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1 beta-adrenoceptor blockade with metoprolol provoked, both at rest and during exercise, a decrease of 'active' renin and angiotensin II together with an increase of 'inactive' renin and unchanged 'total' renin. The significant exercise-provoked increases in angiotensin II, plasma renin activity and 'active', 'inactive' and 'total' renin when on placebo, were reduced by metoprolol. 2 No significant change in serum sodium and potassium and in plasma aldosterone was found during beta-adrenoceptor blockade at rest. During exercise plasma aldosterone dropped significantly without any change in serum sodium or potassium. 3 Plasma noradrenaline increased significantly at rest on metoprolol. The increase in plasma noradrenaline and adrenaline during exercise was similar on placebo and on metoprolol.

Ketanserin (120 mg/day) or placebo was given orally to 14 patients with mild to moderate essential hypertension according to a double blind crossover protocol, each treatment period lasting six weeks. Resting intra-arterial pressure in the recumbent position was reduced from 150/84 to 141/77 mm Hg; the hypotensive effect persisted throughout an uninterrupted graded exercise test to the point of exhaustion. The haemodynamic effects were similar at rest and during exercise. Overall, systemic vascular resistance decreased by 14%, heart rate fell by 5%, but stroke volume and cardiac output increased. Mean pulmonary arterial pressure and capillary wedge pressure were not significantly affected, but pulmonary vascular resistance decreased by 15%. The pressor response to methoxamine was significantly reduced by ketanserin. Both plasma noradrenaline and adrenaline concentrations increased, plasma renin activity and angiotensin II concentration decreased, and plasma aldosterone concentration was unchanged. The data indicate that ketanserin induces arteriolar dilatation, possibly related to an alpha-1-antagonistic action and to a reduced circulating angiotensin II concentration. The haemodynamic response is complex, and an increase in cardiac output limits the hypotensive effect. There is no firm evidence of an effect on venous tone as cardiac filling pressures do not change.

It has been suggested that enkephalins are involved in the gastric relaxation induced by stimulation of the non-adrenergic, non-cholinergic vagal fibres in the cat stomach. Experiments were therefore performed on strips of cat stomach. With longitudinal and circular gastric fundus and corpus strips from reserpinized cats, non-adrenergic, non-cholinergic relaxatory responses could be elicited by transmural electrical stimulation in Tyrode solution containing atropine and 5-hydroxytryptamine. Morphine, leu-enkephalin and met-enkephalin did not influence the tone of the strips or the relaxation evoked by stimulation at 8 Hz, and neither did the opioid antagonist, naloxone. These results do not support the enkephalinergic hypothesis for the non-adrenergic, non-cholinergic vagal fibres in the cat stomach.

SummaryThe author provides a description and discussion of a fluorimetric method for differential estimation of adrenaline and noradrenaline in urine.The importance of this method in differential diagnosis of arterial hypertension is stressed.

The contribution of beta 1-adrenoceptors to the regulation of plasma renin activity was investigated in nine healthy sodium-replete volunteers: seven subjects received a cumulative intravenous dose of 75 micrograms/kg prenalterol, a predominant beta 1-adrenoceptor agonist, and two subjects only vehiculum. In the seven actively treated subjects beta 1-adrenoceptor agonism increased (P less than 0.001) systolic intra-arterial pressure by an average of 16 +/- 4 mm Hg and heart rate by 19 +/- 3 beats min. These increases were significantly (P less than 0.04) different from the changes observed in the two control subjects (+ 3 +/- 4 mm Hg and -1 +/- 4 beats/min, respectively). Plasma renin activity, however, tended to decrease in both the actively (-38%) and saline (-28%) treated subjects. Predominant beta 1-adrenoceptor agonism, powerful enough to increase systolic pressure and heart rate does not increase plasma renin activity in supine sodium-replete normal man.

We studied the effects of labetalol, an alpha- and beta-adrenoceptor antagonist, on maximum exercise heart rate and on plasma renin, aldosterone, noradrenaline, and adrenaline levels at rest and during exercise in hypertensive patients. The dose of labetalol was doubled weekly from 0.3 to 2.4 g per day. The maximum exercise heart rate fell significantly during labetalol treatment, and there was a significant correlation between exercise tachycardia and the dosage of labetalol. Plasma renin activity and aldosterone concentration at rest decreased during treatment with labetalol. The exercise-induced increase in plasma renin activity was reduced by labetalol. Labetalol did not cause any significant changes in plasma noradrenaline and adrenaline at rest or during exercise.

Experiments performed in anesthetized dogs have shown that occlusion of the coeliac and mesenteric arteries may determine minor increases of systemic blood pressure, obviously of hemodynamic nature and not induced by baroreceptive vasomotor reflexes. Increase of pressure into the mesenteric arterial circulation does not decrease the systemic blood pressure. The aortic and carotid sinus baroreceptors are the major means of the reflex blood pressure homeostasis. Evidence for the existence of specific chemoreceptors in the abdominal vascular area could not be obtained.

After 30 min rest in the lying position, 12 healthy male volunteers (average age 22 years) received, in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg iv followed by a continuous infusion of 10 mg/hr). Thereafter they rested for a further 30 min in the recumbent position and for 15 min sitting on a bicycle ergometer; they then exercised to exhaustion. At rest plasma levels of adrenocorticotropin (ACTH), cortisol, and aldosterone increased during infusion of naloxone, while body temperature decreased. During exercise the difference in plasma ACTH between naloxone and saline periods was abolished, while the differences in plasma cortisol and aldosterone lost statistical significance. Intra-arterial pressure, heart rate, ventilation, O2 uptake, and CO2 output were continuously monitored throughout the experiment and were not affected by naloxone. This was also the case for several hormonal and biochemical measurements, including those of plasma renin, angiotensin II, norepinephrine, 13,14-dihydro-15-keto-prostaglandin F2 alpha, glucose and lactate, and serum insulin and growth hormone. Exercise performance was not changed by naloxone. In conclusion (1) during exhaustive graded exercise of short duration opioidergic inhibition of the pituitary-adrenocortical axis is probably not sustained, (2) apart from the latter mechanism, the present study does not support the hypothesis that endogenous opioids are involved in various hemodynamic, respiratory, and hormonal responses to this type of exercise.

Dans 18 cas de neuroblastome humain la noradrenaline (NA) et la dopamine-β-hydroxylase presentent des profils de distribution intracellulaire identiques, suggerant un stockage dans la meme particule. Le contenu en NA de ces particules n'est pas inferieur a celui des particules du nerf splenique; on peut en conclure qu'un stockage defectueux de NA dans les cas de neuroblastome est peu probable.

THE existence of different noradrenaline pools in sympathetically innervated tissues has been proposed on the basis of both pharmacological and biochemical studies1,2. Recent morphological evidence3,4, showing that the terminals of splenic nerves contain two distinct size populations of granulated vesicles and that only one of them is present in the preterminal processes, has given additional support to this theory. We now present biochemical evidence for the existence of two types of noradrenaline storage particles in the dog spleen and compare some of their properties with those of the noradrenaline vesicles of bovine splenic nerve.

Eine einfache, schnelle und empfindliche Methode zur dunnschichtchromatographischen Trennung von 0,2–1µg Menge von Noradrenalin, Adrenalin, Normetanephrin, Metanephrin, 3,4-Dihydroxy-mandelsaure und 3-Methoxy-4-hydroxymandelsaure wird beschrieben.