In contrast to beta-adrenoceptor blocking agents, calcium channel blockers do not appear to affect exercise tolerance in hypertensive subjects. A possible explanation is a difference in the metabolic effects of both types of drugs. Therefore, the effects of 4-week treatment periods with verapamil and propranolol on metabolic parameters during an endurance bicycle ergometer test were studied in eight patients with mild to moderate essential hypertension. Patients exercised at a work load which increased the heart rate to 150 bts/min during placebo. A single-blind, placebo-controlled, randomized cross-over design was used. The dose of propranolol and verapamil was adjusted to lower standing diastolic blood pressure less than 90 mmHg. Average daily doses were 155 +/- 21 mg propranolol and 390 +/- 44 mg verapamil. Exercise heart rate was reduced during propranolol and verapamil (P less than 0.01), but the reduction was more pronounced during propranolol than during verapamil (P less than 0.05). Minute ventilation and oxygen consumption were unchanged during propranolol and verapamil. The respiratory exchange ratio tended to increase during propranolol. Plasma glucose and lactate concentrations were unchanged during propranolol and verapamil. In contrast, plasma glycerol and nonesterified fatty acids were reduced during propranolol (P less than 0.05), but unchanged during verapamil. Plasma potassium levels were increased during propranolol (P less than 0.05). Despite the important direct and indirect role of calcium ions in the regulation of many metabolic processes, no effect of verapamil on metabolic parameters during submaximal exercise was found. In contrast, propranolol had an effect on fat and potassium metabolism during exercise.

A series of measurements of blood pressure in normotensive and hypertensive subjects showed that measurements made with a sphygmomanometer with the arm dependent by the side were consistently higher than those made with the arm horizontal at heart level. The mean difference in a group of 90 hypertensive outpatients was 11/12 mm Hg.Failure to appreciate the importance of arm position may lead to erroneous measurements of blood pressure. This has important implications for clinical practice and research. IntroductionMany factors influence the measurement of blood pressure by sphygmomanometer. Much attention has been paid to the importance of the choice of instrument,' defects of the instrument,2 3 size of the cuff,4 and diastolic end point.5 The influence of changes in arm position on blood pressure measured by sphygmomanometer was first reported 75 years ago.6 7 Our experience led us to believe that this factor has been overlooked by many observers. We undertook a series of investigations to evaluate this aspect of measuring blood pressure.The aim of this study was to estimate the effect on measurement of blood pressure by sphygmomanometer of changes in arm position; we studied this in normotensive subjects, untreated patients with hypertension, and patients with hypertension receiving various antihypertensive drugs.

Adult newts regenerate functional limbs after amputation. This process normally depends on the trophic influence of nerves on the regenerating limbs, particularly in the early stages before differentiation of the regeneration blastema, when it stimulates growth by maintaining high rates of macromolecular synthesis. The sequence of biochemical events involved is unknown, but it has been suggested that intracellular cyclic AMP may be a second messenger within the blastema. Many studies have indicated that the neural agent(s) involved might be protein. The recent finding that blastemata contain high levels of catecholamines, however, has implicated noradrenaline (NA) as the neurotrophic agent, and suggested that it works via stimulation of beta-adrenergic receptors on the blastemal cells, thereby raising the intracellular concentrations of cyclic AMP. To test this hypothesis we studied the ability of NA alone and in combination with alpha-and beta-adrenergic antagonists to increase cyclic AMP levels and to mimic the effects of nerves by maintaining high rates of protein synthesis and high mitotic indices (MI) in denervated blastemata in organ culture. We find that although NA raises cyclic AMP levels through a beta-adrenergic effect, it does not maintain high rates of protein synthesis or high MI in cultured blastemata. It is unlikely therefore, that this hypothesis applies.

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