ABSTRACT
The nucleus tractus solitarii (NTS) receives afferent projections from the arterial baroreceptors, carotid chemoreceptors and cardiopulmonary receptors and as a function of this information produces autonomic adjustments in order to maintain arterial blood pressure within a narrow range of variation.The activation of each of these cardiovascular afferents produces a specific autonomic response by the excitation of neuronal projections from the NTS to the ventrolateral areas of the medulla (nucleus ambiguus, caudal and rostral ventrolateral medulla). The neurotransmitters at the NTS level as well as the excitatory amino acid (EAA) receptors involved in the processing of the autonomic responses in the NTS, although extensively studied, remain to be completely elucidated. In the present review we discuss the role of the EAA L-glutamate and its different receptor subtypes in the processing of the cardiovascular reflexes in the NTS. The data presented in this review related to the neurotransmission in the NTS are based on experimental evidence obtained in our laboratory in unanesthetized rats. The two major conclusions of the present review are that a) the excitation of the cardiovagal component by cardiovascular relfex activation (chemo- and Bezold-Jarisch reflexes) or by L-glutamatae microinjection into the NTS is mediated by N-methyl-D-aspartate (NMDA) receptors, and b) the sympatho-excitatory componente of the chemoreflex and the pressor response to L-glutamate microinjected into the NTS are not affected by an NMDA receptor antagonist, suggesting that the sympatho-excitatory component of these responses is mediated by non-NMDA receptors.
Subject(s)
Rats , Animals , Cardiovascular System/drug effects , Chemoreceptor Cells/physiology , Glutamic Acid/pharmacology , Glycine/pharmacology , Potassium Cyanide/pharmacology , Pressoreceptors/physiology , Receptors, Glutamate/drug effects , Reflex/physiology , Serotonin/pharmacology , Solitary Nucleus/physiology , Chemoreceptor Cells/drug effects , Pressoreceptors/drug effectsABSTRACT
The central injection of clonidine (an alpha2-adrenoceptor agonist) in conscious normotensive rats produces hypertensive responses and breadycardia. The present study performed was performed to investigate the effect of electrolytic lesions of the lateral hypothalamus (LH) on the pressor and bradycardiac responses induced by clonidine injected into the medial septal area (MSA) in conscious and unrestrained rats. Male Holtzman rats weighing 250-300 g were used. Mean arterial pressure and heart rate were recorded in sham- or bilateral LH-lesioned rats with a cerebral stainless steel cannula implanted into the MSA. The injection of clonidine (40 nmol/ul) into the MSDA of sham rats (N=8) produced a pressor response (36 ñ 7 mmHg, P<0.05) and bradycardia (-70 ñ 13 bpmm, P<0.05) compared to saline. Fourteen days after LH-lesion (N=9) the pressor response was reduced (9 ñ 10 mmHg, P<0.05) but no change was observed in the bradycardia (-107 ñ 24 bpm). These results show that LH is an important area involved in the pressor response to clonidine injected into the MSA of rats
Subject(s)
Rats , Arterial Pressure , Bradycardia , Clonidine/administration & dosage , Heart Rate , Hypothalamus/injuries , Receptors, AdrenergicABSTRACT
Natriuresis, kaliuresis, diuresis, arterial pressure and heart rate were studied in rats following dehydration and cholinergic stimulation of the medial septal area (MSA). The increase in renal NA+ and K+ excretion produced by the injection of carbachol (2nmol) into the MSA in normal hydrated rats was abolished in 48-h water-deprived rats. Urinary volume was also reduced. Cholinergic stimulation of the MSA produced a smaller mincrease in arterial pressure in 48-h-deprived rats compared to normal hydrated animals. No change was observed in heart rate. These reults show that hydration state is essential for the central cholinergic control of electrolyte excretion and increase in arterial pressure