cDNA cloning and analysis of tissue-specific gene expression of rat urocortin II

Chae, Jong‐Chan; Ju, Sung Kyu; Lee, M. K.; Park, J. H.; Yoon, Jae-Seung; Shim, Jooyong; Lee, D. S.

doi:10.1134/s0026893309010117

Cited by 3 publications

(1 citation statement)

References 20 publications

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“…24 Intriguingly, hematocrit dropped after Ucn2 treatment, despite an active diuresis and associated negative fluid balance in these animals, conceivably pointing to an acute shift of fluid from the extravascular to vascular compartments. It is also possible that the peptide has an effect on red blood cell production, given the report of Ucn2 gene expression in bone marrow, 37 although this is unlikely to have produced the precipitous hematocrit declines (and posttreatment increases) observed in this study because bone marrow effects are usually seen over days/weeks and months. The Ucn2-induced reduction in hematocrit was mitigated by contemporaneous furosemide administration, presumably reflecting the markedly greater negative fluid balance status demonstrated in this group.…”

Section: Discussionmentioning

confidence: 82%

Urocortin 2 Inhibits Furosemide-Induced Activation of Renin and Enhances Renal Function and Diuretic Responsiveness in Experimental Heart Failure

Rademaker

Charles

Nicholls

et al. 2009

Circ: Heart Failure

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Background— Urocortin 2 (Ucn2), a novel peptide with therapeutic potential in heart failure, and diuretics have opposing effects on renal function and the renin-angiotensin-aldosterone system. Because any prospective new treatment is likely to be used in conjunction with standard diuretic therapy, it is necessary to investigate the combined effects of these agents. Methods and Results— Ucn2 and furosemide were administered for 3 hours, both singly and combined, in 7 sheep with pacing-induced heart failure. Compared with time-matched controls, separate Ucn2 and furosemide administration significantly increased urine output (furosemide>Ucn2), urine sodium (furosemide>Ucn2), potassium (furosemide>Ucn2), and creatinine excretion (Ucn2>furosemide) and creatinine clearance (Ucn2>furosemide). Compared with furosemide treatment alone, Ucn2+furosemide produced a further diuresis ( P <0.05), natriuresis ( P <0.05), and a sustained increase in creatinine excretion ( P <0.05) and clearance ( P <0.05), without additional potassium elimination. All active treatments reduced mean arterial pressure (Ucn2+furosemide=furosemide>Ucn2), left atrial pressure (Ucn2+furosemide>Ucn2>furosemide), and peripheral resistance (Ucn2+furosemide=Ucn2>furosemide), whereas only Ucn2, singly and in combination with furosemide, increased cardiac output and dP/dt(max). In contrast to the increase in plasma renin activity elicited by furosemide alone, Ucn2 and Ucn2+furosemide markedly reduced plasma renin activity. All active treatments decreased plasma aldosterone (Ucn2+furosemide=Ucn2>furosemide), whereas only Ucn2 and Ucn2+furosemide reduced vasopressin and natriuretic peptide concentrations. Conclusion— Ucn2 cotreatment with furosemide enhanced hemodynamic and renal function and diuretic responsiveness (without additional potassium depletion) in experimental heart failure. Furthermore, Ucn2 reversed furosemide-induced increases in plasma renin activity and induced greater decreases in plasma aldosterone and vasopressin. These data indicate that adjunct Ucn2 therapy with diuretics in heart failure is beneficial.

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Section: Discussionmentioning

confidence: 82%

Urocortin 2 Inhibits Furosemide-Induced Activation of Renin and Enhances Renal Function and Diuretic Responsiveness in Experimental Heart Failure

Rademaker

Charles

Nicholls

et al. 2009

Circ: Heart Failure

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Ventromedial prefrontal cortex CRF1 receptors modulate the tachycardic activity of baroreflex

Brufatto

Lagatta

Uliana

et al. 2021

Pflugers Arch - Eur J Physiol

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Key Role of CRF in the Skin Stress Response System

et al. 2013

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The discovery of corticotropin-releasing factor (CRF) or CRH defining the upper regulatory arm of the hypothalamic-pituitary-adrenal (HPA) axis, along with the identification of the corresponding receptors (CRFRs 1 and 2), represents a milestone in our understanding of central mechanisms regulating body and local homeostasis. We focused on the CRF-led signaling systems in the skin and offer a model for regulation of peripheral homeostasis based on the interaction of CRF and the structurally related urocortins with corresponding receptors and the resulting direct or indirect phenotypic effects that include regulation of epidermal barrier function, skin immune, pigmentary, adnexal, and dermal functions necessary to maintain local and systemic homeostasis. The regulatory modes of action include the classical CRF-led cutaneous equivalent of the central HPA axis, the expression and function of CRF and related peptides, and the stimulation of pro-opiomelanocortin peptides or cytokines. The key regulatory role is assigned to the CRFR-1α receptor, with other isoforms having modulatory effects. CRF can be released from sensory nerves and immune cells in response to emotional and environmental stressors. The expression sequence of peptides includes urocortin/CRF→pro-opiomelanocortin→ACTH, MSH, and β-endorphin. Expression of these peptides and of CRFR-1α is environmentally regulated, and their dysfunction can lead to skin and systemic diseases. Environmentally stressed skin can activate both the central and local HPA axis through either sensory nerves or humoral factors to turn on homeostatic responses counteracting cutaneous and systemic environmental damage. CRF and CRFR-1 may constitute novel targets through the use of specific agonists or antagonists, especially for therapy of skin diseases that worsen with stress, such as atopic dermatitis and psoriasis.

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cDNA cloning and analysis of tissue-specific gene expression of rat urocortin II

Cited by 3 publications

References 20 publications

Urocortin 2 Inhibits Furosemide-Induced Activation of Renin and Enhances Renal Function and Diuretic Responsiveness in Experimental Heart Failure

Urocortin 2 Inhibits Furosemide-Induced Activation of Renin and Enhances Renal Function and Diuretic Responsiveness in Experimental Heart Failure

Ventromedial prefrontal cortex CRF1 receptors modulate the tachycardic activity of baroreflex

Key Role of CRF in the Skin Stress Response System

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