Vasopressin and autonomic mechanisms mediate cardiovascular actions of central serotonin

1991 ◽  
Vol 260 (6) ◽  
pp. R1188-R1193 ◽  
Author(s):  
P. E. Pergola ◽  
R. H. Alper

Intracerebroventricular administration of serotonin (5-HT) to conscious rats increases mean arterial pressure (MAP) and decreases heart rate. To determine the mechanisms involved, 5-HT (2.5 micrograms) was injected intracerebroventricularly into conscious rats pretreated with various neurotransmitter and hormone antagonists. The selective 5-HT2 antagonist LY 53857 abolished the increase in MAP and the bradycardia elicited by 5-HT. The increase in MAP produced by 5-HT was potentiated by chlorisondamine (a ganglionic antagonist), unaffected by prazosin (an alpha 1-antagonist) or a vasopressin V1 antagonist alone, but eliminated by the combined pretreatment with prazosin plus the vasopressin antagonist. In contrast, the bradycardia was eliminated by either the vasopressin V1 antagonist or chlorisondamine. In conclusion, 5-HT injected into the lateral cerebral ventricle of conscious rats induces sympathoexcitation and the release of vasopressin, which results in an increase in MAP; 5-HT also elicits a bradycardia mediated through an interaction of the autonomic nervous system with circulating vasopressin.

1991 ◽  
Vol 9 (6) ◽  
pp. S429
Author(s):  
C. Cerutti ◽  
M. Lo ◽  
Claude Julien ◽  
Madelaine Vincent ◽  
C. Paultre ◽  
...  

1997 ◽  
Vol 272 (5) ◽  
pp. H2361-H2368 ◽  
Author(s):  
R. L. Davisson ◽  
M. D. Travis ◽  
J. N. Bates ◽  
A. K. Johnson ◽  
S. J. Lewis

This study examined whether the stereoselective actions of S-nitrosocysteine (SNC) in the central nervous system involves the activation of stereoselective SNC recognition sites. We examined the effects produced by intracerebroventricular injection of the L- and D-isomers of SNC (L- and D-SNC) on mean arterial blood pressure, heart rate, and vascular resistances in conscious rats. We also examined the hemodynamic effects produced by intracerebroventricular injections of 1) L-cystine, the major non-nitric oxide (NO) decomposition product of L-SNC, 2) the parent thiols L- and D-cysteine, and 3) the bulky S-nitrosothiol L-S-nitroso-gamma-glutamylcysteinylglycine [L-S-nitrosoglutathione, (L-SNOG)]. Finally, we examined the decomposition of L- and D-SNC and L-SNOG to NO on their addition to brain homogenates. The intracerebroventricular injection of L-SNC (250-1,000 nmol) produced falls in mean arterial pressure, increases in heart rate, and a dose-dependent pattern of changes in hindquarter, renal, and mesenteric vascular resistances. The intracerebroventricular injections of D-SNC, L-cystine, and L-SNOG produced only minor effects. The intracerebroventricular injection of L-cysteine produced pressor responses and tachycardia, whereas D-cysteine was inactive. L- and D-SNC decomposed equally to NO on addition to brain homogenates. L-SNOG decomposed to similar amounts of NO as L- and D-SNC. These results suggest that SNC may activate stereoselective SNC recognition sites on brain neurons and that S-nitrosothiols of substantially different structure do not stimulate these sites. These recognition sites may be stereoselective membrane-bound receptors for which L-SNC is the unique ligand.


1985 ◽  
Vol 26 (4) ◽  
pp. 631-631
Author(s):  
Yoshiko Kobayashi ◽  
Kenji Shimoda ◽  
Kazushige Kuniyoshi ◽  
Yuji Otsuka ◽  
Hitoshi Kurumatani ◽  
...  

