Search Results
Instituto de Biología Molecular y Celular del Cáncer, CSIC-University of Salamanca, Salamanca, Spain
Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), CSIC-University of Salamanca, Salamanca, Spain
Search for other papers by L Francisco Lorenzo-Martín in
Google Scholar
PubMed
Instituto de Biología Molecular y Celular del Cáncer, CSIC-University of Salamanca, Salamanca, Spain
Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), CSIC-University of Salamanca, Salamanca, Spain
Search for other papers by Mauricio Menacho-Márquez in
Google Scholar
PubMed
Instituto de Biología Molecular y Celular del Cáncer, CSIC-University of Salamanca, Salamanca, Spain
Search for other papers by Salvatore Fabbiano in
Google Scholar
PubMed
Centro de Investigación en Medicina Molecular e Enfermidades Crónicas, University of Santiago de Compostela, Santiago de Compostela, Spain
Centro de Investigación Biomédica en Red de Cáncer sobre la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), University of Santiago de Compostela, Santiago de Compostela, Spain
Search for other papers by Omar Al-Massadi in
Google Scholar
PubMed
Instituto de Biología Molecular y Celular del Cáncer, CSIC-University of Salamanca, Salamanca, Spain
Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), CSIC-University of Salamanca, Salamanca, Spain
Search for other papers by Antonio Abad in
Google Scholar
PubMed
Instituto de Biología Molecular y Celular del Cáncer, CSIC-University of Salamanca, Salamanca, Spain
Search for other papers by Sonia Rodríguez-Fdez in
Google Scholar
PubMed
Instituto de Biología Molecular y Celular del Cáncer, CSIC-University of Salamanca, Salamanca, Spain
Search for other papers by María A Sevilla in
Google Scholar
PubMed
Instituto de Biología Molecular y Celular del Cáncer, CSIC-University of Salamanca, Salamanca, Spain
Search for other papers by María J Montero in
Google Scholar
PubMed
Centro de Investigación en Medicina Molecular e Enfermidades Crónicas, University of Santiago de Compostela, Santiago de Compostela, Spain
Centro de Investigación Biomédica en Red de Cáncer sobre la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), University of Santiago de Compostela, Santiago de Compostela, Spain
Search for other papers by Carlos Diéguez in
Google Scholar
PubMed
Centro de Investigación en Medicina Molecular e Enfermidades Crónicas, University of Santiago de Compostela, Santiago de Compostela, Spain
Centro de Investigación Biomédica en Red de Cáncer sobre la Fisiopatología de la Obesidad y Nutrición (CIBEROBN), University of Santiago de Compostela, Santiago de Compostela, Spain
Search for other papers by Rubén Nogueiras in
Google Scholar
PubMed
Instituto de Biología Molecular y Celular del Cáncer, CSIC-University of Salamanca, Salamanca, Spain
Search for other papers by Xosé R Bustelo in
Google Scholar
PubMed
Multiple crosstalk between peripheral organs and the nervous system are required to maintain physiological and metabolic homeostasis. Using Vav3-deficient mice as a model for chronic sympathoexcitation-associated disorders, we report here that afferent fibers of the hepatic branch of the vagus nerve are needed for the development of the peripheral sympathoexcitation, tachycardia, tachypnea, insulin resistance, liver steatosis and adipose tissue thermogenesis present in those mice. This neuronal pathway contributes to proper activity of the rostral ventrolateral medulla, a sympathoregulatory brainstem center hyperactive in Vav3−/− mice. Vagal afferent inputs are also required for the development of additional pathophysiological conditions associated with deregulated rostral ventrolateral medulla activity. By contrast, they are dispensable for other peripheral sympathoexcitation-associated disorders sparing metabolic alterations in liver.
Search for other papers by Daniela Fernandois in
Google Scholar
PubMed
Search for other papers by Gonzalo Cruz in
Google Scholar
PubMed
Search for other papers by Eun Kyung Na in
Google Scholar
PubMed
Search for other papers by Hernán E Lara in
Google Scholar
PubMed
Search for other papers by Alfonso H Paredes in
Google Scholar
PubMed
two months, all rats were killed by decapitation, and their tissues were collected and stored at −80°C until analysis. To dissect the effect of the sympathetic system over the ovary, we performed a second experiment, in which a physical denervation of
Search for other papers by P. B. MURIUKI in
Google Scholar
PubMed
Search for other papers by M. MUGAMBI in
Google Scholar
PubMed
Search for other papers by K. THAIRU in
Google Scholar
PubMed
Search for other papers by S. MATHAI in
Google Scholar
PubMed
Search for other papers by J. K. G. MATI in
Google Scholar
PubMed
Department of Medical Physiology, University of Nairobi, *Public Health Department, City Council of Nairobi, and †Department of Obstetrics and Gynaecology, University of Nairobi, Box 30197, Nairobi, Kenya
(Received 29 January 1974)
Circulatory changes in normal pregnancy include a fall in peripheral resistance (Bader, Bader, Rose & Braunward, 1955) and blood pressure (Hytten & Leitch, 1971) and an increase in blood volume (Hytten & Paintin, 1963). Human studies have shown that ganglion blockade during normal pregnancy causes a significant fall in blood pressure (Assali, Vergon, Tada & Garber, 1952). This effect is not observed in non-pregnant women, in pre-eclamptics or post partum (Assali et al. 1952). These observations imply that in normal pregnancy there may be a substance produced that reduces the effectiveness of the sympathetic system and the vasoconstrictors in the circulation. The same substance could account for the reduced responsiveness to angiotensin found in pregnancy by Chesley, Wynn &
Search for other papers by F. MENA in
Google Scholar
PubMed
Search for other papers by G. REYES in
Google Scholar
PubMed
Search for other papers by D. AGUAYO in
Google Scholar
PubMed
Search for other papers by C. E. GROSVENOR in
Google Scholar
PubMed
SUMMARY
Milk yield fell in a single rabbit mammary gland within 24 h after the litter had been reduced from six to eight pups to one pup. The diminished secretion lasted 2–3 days, then rebounded to the expected level over the next 1–2 days and thereafter maintained this level. During early to mid-lactation the decrease in milk secretion after reduction of the litter to one pup was prevented either by s.c. injections of prolactin or by s.c. injections of the β-adrenergic blocking drug, propranolol. These results suggest that milk secretion was reduced in the single gland as the result of sympathetic activation, triggered possibly by the turgid state which developed in the remaining glands after the litter was reduced. The results suggest also that the depression of milk secretion by the sympathetic system was due to a reduction in the effective amount of prolactin and probably of other adenohypophysial hormones reaching the mammary secretory cells rather than to an impairment of their release from the anterior pituitary.
