Role of Nitric Oxide in the Cerebral Vasodilatory Responses to Vasopressin and Oxytocin in Dogs

Oyama, Hirofumi; Suzuki, Yoshio; Satoh, Shin’ichi; Kajita, Yasukazu; Takayasu, Misako; Shibuya, Masabumi; Sugita, Kenichiro

doi:10.1038/jcbfm.1993.35

Cited by 77 publications

(36 citation statements)

References 28 publications

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“…73 Less vasoconstriction in coronary and cerebral circulations may be due to the additional NO-mediated vasodilating effect of vasopressin on these circulations. 74,75 The effects of vasopressin on the heart (reduced cardiac output and heart rate) are mainly due to increased vagal tone and decreased sympathetic tone as well as a decrease in coronary blood flow at high circulating levels of vasopressin. 10 Of relevance to septic shock, vasopressin enhances the sensitivity of the vasculature to other pressor agents.…”

Section: Vasoconstrictor Effectsmentioning

confidence: 99%

Physiology of Vasopressin Relevant to Management of Septic Shock

Holmes

Patel

Russell

et al. 2001

Chest

538

395

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Section: Vasoconstrictor Effectsmentioning

confidence: 99%

Physiology of Vasopressin Relevant to Management of Septic Shock

Holmes

Patel

Russell

et al. 2001

Chest

538

395

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“…In the majority of blood vessels, application of CGRP has been reported to cause dilation through an endothelium-independent process. These vessels include cat cerebral (16,48), rat mesenteric (1,20,25,35), rat stomach mucosal (27), rabbit jejunal (34), dog basilar (40), dog lingual (33), and human uterine arteries (5). A primary signal transduction pathway involved in this form of CGRP activation is adenylate cyclase, which increases cAMP and cAMP-dependent protein kinase (PKA)-activating K ϩ channels including ATP-sensitive K ϩ (K ATP ϩ ) channels (37,38,41).…”

mentioning

confidence: 99%

Calcitonin gene-related peptide activates different signaling pathways in mesenteric lymphatics of guinea pigs

Hosaka¹,

Rayner²,

Weid³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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The effects of calcitonin generelated peptide (CGRP) on constriction frequency, smooth muscle membrane potential (V m), and endothelial Vm of guinea pig mesenteric lymphatics were examined in vitro. CGRP (1-100 nM) caused an endothelium-dependent decrease in the constriction frequency of perfused lymphatic vessels. The endothelium-dependent CGRP response was abolished by the CGRP-1 receptor antagonist CGRP-(8 -37) (1 M) and pertussis toxin (100 ng/ml). This action of CGRP was also blocked by the nitric oxide (NO) synthase inhibitor N G -nitro-Larginine (L-NNA; 10 M), an action that was reversed by the addition of L-arginine (100 M). cGMP, adenylate cyclase, cAMP-dependent protein kinase (PKA), and ATP-sensitive K ϩ (K ATP ϩ ) channels were all implicated in the endothelium-dependent CGRP response because it was abolished by methylene blue (20-5-isoquinolinesulfonamide-dichloride (H89; 1 M) and glibenclamide (10 M). CGRP (100 nM), unlike acetylcholine, did not alter endothelial intracellular Ca 2ϩ concentration or V m. CGRP (100 nM) hyperpolarized the smooth muscle Vm, an effect inhibited by L-NNA, H89, or glibenclamide. CGRP (500 nM) also caused a decrease in constriction frequency. However, this was no longer blocked by CGRP-(8 -37). CGRP (500 nM) also caused smooth muscle hyperpolarization, an action that was now not blocked by L-NNA (100 M). It was most likely mediated by the activation of the cAMP/PKA pathway and the opening of K ATP ϩ channels because it was abolished by H89 or glibenclamide. We conclude that CGRP, at low to moderate concentrations (i.e., 1-100 nM), decreases lymphatic constriction frequency primarily by the stimulation of CGRP-1 receptors coupled to pertussis toxin-sensitive G proteins and the release of NO from the endothelium or enhancement of the actions of endogenous NO. At high concentrations (i.e., 500 nM), CGRP also directly activates the smooth muscle independent of NO. Both mechanisms of activation ultimately cause the PKA-mediated opening of K ATP ϩ channels and resultant hyperpolarization. smooth muscle; endothelium; nitric oxide; adenosine 3Ј,5Ј-cyclic monophosphate-dependent protein kinase; vasomotion CALCITONIN GENE-RELATED PEPTIDE (CGRP), like substance P, is a dominant neurotransmitter in vascular sensory nerves and is a potent vasodilator, which may play a role in modulation of total peripheral resistance of the systemic circulation (6,22,30). The pathways by which CGRP produces vasodilation vary between vascular beds. In the majority of blood vessels, application of CGRP has been reported to cause dilation through an endothelium-independent process. These vessels include cat cerebral (16, 48), rat mesenteric (1, 20, 25, 35), rat stomach mucosal (27), rabbit jejunal (34), dog basilar (40), dog lingual (33), and human uterine arteries (5). A primary signal transduction pathway involved in this form of CGRP activation is adenylate cyclase, which increases cAMP and cAMP-dependent protein kinase (PKA)-activating K ϩ channels including ATP-sensitive K ϩ (K ATP ϩ ) channels (37,...

