Locally produced dopamine (DA) causes a reversible and dose-dependent inhibition in Na+-K+-ATPase activity in rat proximal tubule (PT) segments [A. Aperia, A. Bertorello, and I. Seri. Am. J. Physiol. 252 (Renal Fluid Electrolyte Physiol. 21): F32-F45, 1987.]. To examine whether this effect might be of physiological importance, rats were given normal-salt (NS) or high-salt (HS) diet for 10 days. HS diet significantly increased Na excretion but did not alter glomerular filtration rate (GFR). Benserazide (Bz), an inhibitor of the enzyme L-aromatic amino acid decarboxylase (AADC) that converts L-dopa to DA, significantly attenuated the natriuresis in HS rats but had no effect on GFR. By use of immunofluorescence (IF) studies AADC was localized to the PT. Specific AADC IF was not observed in the medulla. In AADC-positive PT segments, Na+-K+-ATPase activity was significantly lower in HS rats than in NS rats (P less than 0.001). In AADC-negative medullary thick ascending limb, Na+-K+-ATPase activity was the same in NS and HS rats. If HS rats were given Bz just before study, PT Na+-K+-ATPase activity increased significantly and was not different from Na+-K+-ATPase activity in PT segments from NS rats. Bz had no significant effect on PT Na+-K+-ATPase activity in NS rats. In PT segments from Bz-treated rats, DA inhibited Na+-K+-ATPase activity already at a dose of 10(-8) M, whereas in segments from NS rats, significant inhibition of Na+-K+-ATPase activity was not observed until DA was increased to 10(-7) M.(ABSTRACT TRUNCATED AT 250 WORDS)

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Using in situ hybridization histochemistry we have studied the effect of glucose and fat deprivation on galanin-R1 receptor (GAL-R1-R) mRNA levels in the rat paraventricular (PVN) and supraoptic (SON) nuclei after single and repeated i.p. administration of a glucose antimetabolite 2-deoxy-D-glucose (DG), as well as of a fatty acid antimetabolite, sodium mercaptoacetate (MA), treatments known to increase food intake. Both DG and MA injections caused an increase in levels of GAL-R1 mRNA transcripts in the PVN and SON. These results indicate that glucose and fat deprivation increase the sensitivity of PVN and SON neurons to galanin, and that regulation of receptor levels may be an important mechanism in galaninergic signalling.

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Pregnant mare’s serum gonadotropin (PMS; 10 IU day 3O)-induced ovulation was used as a model to study the effect of drugs interfering with monoamine neurotransmission on CNS processes controlling ovulation. The drugs were administered during the critical period on day 32 and tubal eggs were counted in the morning of day 33. When injected during the critical period, dopamine (DA) receptor agonists such as apomorphine, ET 495, ergotamine, 2-bromo-α-ergocryptine, lergotrile and ergocornine inhibited ovulation, an effect which was counteracted by the DA receptor blocking agent, pimozide. However, by itself pimozide had no significant effect, whereas combined noradrenahne (NA) and DA receptor blocking agents such as chlorpromazine and clozapine inhibited ovulation. α- and β-adrenergic blocking agents and drugs influencing 5-hydroxytryptamine (5-HT) neurotransmission did not affect ovulation. LH-RH removed the ovulatory blockade induced by ET 495 in the same dose-range as it removed pentobarbital-induced blockade of ovulation. Furthermore, ergocornine did not block ovulation after the critical period and was less effective when given prior to the critical period. Therefore it is likely that the DA receptor agonists act via a central action. Thus, the present findings give further support for the existence of a central inhibitory DA and facilitory NA mechanism in the control of PMS-induced ovulation in the immature female rat.