Chemical sympathectomy was produced in spontaneously hypertensive rats by intraperitoneal injection of 6-hydroxydopamine hydrobromide (6-OHD) (100 μg/g body weight) on days 1, 4 and 7 neonatal life and weekly thereafter until 6 weeks of age. The dose was then reduced to 50 μg g body weight and injected every 2 weeks. Studies were performed at 6 and 12 weeks of age in pentobarbital-anaesthetized rats. Plasma renin activity was measured before and 5 and 15 min after the administration of intravenous hydrallazine (5 mg/kg). Tissue noradrenaline concentration was determined in brains, hearts and kidneys from rats killed immediately upon completion of blood sampling. The blood pressure of 6-OHD-treated rats was significantly lower than in untreated rats at 6 weeks (117 ± 3 and 146 ± 2 mmHg respectively) and 12 weeks (151 ± 5 and 196 ± 4 mmHg respectively). Kidneys and hearts from 6-OHD-treated rats demonstrated a highly significant reduction in noradrenaline concentration at both 6 and 12 weeks; brain noradrenaline in treated rats was normal at 6 weeks and reduced only to 80% of normal at 12 weeks. Control (pre-hydrallazine) plasma renin activity was significantly lower in 6-OHD-treated rats at 6 and 12 weeks. Nevertheless, renin release in response to intravenous hydrallazine, expressed in terms of absolute values of plasma renin activity, was not significantly different in the treated and untreated rats. When the percentage increase in plasma renin activity from control to 15 min post-hydrallazine samples was calculated, the response of the 6-OHD-treated rats was found to be significantly greater than the response in the untreated rats at each age. These data show that treatment of neonatal rats with 6-OHD results in a significant reduction in basal activity of the renin-angiotensin system but does not interfere with the release of renin in response to hypotensive stress. In cases of severe compromise of adrenergic nervous system function, alternative mechanism exist which allow the renin-angiotensin system to manifest a maximal response in order to maintain cardiovascular homeostasis.
|Original language||English (US)|
|Number of pages||7|
|State||Published - 1980|