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“…Third, we determined whether nitric oxide (NO) plays a role in mediating oxyto cin-induced arteriolar dilation. Recent evidence indicates that dilator prostaglandin effects are mediated via a NO mechanism in newborn pigs [23], and other investigators have shown that inhibition of nitric oxide synthase (NOS) eliminates cerebral hyperemia to oxytocin [12], Fourth, we determined the role of ATP-sensitive potassium chan nels (K atp) in mediating cerebral arteriolar dilation to oxytocin. We have shown that KATp-mediated cerebral arteriolar dilation is virtually eliminated following isch emia [3].…”

Section: Introductionmentioning

confidence: 99%

Influence of Hypoxia/lschemia on Cerebrovascular Responses to Oxytocin in Piglets

Bari

Errico²,

Louis

et al. 1997

J Vasc Res

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We examined the effects of hypoxic/ischemic stress on cerebral arteriolar responses to oxytocin in anesthetized piglets. Pial arteriolar diameters were measured using a cranial window and intravital microscopy. First, we evaluated arteriolar responses to topical application of oxytocin during normoxic conditions. We then determined whether 5–10 min of arterial hypoxia, ischemia, or asphyxia alters oxytocin-induced responses. Arterial hypoxia was produced by inhalation of 7.5% O₂-92.5% N₂ for 10 min. Ischemia was achieved by increasing intracranial pressure for 10 min. Asphyxia was achieved by turning off the ventilator for 5 min. During normoxic conditions, oxytocin dilated pial arterioles by 9 ± 1% at 10^-8 and by 16 ± 1% at 10^–6 mol/l (n = 47, p < 0.05). Arteriolar responses to oxytocin did not change with repeated applications (n = 10). Following hypoxia, dilator effect of oxytocin was not changed at 10^–8 (8 ± 2%) but it was reduced at 10^–6 mol/l (7 ± 2%; p < 0.05, n = 8). After asphyxia or ischemia, oxytocin did not dilate arterioles at 10^–8 mol/l, whereas 10^-6 mol/l resulted in a mild vasoconstriction (-4 ± 3 to -6 ± 4%, n = 6 and 8). Topically applied superoxide dismutase did not preserve arteriolar responses to oxytocin after asphyxia although the arterioles did not constrict to 10^–6 mol/l oxytocin (n = 5). Dilatation of cerebral arterioles in response to oxytocin was reversed to constriction by N^ω-nitro-L-arginine methyl ester (L-NAME) (15 mg/kg, i.v.; n = 5) and by endothelial impairment by intra-arterial infusion of phorbol ester (10^–5 mol/l; n = 5). We conclude that the absence of pial arteriolar dilation to oxytocin after ischemia and asphyxia indicates endothelial dysfunction which may be involved in the pathology of perinatal brain injury.

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Role of Nitric Oxide in the Cerebral Vasodilatory Responses to Vasopressin and Oxytocin in Dogs

Cited by 77 publications

References 28 publications

Physiology of Vasopressin Relevant to Management of Septic Shock

Physiology of Vasopressin Relevant to Management of Septic Shock

Calcitonin gene-related peptide activates different signaling pathways in mesenteric lymphatics of guinea pigs

Influence of Hypoxia/lschemia on Cerebrovascular Responses to Oxytocin in Piglets

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