Elsevier

Regulatory Peptides

Volume 25, Issue 3, May–June 1989, Pages 315-324
Regulatory Peptides

Central nervous system actions of corticotropin-releasing factor on cardiovascular function in the absence of locomotor activity

https://doi.org/10.1016/0167-0115(89)90179-1Get rights and content

Abstract

Studies were performed in conscious and anesthetized Sprague-Dawley rats to examine whether the cardiovascular responses to intracerebroventricular (i.c.v.) administration of corticotropin-releasing factor (CRF) required concomitant locomotor activation. I.c.v. administration of CRF to conscious animals elicited significant increases in arterial pressure, heart rate, mesenteric resistance, and iliac blood flow, as well as intermittent locomotor, grooming and chewing activity. Intravenous infusion of the anesthetic agent, Saffan, at the minimal dose required to abolish locomotor activity caused slight but significant elevations of heart rate and mesenteric vascular resistance. I.c.v. administration of CRF to anesthetized animals produced delayed, yet significant and sustained increases in the heart rate and arterial pressure, without altering regional blood flow. These results demonstrate that locomotor activation is not requisite for the expression of CRF-induced pressor and tachycardic responses. It is concluded that CRF acts within the central nervous system to influence cardiovascular function in the absence of locomotor activity.

Cited by (26)

  • Cardiovascular functions of central corticotropin-releasing factor related peptides system

    2019, Neuropeptides
    Citation Excerpt :

    CRF 1 type receptor (CRFR1) and CRF 2 type receptor (CRFR2) mediate actions of CRF related peptides. CRF related peptide was injected into intracerebroventricular to increase blood pressure (BP) and heart rate (HR) (Briscoe et al., 2000; Brown and Fisher, 1983; Kalin et al., 1983; Nijsen et al., 2000; Overton et al., 1990a, 1990b; Overton and Fisher, 1989; Richter and Mulvany, 1995; Scoggins et al., 1984), and produce a reduction in baroreflex sensitivity (Fisher, 1988, 1989; Turnbull et al., 1993) in conscious or anesthetized animals. In addition, microinjection of CRF related peptides receptors antagonist into intracerebroventricular decreased pressor and tachycardia responses and reduction in baroreflex sensitivity induced by diverse stimulations (Dedeoglu and Fisher, 1994; Dong et al., 2001; Kregel et al., 1990; Nakamori et al., 1993; Tan et al., 2003; Wang et al., 2018; Yamada et al., 2009).

  • Chapter 2.4 The roles of urocortins 1, 2, and 3 in the brain

    2005, Techniques in the Behavioral and Neural Sciences
    Citation Excerpt :

    The increased metabolism achieved by CRF occurs through activation of diverse behavioral, thermogenic, and other autonomic pathways. Independent of its effects on behavioral activation (Overton and Fisher, 1989; Diamant et al., 1992b), i.c.v, administration of CRF elevated mean arterial pressure (Fisher and Brown, 1984; Lenz et al., 1987; Grosskreutz and Brody, 1988; Overton and Fisher, 1989; Richter and Mulvany, 1995), elevated heart rate (Fisher and Brown, 1984; Lenz et al., 1987; Grosskreutz and Brody, 1988; Overton and Fisher, 1989; Diamant and de Wied, 1991; Korte et al., 1992; Diamant et al., 1992b; Richter and Mulvany, 1995; Nijsen et al., 2000), increased plasma catecholamine levels (Fisher and Brown, 1984; Lenz et al., 1987; Overton and Fisher, 1989; Irwin et al., 1992; Nijsen et al., 2000), increased firing of sympathetic nerves to brown adipose tissue (Holt and York, 1989), increased brown adipose tissue thermogenesis (LeFeuvre et al., 1987; Arase et al., 1988, 1989a,b), increased core body temperature (Diamant and de Wied, 1991; Buwalda et al., 1997; Linthorst et al., 1997), and increased resting whole body oxygen consumption (VO2) (Rothwell et al., 1991). Consistent with these findings, i.c.v. CRF reduced body weight gain even after reductions in food intake were accounted for by pair-feeding (Rohner-Jeanrenaud et al., 1989; Hotta et al., 1991; Cullen et al., 2001).

  • Central corticotropin releasing factor (CRF) and adrenergic receptors mediate hemodynamic responses to cocaine

    2001, Brain Research
    Citation Excerpt :

    By definition, vascular responders are dependent on greater increases in systemic vascular resistance to cocaine compared to mixed responders. Central administration of CRF elevates mesenteric and renal arterial resistance in conscious animals [16,33]. Cocaine also elicits an increase in mesenteric and renal vascular resistance in conscious rats ( [5], Knuepfer and Wehner, unpublished data).

View all citing articles on Scopus
View full text