on the subject the reader is referred to the papers by BIEL (1970), vANRossuM and SIMONS (1969) and VREE (1973. The effect of ring and side-chain substitution on distribution and elimination of the amphetamines has been discussed by BECKETT and BROOKES (1970). recently reviewed the biochemical pharmacology of the amphetamines. The metabolism and disposition of methylphenidate were reported by F ARAJ et al.

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Resistance of rat fetuses to nicotine‐induced lipolysis

Mosier

Capodanno

et al. 1974

Teratology

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Pregnant Long-Evans rats were fed stock diets containing 50 or 100 mg/kg of added nicotine during days 10-20 or 0-20 of pregnancy. Control rats were given stock diet during days 0-20. The mean nicotine intake ranged up to 6.03 mg/kg/day. In fetuses bled on day 20 there were no differences in levels of fetal plasma triglycerides, phospholipids, and cholesterol between the experimental and control groups. In another experiment single doses of 1 mglkg

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Drug-induced changes of urinary catecholamines in the rat: Role of the adrenal medulla

Cited by 4 publications

References 12 publications

Development of Tolerance to the Metabolic Actions of β²‐Adrenoceptor Stimulating Drugs

Development of Tolerance to the Metabolic Actions of β²‐Adrenoceptor Stimulating Drugs

General Pharmacology of Amphetamine-Like Drugs

Resistance of rat fetuses to nicotine‐induced lipolysis

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Drug-induced changes of urinary catecholamines in the rat: Role of the adrenal medulla

Cited by 4 publications

References 12 publications

Development of Tolerance to the Metabolic Actions of β2‐Adrenoceptor Stimulating Drugs

Development of Tolerance to the Metabolic Actions of β2‐Adrenoceptor Stimulating Drugs

General Pharmacology of Amphetamine-Like Drugs

Resistance of rat fetuses to nicotine‐induced lipolysis

Contact Info

Product

Resources

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Development of Tolerance to the Metabolic Actions of β²‐Adrenoceptor Stimulating Drugs

Development of Tolerance to the Metabolic Actions of β²‐Adrenoceptor Stimulating Drugs