Endorphinergic Neurons in the Brainstem: Role in Cardiovascular Regulation

Kunos, George; Mastrianni, James A.; Mosqueda‐Garcia, Rogelio; Varga, K

doi:10.1007/978-1-4615-9834-3_10

Cited by 7 publications

(5 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We have ear lier reported that microinjection of clonidine into the arcuate nucleus of urethane-anesthetized rats caused hy potension and bradycardia, and that these effects oc curred at doses similar to those effective in producing the same effects in the rostral ventrolateral medulla [8], In the present experiments, intra-arcuate microinjection of aMN caused hypotension and bradycardia that could be inhibited by microinjection of yohimbine into the same site. Unlike clonidine, aMN does not interact with imida zoline receptors, therefore the present findings unequivo cally implicate aj-receptors in the arcuate nucleus in…”

Section: Discussionmentioning

confidence: 58%

“…The arcuate nucleus also has neural projec tions to brainstem sites of cardiovascular regulation, in cluding the nucleus tractus solitarii (NTS) [3,4] can be activated via catecholaminergic afferents [1] or by synthetic a2-selective agonists, such as clonidine and amethylnorepinephrine. Stimulation of these receptors in creases growth hormone [6,7] and prolactin release [6], and can also cause hypotension and bradycardia [8,9], The arcuate nucleus is the bed nucleus for proopiome lanocortin (POMC)-containing neurons [10], which pro ject to a variety of brain regions [11], including the NTS …”

mentioning

confidence: 99%

See 1 more Smart Citation

Alpha-2-Adrenergic Activation of Proopiomelanocortin-Containing Neurons in the Arcuate Nucleus Causes Opioid-Mediated Hypotension and Bradycardia

Scanlon

Járai

et al. 1996

Neuroendocrinology

Self Cite

View full text Add to dashboard Cite

Treatment of rats for 4 days with α-methyldopa, 200 mg/kg/day i.p., increases steady state levels of proopiomelanocortin (POMC) mRNA in the mediobasal hypothalamus, as measured by DNA excess solution hybridization. The increase is prevented by parallel treatment with yohimbine, 2 mg/kg/day i.p., but not by naltrexone, 2 mg/kg/day i.p. Treatment with the peripheral vasodilator hydralazine, 2 mg/kg/day, does not affect POMC mRNA levels. In situ hybridization histochemistry with a cRNA probe for POMC indicates that POMC-containing cells are located within the confines of the arcuate nucleus both in control and in α-methyldopa-treated rats, and confirms the increase in POMC mRNA in the latter. Microinjection of 2 µg of α-methylnorepinephrine unilaterally into the arcuate nucleus of urethane-anesthetized rats causes hypotension and bradycardia, which can be inhibited by 200 ng of yohimbine microinjected into the same site, or by 100 ng l-naloxone microinjected into the ipsilateral nucleus tractus solitarii, but not into the arcuate nucleus. These findings are interpreted to indicate that activation of α₂-adrenergic receptors located on POMC-containing neurons in the arcuate nucleus causes β-endorphin release and stimulation of opiate receptors in the NTS, which results in hypotension and bradycardia, and that this mechanism contributes to the hypotensive action of α-methyldopa.

show abstract

Section: Discussionmentioning

confidence: 58%

mentioning

confidence: 99%

Alpha-2-Adrenergic Activation of Proopiomelanocortin-Containing Neurons in the Arcuate Nucleus Causes Opioid-Mediated Hypotension and Bradycardia

Scanlon

Járai

et al. 1996

Neuroendocrinology

Self Cite

View full text Add to dashboard Cite

show abstract

“…Дорсальные ядра Х пары черепномозговых нервов, находящиеся в нижней части ствола мозга -это ядро одиночного пути и прилегающее дорсальное ядро блуждающего нерва. Как известно, эти структуры играют ключевую роль в рефлекторной парасимпатической регуляции АД (снижение) и частоты сердечных сокращений (урежение), что происходит за счет активации первого нейрона барорефлекса, содержащегося в этих ядрах [19]. В данном контексте значение имеет то, что обратная зависимость между уровнем АД и чувствительностью к болевым раздражителям простирается в пределах диапазона нормальных и умеренных значений АД.…”

