ABSTRACT
In the present study we used intracerebral microdialysis techniques to examine whether angiotensin II (ANG II) modulates the release of serotonin (5-hydroxytryptamine, 5-HT) in the subfornical organ (SFO) in freely moving rats. Extracellular concentrations of 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the region of the SFO were significantly decreased by microinjection of ANG II (10 pmol, 50 nl), but not by vehicle, into the dialysis site. No significant changes in the 5-HT and 5-HIAA levels caused by ANG II were observed in the sites away from the SFO. Water ingestion significantly enhanced the amount of the decrease in the 5-HT and 5-HIAA concentrations in the SFO area elicited by the ANG II injection. These results show that ANG II may reduce the release of 5-HT in the SFO area, and imply that the 5-HT receptor mechanism in the SFO area may participate in the elicitation of the drinking behavior to ANG II.
Subject(s)
Angiotensin II/pharmacology , Serotonin/metabolism , Subfornical Organ/drug effects , Subfornical Organ/metabolism , Animals , Drinking/drug effects , Enzyme Activation , Hydroxyindoleacetic Acid/analysis , Male , Microdialysis , Microinjections , Rats , Rats, Wistar , WaterABSTRACT
Experiments were conducted to investigate the role of noradrenergic systems in the lateral hypothalamus area (LHA) in the water intake caused by injection of angiotensin II (ANG II) into the subfornical organ (SFO) in rats. Intracerebral microdialysis techniques were utilized to quantify the extracellular content of noradrenaline (NA) in the LHA. Microinjection of ANG II into the SFO significantly increased NA release in the LHA when water was not available for drinking. The increase in the release of NA in the LHA was significantly attenuated by water intake. In urethane-anesthetized rats, injections of ANG II into the SFO significantly enhanced the release of NA in the LHA that accompanied an elevation in mean arterial pressure (MAP). Intravenous administration of the alpha-agonist metaraminol, on the other hand, significantly decreased the NA release in the LHA that accompanied an increase in MAP, suggesting that the enhanced NA release in the LHA caused by ANG II into the SFO may be not mediated by increasing in arterial pressure. These results show the involvement of the noradrenergic systems in the LHA in the dipsogenic response induced by angiotensinergic activation of the SFO.
Subject(s)
Angiotensin II/pharmacology , Drinking/physiology , Hypothalamic Area, Lateral/metabolism , Norepinephrine/metabolism , Subfornical Organ/drug effects , Vasoconstrictor Agents/pharmacology , Adrenergic alpha-Agonists/pharmacology , Animals , Blood Pressure/drug effects , Extracellular Space , Hypothalamic Area, Lateral/drug effects , Male , Metaraminol/pharmacology , Microdialysis/methods , Rats , Rats, Wistar , Time FactorsABSTRACT
The present study was carried out to examine whether estrogen modulates the drinking response caused by activation of neural pathways from the subfornical organ (SFO) to the hypothalamic paraventricular nucleus (PVN) in the female rat. Microinjection of angiotensin II (ANG II) into the SFO elicited drinking in ovariectomized female rats that were treated with either propylene glycol (PG) vehicle or estradiol benzoate (EB). The amount of water intake induced by the ANG II injection was significantly greater in the PG-treated than in the EB-treated animals. In both groups, previous injections of either saralasin, an ANG II antagonist, or phentolamine, an alpha-adrenoceptor antagonist, bilaterally into the PVN resulted in the significant attenuation of the drinking response to ANG II, whereas similar injections of saline vehicle into the PVN were without effect. These results suggest that the circulating estrogen may act to reduce the drinking response that is mediated through angiotensinergic and alpha-adrenergic mechanisms in the PVN in response to angiotensinergic activation of SFO efferent projections.
Subject(s)
Angiotensins/metabolism , Drinking/physiology , Estrogens/metabolism , Neural Pathways/metabolism , Neurons/metabolism , Paraventricular Hypothalamic Nucleus/metabolism , Subfornical Organ/metabolism , Angiotensins/pharmacology , Animals , Antihypertensive Agents/pharmacology , Drinking/drug effects , Drug Interactions/physiology , Estrogens/pharmacology , Estrus/physiology , Female , Neural Inhibition/drug effects , Neural Inhibition/physiology , Neural Pathways/cytology , Neural Pathways/drug effects , Neurons/drug effects , Ovariectomy , Paraventricular Hypothalamic Nucleus/cytology , Paraventricular Hypothalamic Nucleus/drug effects , Phentolamine/pharmacology , Rats , Rats, Wistar , Reaction Time/drug effects , Reaction Time/physiology , Saralasin/pharmacology , Sodium Chloride/pharmacology , Subfornical Organ/cytology , Subfornical Organ/drug effectsABSTRACT
The present study was designed to examine the role of noradrenergic systems in the hypothalamic paraventricular nucleus (PVN) in the drinking response induced by microinjection of angiotensin II (ANG II) into the subfornical organ (SFO) in the awake rat. Intracerebral microdialysis techniques were utilized to quantify the extracellular concentration of noradrenaline (NA) in the region of the PVN. Injections of ANG II (10(-6)M, 0.2 microl) into the SFO significantly increased NA release in the PVN area. The increase in the NA concentration caused by the ANG II injection was significantly attenuated by water ingestion. In urethane-anesthetized rats, injections of ANG II into the SFO elicited an elevation in mean arterial pressure (MAP). On the other hand, intravenous injections of the alpha-agonist metaraminol (5 microg) slightly decreased the release of NA in the PVN area that accompanied an elevation in MAP. These results show that the noradrenergic system in the PVN area may be involved in the dipsogenic response induced by ANG II acting at the SFO.
