Clinical Pharmacology & Therapeutics · 1987 · 21 citations · 0 references
MedicinePharmacologyPhysiologyExercise PhysiologyPharmacodynamicsPhysical ActivityAerobic ExerciseCardiopulmonary Exercise TestingExercise TherapyTherapeutic ExerciseAntihypertensive TreatmentAutonomic Response To ExerciseAutonomic Responses To ExerciseBlood PressureCyclic Adenosine Monophosphate PathwayCyclic Adenosine Monophosphate SignalingDynamic Exercise TrainingExercise Blood Pressure Response
We compared the effects of acute stimulation of sympathetic activity by dynamic exercise on a bicycle on lymphocyte beta 2-adrenoceptor density and 10 mumol/L (-)-isoprenaline-evoked lymphocyte cyclic adenosine monophosphate increases in normotensive volunteers with those in patients with essential hypertension. In normotensive subjects exercise increased lymphocyte beta 2-adrenoceptors by about 100%. This effect seems to be a beta 2-dependent process, since it is prevented by propranolol (5 mg administered intravenously) and the beta 2-selective antagonist ICI 118,551 (25 mg t.i.d. orally for 2 weeks) but not by the beta 1-selective antagonist bisoprolol (2.5 mg administered intravenously). In patients with essential hypertension who have elevated lymphocyte beta 2-adrenoceptors, dynamic exercise caused only marginal beta 2-adrenoceptor changes, suggesting an impairment of the acute beta-adrenoceptor regulation. Normalization of blood pressure by antihypertensive treatment resulted in a significant fall in lymphocyte beta 2-adrenoceptors and in a restoration of exercise-induced beta 2-adrenoceptor increases. It is concluded that in essential hypertension the impairment of beta-adrenoceptor regulation is directly linked to the elevated blood pressure.