Articles: pressoreceptors-physiology.
-
The vasopressin receptor subtype involved in the enhancement by vasopressin of adrenoceptor-mediated vasoconstriction was investigated in rat isolated perfused mesenteric arteries. [Arg8]vasopressin (1-10 nM) dose-dependently increased the perfusion pressure and enhanced the pressor response to the adrenoceptor agonist methoxamine (40 nmol) or electrical stimulation of periarterial nerves (16 Hz), at the concentration of 10 nM of [Arg8]vasopressin up to 4 and 3 fold, respectively. During prolonged exposure (45 min) the direct vasoconstrictor effect of [Arg8]vasopressin (10 nM) rapidly declined whereas the potentiation of methoxamine-induced vasoconstriction was maintained. The selective vasopressin V1A receptor antagonist SR 49,059 (1-3 nM) and the non-selective V1A/B and oxytocin receptor antagonist [deamino-Pen1,Tyr(Me)2,Arg8]vasopressin (15-45 nM) inhibited the direct vasoconstrictor action of [Arg8]vasopressin but had no effect on the enhancement of the pressor response to methoxamine or electrical stimulation. ⋯ In arteries precontracted with methoxamine (7.5 microM) pressor responses to [Arg8]vasopressin (3-10 nM) were not inhibited by a dose of SR 49,059 (3 nM) which abolished the peptide's vasoconstrictor effect under control conditions. These data show that the direct vasoconstrictor effect of [Arg8]vasopressin is mediated by V1A receptors while the enhancement of adrenoceptor-mediated pressor responses is insensitive to V1A, V1B, and oxytocin receptor antagonists and is not mimicked by selective agonists of V1B and V2 receptors. In conclusion, an unusual interaction of vasopressin with V1A receptors, or even the existence of a novel receptor subtype, has to be considered.
-
Experiments were performed on male SD rats anaesthetized with urethane (700 mg/kg) and chloralose (35 mg/kg). The results showed that mean arterial pressure (MBP) increased signifigantly and heart rate (HR) had no signifigant change by bilateral microinjection AVP(10 pmol/0.1 microliter/site) into the rostral ventrolateral medulla (rVLM), while both MBP and HR were not changed by application of an AVP-V1 receptor antagnoist. ⋯ The above results suggest that AVP in the rVLM can elevate MBP and midbrain defence area stimulation can cause pressor response. Both these effects are related to activation of AVP-V1 receptors in the rVLM.
-
Int J Psychophysiol · Apr 1997
Clinical TrialSomatotosensory evoked potentials during baroreceptor stimulation in chronic low back pain patients and normal controls.
Nineteen chronic low back pain patients (aged 19-63) and 17 controls (aged 20-41) received electrical pain stimuli during manipulation of their carotid baroreceptors. The non-invasive mechanical manipulation of baroreceptors, using the PRES technique (Phase Related External Suction), simulates the end-effects of phasic blood pressure changes. This technique was developed to assess pain responses induced by changes in blood pressure without the typical shortcomings of pharmacological manipulation or lack of a control condition. ⋯ Results showed that lower tonic blood pressures are associated with greater baroreceptor activity amplifying pain, while higher blood pressure is associated with pain dampening during high baroreceptor activity. Data suggested that the differences in pain responses found in low back pain patients were associated with their lower tonic blood pressure levels. It is proposed that in general, lower blood pressures may be associated with greater pain during baroreceptor activation.
-
The inhalation of high concentrations of isoflurane has been reported to increase the heart rate and the concentration of serum catecholamines. Although the precise mechanisms for the sympathetic activation of isoflurane have yet to be clearly elucidated, they are considered to possibly originate from the stimulation of airway sensory afferents, the baroreceptor reflex, or the direct stimulation of the central nervous system. To determine how these three mechanisms contribute to sympathetic augmentation, the effects of lower airway deafferentation and baroreceptor deafferentation on the isoflurane-induced changes in the renal sympathetic nerve activity (RSNA) in tracheally intubated rabbits were examined. ⋯ The inhalation of isoflurane caused an increase of RSNA in intact, baroreceptor-deafferented, and lower airway-deafferented rabbits. The extent of the increases in RSNA was greater in intact and lower airway-deafferented rabbits than in baroreceptor-deafferented rabbits. Therefore, it is suggested that isoflurane may increase the efferent sympathetic nerve activity via the direct stimulation of the central nervous system and via the arterial baroreceptor reflex reflecting the reduction in arterial blood pressure. The stimulation of the vagally innervated airway may not contribute to the increase in the sympathetic nerve activity by isoflurane.
-
J. Auton. Nerv. Syst. · Dec 1994
Neuronal expression of Fos protein in the rat brain after baroreceptor stimulation.
The purpose of this study was to identify the CNS neurons that express Fos protein after repeated activation of the baroreceptor reflex. This was done in Wistar rats anesthetized with urethane and alpha-chloralose with careful physiological controls. The intact control rat showed few Fos-immunoreactive (ir) neurons, whereas the anesthetized control rat showed many Fos-ir neurons in the CNS from the medulla oblongata to the forebrain. ⋯ No significant correlation was found in the humoral control nuclei in the preoptico-hypothalamic structure. Fos expression was never detected in the sensory neurons in the ganglia petrosum and nodosum, and in the sympathetic preganglionic neurons in the intermediolateral nucleus of the thoracic spinal cord. This study shows that Fos expression in the CNS neurons is induced not only by baroreceptor stimulation but also by anesthesia and/or sham-operation, and that Fos expression in the NTSm and PAG neurons faithfully responds to baroreceptor stimulation.