Section: история изучения и новые взгляды на фенотип «аг+гб»unclassified

Comorbidity of arterial hypertension and tension-type headache

2020

View full text Add to dashboard Cite

Arterial hypertension (AH) and exertional headache (EHA) are comorbidities. The article presents a nonsystematic review focused on studying the AH+EHA phenotype. The authors addressed the history of studying the phenotype, several theories about its pathophysiological causes (psychosomatic, neuroanatomical, and baroreflector). The protective “hypertension-associated hypoalgesia” phenotype, a mechanism of its change in AH chronization, and difficulties of differential diagnosis are described. The AH+EHA phenotype requires further study since its incidence is quite high. This will allow developing an individualized approach in prevention and treatment of EHA attacks, decreasing the risk of life-threatening cardiovascular complications, and avoiding iatrogenic complications in patients with AH. The main way to prevent the development of AH+EHA phenotype is patient’s compliance, which can be provided by using combination hypotensive drugs to reduce the number of pills and dosing. It is important to take into account possible adverse reactions of the nervous system (medication-overuse headache or EHA aggravation). Considering these conditions, the drug Triplixam can be used for prevention of complications in the AH+EHA phenotype. Triplixam is a fixed triple combination of amlodipine/indapamide/perindopril, and its individual components have low and medium risk for development of headache.

show abstract

“…Increased MOR signalling along the nucleus accumbens, ventral pallidum and central amygdala nucleus (CeA) has been mainly associated with the hedonic palatability of NaCl when it is tasted . MOR activity along the brainstem, within the lateral parabrachial nucleus (LPBN) and the nucleus of the solitary tract (NTS), mainly modulates motivated sodium/food intake and blood pressure …”

Section: Introductionmentioning

confidence: 99%

“…5,[15][16][17] MOR activity along the brainstem, within the lateral parabrachial nucleus (LPBN) and the nucleus of the solitary tract (NTS), mainly modulates motivated sodium/food intake and blood pressure. [18][19][20][21] However, experiments such as these fail to determine the mechanisms by which endogenous MOR signalling acts to modulate sodium appetite and blood pressure regulation. The present study aimed to investigate the effect of increased salt intake (2% NaCl solution) in rats during a short period of time (4 days) on MOR mRNA expression along the MnPO and the NTS.…”

mentioning

confidence: 99%

The effect of increased NaCl intake on rat brain endogenous μ‐opioid receptor signalling

Dadam

Zádor

Caeiro

et al. 2018

J Neuroendocrinology

View full text Add to dashboard Cite

Numerous studies demonstrate the significant role of central β-endorphin and its receptor, the μ-opioid receptor (MOR), in sodium intake regulation. The present study aimed to investigate the possible relationship between chronic high-NaCl intake and brain endogenous MOR functioning. We examined whether short-term (4 days) obligatory salt intake (2% NaCl solution) in rats induces changes in MOR mRNA expression, G-protein activity and MOR binding capacity in brain regions involved in salt intake regulation. Plasma osmolality and electrolyte concentrations after sodium overload and the initial and final body weight of the animals were also examined. After 4 days of obligatory hypertonic sodium chloride intake, there was clearly no difference in MOR mRNA expression and G-protein activity in the median preoptic nucleus (MnPO). In the brainstem, MOR binding capacity also remained unaltered, although the maximal efficacy of MOR G-protein significantly increased. Finally, no significant alterations were observed in plasma osmolality and electrolyte concentrations. Interestingly, animals that received sodium gained significantly less weight than control animals. In conclusion, we found no significant alterations in the MnPO and brainstem in the number of available cell surface MORs or de novo syntheses of MOR after hypertonic sodium intake. The increased MOR G-protein activity following acute sodium overconsumption may participate in the maintenance of normal blood pressure levels and/or in enhancing sodium taste aversion and sodium overload-induced anorexia.

show abstract

Endorphinergic Neurons in the Brainstem: Role in Cardiovascular Regulation

Cited by 7 publications

References 37 publications

Alpha-2-Adrenergic Activation of Proopiomelanocortin-Containing Neurons in the Arcuate Nucleus Causes Opioid-Mediated Hypotension and Bradycardia

Alpha-2-Adrenergic Activation of Proopiomelanocortin-Containing Neurons in the Arcuate Nucleus Causes Opioid-Mediated Hypotension and Bradycardia

Comorbidity of arterial hypertension and tension-type headache

The effect of increased NaCl intake on rat brain endogenous μ‐opioid receptor signalling

Contact Info

Product

Resources

About

Endorphinergic Neurons in the Brainstem: Role in Cardiovascular Regulation

Cited by 7 publications

References 37 publications

Alpha-2-Adrenergic Activation of Proopiomelanocortin-Containing Neurons in the Arcuate Nucleus Causes Opioid-Mediated Hypotension and Bradycardia

Alpha-2-Adrenergic Activation of Proopiomelanocortin-Containing Neurons in the Arcuate Nucleus Causes Opioid-Mediated Hypotension and Bradycardia

Comorbidity of arterial hyperten­sion and tension-type headache

The effect of increased NaCl intake on rat brain endogenous μ‐opioid receptor signalling

Contact Info

Product

Resources

About

Comorbidity of arterial hypertension and tension-type headache