Consequences of cerebroventricular insulin injection on renal sodium handling in rats: effect of inhibition of central nitric oxide synthase

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.

Renal handling of sodium and potassium in cadmium exposed rats

Effects of cadmium exposure on renal Na+ and K+ transports were studied in rats. During the course of cadmium treatment (2 mg Cd/kg/day, s.c. injections for 3 weeks) renal tubular transports of Na+ and K+ were evaluated by lithium clearance technique. During the early phase (first week) of cadmium treatment, urinary Na+ excretion decreased drastically and this was due to an increased Na+ reabsorption both in the proximal and distal nephrons. During the late phase (third week) of cadmium treatment, filtered Na+ load was decreased by reduction in GFR, but the renal Na+ excretion returned to the control level due to impaired Na+ transport in the proximal tubule. Urinary excretion of K+ did not change during the early phase, but it rose markedly during the late phase of cadmium treatment. These results indicate that a light cadmium intoxication induces a Na+ retention, and a heavy intoxication results in a K+ loss. Possible mechanisms for these changes are discussed.