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 Δ%/min; 126 ng insulin: 2055 ± 310.6 Δ%/min; P = 0.005) and potassium (NaCl: 460.4 ± 100 Δ%/min; 126 ng insulin: 669.2 ± 60.8 Δ%/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 Δ%/min; L-NAME + 126 ng insulin: 582.3 ± 69.6 Δ%/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.
Highlights
Chronic elevated plasma insulin levels and resistance to the hypoglycemic effect of insulin have been associated with increased blood pressure in human and animal models of hypertension
We suggest that the action of insulin in the central nervous system (CNS) may be modulated by nitric oxide (NO) synthase activity, altering urinary sodium excretion
There were no significant differences in daily solid rat chow intake, cerebrospinal fluid (CSF) osmolarity, serum sodium, potassium, and lithium levels and systolic blood pressure (Table 1) in icv 0.15 M NaCl-injected rats compared with the other groups
Summary
Chronic elevated plasma insulin levels and resistance to the hypoglycemic effect of insulin have been associated with increased blood pressure in human and animal models of hypertension. This observation has led to speculation that insulin may play a role in the development of increased blood pressure [1,2]. The role of the central nervous system (CNS) in the control of blood pressure and hydroelectrolyte homeostasis has been demonstrated by several studies [3,4,5]. Exploration of the mechanisms by which insulin controls the CNS activity may offer insights into central mechanisms of insulin resistance and cardiovascular diseases, including hypertension. It has been shown that the peripheral action of insulin reduces urinary sodium excretion, suggesting an attractive reciprocal link between the renal effect of insulin, urinary sodium excre-
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Brazilian Journal of Medical and Biological Research
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