2003 ◽  
Vol 284 (3) ◽  
pp. H987-H993 ◽  
Author(s):  
Carlos Daniel Almeida Pitanga Landulpho ◽  
Ana Carolina Rodrigues Dias ◽  
Eduardo Colombari

The peripheral mechanisms responsible for pressor response produced by microinjections of baclofen (GABAB agonist) into the nucleus tractus solitarii (NTS) of conscious rats were studied. Bilateral microinjections of baclofen (10–1,000 pmol/100 nl) produced a dose-related increase in mean arterial pressure (MAP) and heart rate. The maximal response was observed after 15 min. Intravenous injection of prazosin decreased MAP to control levels. Subsequent treatment with Manning compound (vasopressin receptor antagonist; iv) produced an additional decrease in MAP. In a different group of rats, vasopressin antagonist was injected first and MAP was significantly decreased; however, it remained elevated compared with prebaclofen injection levels. Subsequent treatment with prazosin abolished the baclofen-induced pressor response. Reductions in baclofen-induced pressor response with prazosin treatment were followed by a reflex tachycardia in animals that received a 100 pmol/100 nl dose of baclofen. The tachycardia was not observed with a dose of 1,000 pmol/100 nl. The pressor response induced by microinjection of baclofen into the NTS of conscious rats may be produced by both increases in sympathetic tonus and vasopressin release.


1990 ◽  
Vol 258 (3) ◽  
pp. R596-R601
Author(s):  
J. M. Overton ◽  
G. Davis-Gorman ◽  
L. A. Fisher

Studies were performed in unrestrained conscious Sprague-Dawley rats to examine the central nervous system (CNS) mechanism by which corticotropin-releasing factor (CRF) produces simultaneous elevations of arterial pressure and heart rate. To test the hypothesis that CRF inhibits ongoing impulse transmission through and/or transmitter release from the CNS terminations of baroreceptor afferents, the cardiovascular effects of intracerebroventricular administration of CRF were compared in rats subjected to prior sham surgery (Sham) or sinoaortic denervation (SAD). Resting levels of arterial pressure and heart rate were elevated after SAD. In addition, SAD resulted in greater chronotropic sympathetic tone and reduced chronotropic parasympathetic tone as assessed by intravenous injections of atropine methyl nitrate and DL-propranolol. Intracerebroventricular administration of CRF in both surgical groups elicited significant increases in arterial pressure and heart rate, although a tendency for reduced tachycardic responses after SAD was apparent. Pretreatment with atropine or propranolol revealed that both the parasympathetic and sympathetic nervous systems contribute to CRF-induced heart rate responses in both surgical groups. These results suggest that ongoing baroreceptor afferent transmission is not requisite for the expression of CRF-induced cardiovascular changes. Thus it is unlikely that CRF elevates arterial pressure and heart rate through an exclusive action at the CNS terminations of baroreceptor sensory fibers.


1991 ◽  
Vol 9 ◽  
pp. S429
Author(s):  
C. Cerutti ◽  
M. Lo ◽  
Claude Julien ◽  
Madelaine Vincent ◽  
C. Paultre ◽  
...  

2016 ◽  
Vol 17 (5) ◽  
pp. 498
Author(s):  
Alyssa Conte Da Silva ◽  
Juliana Falcão Padilha ◽  
Jefferson Luiz Brum Marques ◽  
Cláudia Mirian De Godoy Marques

Introdução: Existem poucos estudos que evidenciam a manipulação vertebral relacionada à modulação autonômica cardíaca. Objetivo: Revisar a literatura sobre os efeitos da manipulação vertebral sobre a modulação autonômica cardíaca. Métodos: Foi realizada uma busca bibliográfica nas bases de dados da saúde Medline, Pubmed e Cinahl, no período correspondido entre setembro e novembro de 2014. Foram utilizados os descritores em inglês Spinal Manipulation, Cardiac Autonomic Modulation, Autonomic Nervous System, Heart Rate Variability, além de associações entre eles. Resultados: Foram encontrados 190 artigos, sendo excluídos 39 por serem repetidos, restando 151. Destes, 124 não se encaixaram nos critérios de inclusão e após leitura crítica e análise dos materiais foram selecionados 7 artigos. Grande parte dos estudos revelou que a manipulação da coluna, independente do segmento, demonstra alterações autonômicas, tanto em nível simpático quanto parassimpático. Conclusão: Existem diferentes metodologias para avaliação da modulação autonômica cardíaca, sendo a Variabilidade da Frequência cardíaca através do eletrocardiograma a mais utilizada. A manipulação vertebral exerceu influência, na maioria dos artigos, sobre a modulação autonômica cardíaca.Palavras-chave: manipulação da coluna, sistema nervoso autônomo, variabilidade da frequência cardíaca. 


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