It has been previously reported that the peptide neurotensin (NT) produces an inhibitory effect on Na+, K+-ATPase (NKA) activity without changes in Mg2+-ATPase activity in Wistar rats. Clozapine i.p. administration, an atypical antipsychotic, 30 min before cortical membrane preparation produced a stimulatory effect at 10 mg/kg clozapine. Taking into account these results, it is of interest to study the effect of neurotensin after clozapine administration on spontaneously hypertensive (SH) and Wistar Kyoto (WKY) rats. Spontaneously hypertensive rat is considered as a model of schizophrenia because this strain develops behavioural deficits in a social context which are attenuated by acute clozapine administration. Experiments conducted in cortical synaptosomal membranes led to a significant increase in NKA activity in both SH and WKY rats after clozapine administration. Neurotensin only produced NKA inhibition in WKY rats, which were previously administered with clozapine. It was observed that this treatment increases the NKA activity values, making it possible to observe the inhibitory effect of neurotensin. But, the increase in NKA activity values were not enough to confirm the inhibitory effect of neurotensin on NKA activity in SH rats. The lack of this neurotensin effect can be explained by the existence of plasma membrane alteration due to hypertensive state, which resulted in modifications of enzymes or receptors inserted into the plasma membrane, and hence the ATPase modulation by the peptide was also modified.
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