Effects of human urotensin II in isolated vessels of various species; comparison with other vasoactive agents

Camarda, Valeria; Rizzi, Anna; Calò, Girolamo; Gendron, Gabrielle; Perron, Stéphan; Kostenis, Evi; Zamboni, Paolo; Mascoli, Francesco; Regoli, Doménico

doi:10.1007/s00210-001-0503-0

Cited by 100 publications

(74 citation statements)

References 28 publications

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“…A possible explanation for this result could be the desensitization of UII responses, as suggested by our whole-cell recordings. This is supported by studies showing that UII receptors located in the aorta of rats desensitize after a double treatment at intervals of 5 h, with different doses of human UII (Camarda et al, 2002). Moreover, UII receptors heterologously expressed in cell lines desensitize after repeated UII treatment (H.-P. Nothacker, personal communication).…”

Section: Discussionmentioning

confidence: 77%

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Huitrón‐Reséndiz

Kristensen²,

Sanchez‐Alavez³

et al. 2005

Journal of Neuroscience

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Urotensin II (UII) is a cyclic neuropeptide with strong vasoconstrictive activity in the peripheral vasculature. UII receptor mRNA is also expressed in the CNS, in particular in cholinergic neurons located in the mesopontine tegmental area, including the pedunculopontine tegmental (PPT) and lateral dorsal tegmental nuclei. This distribution suggests that the UII system is involved in functions regulated by acetylcholine, such as the sleep-wake cycle. Here, we tested the hypothesis that UII influences cholinergic PPT neuron activity and alters rapid eye movement (REM) sleep patterns in rats. Local administration of UII into the PPT nucleus increases REM sleep without inducing changes in the cortical blood flow. Intracerebroventricular injection of UII enhances both REM sleep and wakefulness and reduces slow-wave sleep 2. Intracerebroventricular, but not local, administration of UII increases cortical blood flow. Moreover, whole-cell recordings from rat-brain slices show that UII selectively excites cholinergic PPT neurons via an inward current and membrane depolarization that were accompanied by membrane conductance decreases. This effect does not depend on action potential generation or fast synaptic transmission because it persisted in the presence of TTX and antagonists of ionotropic glutamate, GABA, and glycine receptors. Collectively, these results suggest that UII plays a role in the regulation of REM sleep independently of its cerebrovascular actions by directly activating cholinergic brainstem neurons.

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Section: Discussionmentioning

confidence: 77%

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Huitrón‐Reséndiz

Kristensen²,

Sanchez‐Alavez³

et al. 2005

Journal of Neuroscience

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“…In this regard, the U-II effects showed a marked desensitization in rat vasculature (Camarda et al 2002). However, in spinal cord neurons, 10-15 min washing is enough to restore most of the U-II-induced [Ca 2+ ] i increase.…”

Section: Discussionmentioning

confidence: 90%

Urotensin‐II regulates intracellular calcium in dissociated rat spinal cord neurons

Filipeanu

Brǎiloiu

Dun

et al. 2002

Journal of Neurochemistry

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Urotensin-II (U-II), a peptide with multiple vascular effects, is detected in cholinergic neurons of the rat brainstem and spinal cord. Here, the effects of U-II on [Ca 2+ ] i was examined in dissociated rat spinal cord neurons by fura 2 microfluorimetry. The neurons investigated were choline acetyltransferasepositive and had morphological features of motoneurons. U-II induced [Ca 2+ ] i increases in these neurons with a threshold of 10 )9 M, and a maximal effect at 10 )6 M with an estimated EC 50 of 6.2 · 10 )9 M. The [Ca 2+ ] i increase induced by U-II was mainly caused by Ca 2+ influx from extracellular space, as the response was markedly attenuated in a Ca 2+ -free medium. Omega-conotoxin GVIA (10 )7 M), a N-type Ca 2+ channel blocker, largely inhibited these increases, whereas the P/Q Ca 2+ channel blocker, omega-conotoxin GVIIC (10 )7 M) and the L-type Ca 2+ channel blocker, verapamil (10 )5 M) had minimal effects. Down-regulation of protein kinase C by 4-aphorbol 12-myristate 13-acetate (10 )6 M) or enzyme inhibition using the specific inhibitor bisindolylmaleimide I (10 )6 M) did not inhibit the observed effects. Similarly, inhibition of protein kinase G with KT5823 (10 )6 M) or Rp-8-pCPT-cGMPS (3 · 10 )5 M) did not modify U-II-induced [Ca 2+ ] i increases. In contrast, protein kinase A inhibitors KT5720 (10 )6 M) and Rp-cAMPS (3 · 10 )5 M) reduced the response to 25 ± 3% and 42 ± 8%, respectively. Present results demonstrate that U-II modulates [Ca 2+ ] i in rat spinal cord neurons via protein kinase A cascade.

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“…The most studied aspect of UII is its vascular activity (Camarda et al, 2002b;Kompa et al, 2004;Barrette and Schwertani, 2012;Zemanciková and Török, 2013). Although previously thought to be endothelin-1, UII has been demonstrated to be the most potent physiologic vasoconstrictor peptide (Ames et al, 1999).…”

Section: B Effect Of Urotensin Ii/urotensin Ii-related Peptide On Thmentioning

confidence: 99%

International Union of Basic and Clinical Pharmacology. XCII. Urotensin II, Urotensin II–Related Peptide, and Their Receptor: From Structure to Function

et al. 2014

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Effects of human urotensin II in isolated vessels of various species; comparison with other vasoactive agents

Cited by 100 publications

References 28 publications

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Urotensin‐II regulates intracellular calcium in dissociated rat spinal cord neurons

International Union of Basic and Clinical Pharmacology. XCII. Urotensin II, Urotensin II–Related Peptide, and Their Receptor: From Structure to Function

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