Inhibitory mechanism of the nucleus of the solitary tract involved in the control of cardiovascular, dipsogenic, hormonal, and renal responses to hyperosmolality.
Am J Physiol Regul Integr Comp Physiol
; 304(7): R531-42, 2013 Apr 01.
Article
em En
| MEDLINE
| ID: mdl-23364528
ABSTRACT
The nucleus of the solitary tract (NTS) is the primary site of visceral afferents to the central nervous system. In the present study, we investigated the effects of lesions in the commissural portion of the NTS (commNTS) on the activity of vasopressinergic neurons in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, plasma vasopressin, arterial pressure, water intake, and sodium excretion in rats with plasma hyperosmolality produced by intragastric 2 M NaCl (2 ml/rat). Male Holtzman rats with 15-20 days of sham or electrolytic lesion (1 mA; 10 s) of the commNTS were used. CommNTS lesions enhanced a 2 M NaCl intragastrically induced increase in the number of vasopressinergic neurons expressing c-Fos in the PVN (28 ± 1, vs. sham 22 ± 2 c-Fos/AVP cells) and SON (26 ± 4, vs. sham 11 ± 1 c-Fos/AVP cells), plasma vasopressin levels (21 ± 8, vs. sham 6.6 ± 1.3 pg/ml), pressor responses (25 ± 7 mmHg, vs. sham 7 ± 2 mmHg), water intake (17.5 ± 0.8, vs. sham 11.2 ± 1.8 ml/2 h), and natriuresis (4.9 ± 0.8, vs. sham 1.4 ± 0.3 meq/1 h). The pretreatment with vasopressin antagonist abolished the pressor response to intragastric 2 M NaCl in commNTS-lesioned rats (8 ± 2.4 mmHg at 10 min), suggesting that this response is dependent on vasopressin secretion. The results suggest that inhibitory mechanisms dependent on commNTS act to limit or counterbalance behavioral, hormonal, cardiovascular, and renal responses to an acute increase in plasma osmolality.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Desequilíbrio Hidroeletrolítico
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Pressão Sanguínea
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Núcleo Solitário
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Ingestão de Líquidos
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Rim
Limite:
Animals
Idioma:
En
Revista:
Am J Physiol Regul Integr Comp Physiol
Assunto da revista:
FISIOLOGIA
Ano de publicação:
2013
Tipo de documento:
Article
País de afiliação:
Brasil