ABSTRACT
In the present study, we investigated the effects of acute intracerebroventricular (icv) insulin administration on central mechanisms regulating urinary sodium excretion in simultaneously centrally NG-nitro-L-arginine methylester (L-NAME)-injected unanesthetized rats. Male Wistar-Hannover rats were randomly assigned to one of five groups: a) icv 0.15 M NaCl-injected rats (control, N = 10), b) icv dose-response (1.26, 12.6 and 126 ng/3 µL) insulin-injected rats (N = 10), c) rats icv injected with 60 µg L-NAME in combination with NaCl (N = 10) or d) with insulin (N = 10), and e) subcutaneously insulin-injected rats (N = 5). Centrally administered insulin produced an increase in urinary output of sodium (NaCl: 855.6 ± 85.1 Ä percent/min; 126 ng insulin: 2055 ± 310.6 Ä percent/min; P = 0.005) and potassium (NaCl: 460.4 ± 100 Ä percent/min; 126 ng insulin: 669.2 ± 60.8 Ä percent/min; P = 0.025). The urinary sodium excretion response to icv 126 ng insulin microinjection was significantly attenuated by combined administration of L-NAME (126 ng insulin: 1935 ± 258.3 Ä percent/min; L-NAME + 126 ng insulin: 582.3 ± 69.6 Ä percent/min; P = 0.01). Insulin-induced natriuresis occurred by increasing post-proximal sodium excretion, despite an unchanged glomerular filtration rate. Although the rationale for decreased urinary sodium excretion induced by combined icv L-NAME and insulin administration is unknown, it is tempting to suggest that perhaps one of the efferent signals triggered by insulin in the CNS may be nitrergic in nature.
Subject(s)
Animals , Male , Rats , Brain/enzymology , Insulin/pharmacology , Natriuresis/drug effects , Nitric Oxide Synthase/antagonists & inhibitors , Injections, Intraventricular , Insulin/administration & dosage , Microinjections , NG-Nitroarginine Methyl Ester/administration & dosage , Random Allocation , Rats, WistarABSTRACT
In the present study, we investigated the effects of acute intracerebroventricular (icv) insulin administration on central mechanisms regulating urinary sodium excretion in simultaneously centrally NG-nitro-L-arginine methylester (L-NAME)-injected unanesthetized rats. Male Wistar-Hannover rats were randomly assigned to one of five groups: a) icv 0.15 M NaCl-injected rats (control, N = 10), b) icv dose-response (1.26, 12.6 and 126 ng/3 microL) insulin-injected rats (N = 10), c) rats icv injected with 60 microg L-NAME in combination with NaCl (N = 10) or d) with insulin (N = 10), and e) subcutaneously insulin-injected rats (N = 5). Centrally administered insulin produced an increase in urinary output of sodium (NaCl: 855.6 +/- 85.1 Delta%/min; 126 ng insulin: 2055 +/- 310.6 Delta%/min; P = 0.005) and potassium (NaCl: 460.4 +/- 100 Delta%/min; 126 ng insulin: 669.2 +/- 60.8 Delta%/min; P = 0.025). The urinary sodium excretion response to icv 126 ng insulin microinjection was significantly attenuated by combined administration of L-NAME (126 ng insulin: 1935 +/- 258.3 Delta%/min; L-NAME + 126 ng insulin: 582.3 +/- 69.6 Delta%/min; P = 0.01). Insulin-induced natriuresis occurred by increasing post-proximal sodium excretion, despite an unchanged glomerular filtration rate. Although the rationale for decreased urinary sodium excretion induced by combined icv L-NAME and insulin administration is unknown, it is tempting to suggest that perhaps one of the efferent signals triggered by insulin in the CNS may be nitrergic in nature.
Subject(s)
Brain/enzymology , Insulin/pharmacology , Natriuresis/drug effects , Nitric Oxide Synthase/antagonists & inhibitors , Animals , Injections, Intraventricular , Insulin/administration & dosage , Male , Microinjections , NG-Nitroarginine Methyl Ester/administration & dosage , Random Allocation , Rats , Rats, WistarABSTRACT
The aim of this study was to evaluate the blood lead levels in a sample of Bologna's population, 12 years after the previous screening campaign carried out in 1984. The investigated sample was divided, as in 1984, by age, sex, occupational exposure and selected life style factors. The blood lead levels presented a sharp reduction in comparison with the values observed in the previous study. In 1996, the 50 degrees, 90 degrees and 98 degrees percentile of blood lead were 50 micrograms/l, 90 micrograms/l and 140 micrograms/l whereas in 1984 they were 129 micrograms/l, 242 micrograms/l and 329 micrograms/l, respectively. Possibly, this result is related to a lower level of environmental lead pollution as a result of the increasing use of unleaded gasoline in new cars.
