RESUMEN
The aim of the study was to prove the correlations between systolic and diastolic blood pressure (BP), heart rate (HR) and plasma renin activity (PRA) under mental arithmetic stress without and with beta-blockade. 22 male hypertensive patients (aged 19-39 years) were examined, divided into a group treated with d, 1-propranolol (Obsidan) and a control group receiving placebo. Under arithmetic stress the kinetics of systolic BP showed no differences even after beta-blockade. In contrast, the increases of HR and PRA before, during and after mental arithmetic were either significantly reduced (HR) or completely blocked (PRA) under beta-blockade. However, these suppressions of HR and PRA did not prevent the stress-induced elevations of systolic and diastolic BP under beta-blockade.
Asunto(s)
Hipertensión/tratamiento farmacológico , Propranolol/uso terapéutico , Sistema Renina-Angiotensina/efectos de los fármacos , Estrés Psicológico , Adulto , Presión Sanguínea , Frecuencia Cardíaca , Humanos , Masculino , Renina/sangreAsunto(s)
Miocardio/metabolismo , Compuestos de Organotecnecio , Fosfinas/metabolismo , Tecnecio/metabolismo , Animales , Semivida , Cinética , Masculino , Ratas , Ratas Endogámicas , Porcinos , Distribución TisularRESUMEN
The renal nerve activity plays an essential role in the stimulation of plasma renin activity (PRA), which may be involved in the pathomechanism of neurogenic hypertension after sino-aortic denervation (SAD). Therefore, studies were conducted on unanesthetized rabbits (10 animals; 3-4 kg) after bilateral carotid sinus denervation plus section of cervical aortic nerves and the patterns of blood pressure (BP), heart rate (HR), and PRA were measured after a single injection-dosis of Saralasin (i.v., 10 micrograms/kg). After SAD the BP increased rapidly to 190 mm Hg within one week and remained at this high level (190-220 mm Hg) throughout the whole experiment (120 weeks). No change in BP of control rabbits (100-110 mm Hg) could be observed. Two weeks after SAD, the PRA showed a short elevation (approx. 25 ng) which subsequently returned to the levels of control rabbits (approx. 19 ng). Only in hypertensive rabbits Saralasin produced a short decrease of BP during both the initial and the whole chronic phases of hypertension, which was associated with a larger decrease of HR (1st to 5th min). Surprisingly, Saralasin induced a drop of HR also in the control rabbits. Our results suggest that also the normalized renin-angiotensin system is involved in the pathomechanism of sympathetic induced SAD-hypertension and probable permanently support the chronic state of hypertension by a relative "reninism".