The magnitude of the depression and rebound in milk secretion of a single rabbit mammary gland, and the effectiveness of the preventive action of either propranolol or prolactin, was considerably less during late as compared with early to mid-lactation. We postulate from these results that the mammary gland of the rabbit has a functional lability, i.e. responsiveness, which diminishes as lactation progresses and which dictates the extent to which local, neural and humoral factors may alter the milk secretory function of the mammary gland. Since suckling in the rabbit does not change from a once-a-day frequency throughout lactation, a diminishing lability may be an important factor in the decline and cessation of lactation in this species.
Search for other papers by Raul Riquelme in
Google Scholar
PubMed
Search for other papers by Freddy Ruz in
Google Scholar
PubMed
Search for other papers by Artur Mayerhofer in
Google Scholar
PubMed
Search for other papers by Hernán E Lara in
Google Scholar
PubMed
the sympathetic system. As previously described ( Dorfman et al. 2003 ), we also found that exposure to cold stress decreased the number of secondary follicles after the first month of stress exposure and as Bernuci et al. (2013) described, the
Search for other papers by Florencia Figueroa in
Google Scholar
PubMed
Search for other papers by Gisela Mendoza in
Google Scholar
PubMed
Search for other papers by Darío Cardozo in
Google Scholar
PubMed
Search for other papers by Fabián Mohamed in
Google Scholar
PubMed
Search for other papers by Liliana Oliveros in
Google Scholar
PubMed
Search for other papers by Myriam Forneris in
Google Scholar
PubMed
al . 2016 ). Although its etiology remains unknown, a potential contribution of the peripheral sympathetic system in the initiation and/or perpetuation of PCOS has been proposed ( Stener-Victorin et al . 2005 , Wojtkiewicz et al . 2014 ). In
Search for other papers by S C P Dutra in
Google Scholar
PubMed
Search for other papers by E G Moura in
Google Scholar
PubMed
Search for other papers by A L Rodrigues in
Google Scholar
PubMed
Search for other papers by P C Lisboa in
Google Scholar
PubMed
Search for other papers by I Bonomo in
Google Scholar
PubMed
Search for other papers by F P Toste in
Google Scholar
PubMed
Search for other papers by M C F Passos in
Google Scholar
PubMed
. Trayhurn P , Duncan JS & Rayner DV 1995 Acute cold-induced suppression of ob (obese) gene expression in white adipose tissue of mice: mediation by the sympathetic system. Biochemical Journal 311 729 –733. Trevenzoli IH
Search for other papers by A E Andreazzi in
Google Scholar
PubMed
Search for other papers by D X Scomparin in
Google Scholar
PubMed
Search for other papers by F P Mesquita in
Google Scholar
PubMed
Search for other papers by S L Balbo in
Google Scholar
PubMed
Search for other papers by C Gravena in
Google Scholar
PubMed
Search for other papers by J C De Oliveira in
Google Scholar
PubMed
Search for other papers by W Rinaldi in
Google Scholar
PubMed
Search for other papers by R M G Garcia in
Google Scholar
PubMed
Search for other papers by S Grassiolli in
Google Scholar
PubMed
Search for other papers by P C F Mathias in
Google Scholar
PubMed
neural endings at the pancreatic β-cells ( Lustig 2003 ). During glucose blood level oscillations, β-cells receive inputs from the parasympathetic and sympathetic systems to aid glycemia regulation. As a rule, acetylcholine released from parasympathetic
Search for other papers by Estíbaliz Castillero in
Google Scholar
PubMed
Search for other papers by María López-Menduiña in
Google Scholar
PubMed
Search for other papers by Ana Isabel Martín in
Google Scholar
PubMed
Search for other papers by María Ángeles Villanúa in
Google Scholar
PubMed
Search for other papers by Asunción López-Calderón in
Google Scholar
PubMed
sympathetic systems in adjuvant arthritis in Lewis rats . Brain Research Bulletin 39 33 – 37 doi:10.1016/0361-9230(95)02037-3 . Tashiro T Yamamori H Takagi K Hayashi N Furukawa K Nakajima N 1998 n-3 versus n-6 polyunsaturated fatty acids
Search for other papers by M Granado in
Google Scholar
PubMed
Search for other papers by A I Martín in
Google Scholar
PubMed
Search for other papers by T Priego in
Google Scholar
PubMed
Search for other papers by A López-Calderón in
Google Scholar
PubMed
Search for other papers by M A Villanúa in
Google Scholar
PubMed
, endocrine and sympathetic systems in adjuvant artritis in Lewis rats. Brain Research Bulletin 39 33 –37. Tisdale MJ 2000 Protein loss in cancer cachexia. Science 289 2293 –2294. Tracey KJ
