Enhanced reactivity to vasopressin in rat basilar arteries during vasospasm after subarachnoid hemorrhage

Nishihashi, Tsuyoshi; Trandafir, Cristina C.; Wang, Aiming; Ji, Xu; Kurahashi, Kazuyoshi

doi:10.1016/j.ejphar.2005.01.051

Cited by 18 publications

(11 citation statements)

References 32 publications

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“…V 1a antagonists may also be effective for the treatment of vasospasm in subarachnoid hemorrhage. In a rat model of subarachnoid hemorrhage, both plasma AVP concentration and sensitivity to AVP were increased (36,44). This effect was accompanied by basilar artery vasospasm, which was attenuated by a V 1a vasopressin receptor antagonist.…”

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confidence: 90%

Vasopressin-induced vasoconstriction: two concentration-dependent signaling pathways

Henderson

Byron²

2007

Journal of Applied Physiology

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Current scientific literature generally attributes the vasoconstrictor effects of [Arg(8)]vasopressin (AVP) to the activation of phospholipase C (PLC) and consequent release of Ca(2+) from the sarcoplasmic reticulum. However, half-maximal activation of PLC requires nanomolar concentrations of AVP, whereas vasoconstriction occurs when circulating concentrations of AVP are orders of magnitude lower. Using cultured vascular smooth muscle cells, we previously identified a novel Ca(2+) signaling pathway activated by 10-100 pM AVP. This pathway is distinguished from the PLC pathway by its dependence on protein kinase C (PKC) and L-type voltage-sensitive Ca(2+) channels (VSCC). In the present study, we used isolated, pressurized rat mesenteric arteries to examine the contributions of these different Ca(2+) signaling mechanisms to AVP-induced vasoconstriction. AVP (10(-14)-10(-6) M) induced a concentration-dependent constriction of arteries that was reversible with a V(1a) vasopressin receptor antagonist. Half-maximal vasoconstriction at 30 pM AVP was prevented by blockade of VSCC with verapamil (10 microM) or by PKC inhibition with calphostin-C (250 nM) or Ro-31-8220 (1 microM). In contrast, acute vasoconstriction induced by 10 nM AVP (maximal) was insensitive to blockade of VSCC or PKC inhibition. However, after 30 min, the remaining vasoconstriction induced by 10 nM AVP was partially dependent on PKC activation and almost fully dependent on VSCC. These results suggest that different Ca(2+) signaling mechanisms contribute to AVP-induced vasoconstriction over different ranges of AVP concentration. Vasoconstrictor actions of AVP, at concentrations of AVP found within the systemic circulation, utilize a Ca(2+) signaling pathway that is dependent on PKC activation and can be inhibited by Ca(2+) channel blockers.

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confidence: 90%

Vasopressin-induced vasoconstriction: two concentration-dependent signaling pathways

Henderson

Byron²

2007

Journal of Applied Physiology

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“…These results suggest that pathological cerebral vasospasms observed in SAH rats are due, at least in part, to the promoted 5-lipoxygenase activities stimulated by endogenous AVP. Therefore, SR49059 may represent a potential therapeutic agent in the treatment of cerebral vasospasms (373,507). It should be noted that a part of the intracranial artery causes vasodilatation upon AVP stimulation in an endothelium-dependent manner (264,386 Cerebral edema is a devastating consequence of brain injury that leads to compromised cerebral blood flow and worsening parenchymal damage.…”

Section: Cerebral Vasospasm and Brain Edemamentioning

confidence: 99%

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Koshimizu

Nakamura

Egashira

et al. 2012

Physiological Reviews

334

297

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The neurohypophysial hormone arginine vasopressin (AVP) is essential for a wide range of physiological functions, including water reabsorption, cardiovascular homeostasis, hormone secretion, and social behavior. These and other actions of AVP are mediated by at least three distinct receptor subtypes: V1a, V1b, and V2. Although the antidiuretic action of AVP and V2 receptor in renal distal tubules and collecting ducts is relatively well understood, recent years have seen an increasing understanding of the physiological roles of V1a and V1b receptors. The V1a receptor is originally found in the vascular smooth muscle and the V1b receptor in the anterior pituitary. Deletion of V1a or V1b receptor genes in mice revealed that the contributions of these receptors extend far beyond cardiovascular or hormone-secreting functions. Together with extensively developed pharmacological tools, genetically altered rodent models have advanced the understanding of a variety of AVP systems. Our report reviews the findings in this important field by covering a wide range of research, from the molecular physiology of V1a and V1b receptors to studies on whole animals, including gene knockout/knockdown studies.

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“…In our previous study, we reported hypersensitivity to vasopressin in rat basilar arteries in the vasospasm phase after subarachnoid hemorrhage (SAH) and vasopressin-induced contraction at lower concentration was endothelium-dependent (1). Reactive oxygen species have been reported to be a possible endothelium-derived contracting factor (2,3).…”

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confidence: 99%

“…The contraction induced by 80 mM KCl was used as a measure of tissue contractile effect. There were no significant differences (unpaired Student's t-test) in the response to 80 mM KCl between arteries from control and SAH rats (control, 51 ± 2 mg, n = 55; SAH, 51 ± 3 mg, n = 41), as described in our previous study (1). As for comparisons, one-way analysis of variance (ANOVA), followed by the unpaired Student's t-test was used (JMP; SAS Institute, Cary, NC, USA).…”

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Hypersensitivity to Hydroxyl Radicals in Rat Basilar Artery After Subarachnoid Hemorrhage

et al. 2006

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Abstract. Vasospasm after subarachnoid hemorrhage (SAH) is a serious complication and we have been investigating the relationship between vasoconstrictors and vasospasm after SAH. The present study was designed to investigate the vasocontractile responses to reactive oxygen species in isolated rat basilar arteries from the control and experimental SAH rats. Contractile responses to hydroxyl radicals in basilar arteries from SAH rats were 3 -6-fold higher than those in control rats. The present results clearly indicate that hypersensitivity to hydroxyl radicals may contribute to the vasospasm after SAH.Keywords: subarachnoid hemorrhage, hydroxyl radical, rat basilar arteryIn our previous study, we reported hypersensitivity to vasopressin in rat basilar arteries in the vasospasm phase after subarachnoid hemorrhage (SAH) and vasopressin-induced contraction at lower concentration was endothelium-dependent (1). Reactive oxygen species have been reported to be a possible endothelium-derived contracting factor (2, 3). Reactive oxygen species have also been reported to be a possible spasmogen (4, 5). Especially, hydroxyl radicals, one of the most aggressive species, have been reported to play an important role in the development of the vasospasm and various kinds of hydroxyl radical scavengers have been tried to treat the vasospasm (6 -9). Of all the reports on the relationship between vasospasm and reactive oxygen species, there has been no report about the contractile effect of reactive oxygen species after SAH. In the present study, we examined the contractile effect of reactive oxygen species in rat basilar arteries, using both control and SAH rats.Male Sprague-Dawley rats, weighing 250 -350 g, were supplied by Shimizu Laboratory Supplies Co., Ltd. (Kyoto). The animals were housed in steel cages at 22°C -24°C with a 12-h light / dark cycle and humidity of approximately 60%, and allowed free access to food and water. Animal care and the general protocol for animal use conformed to the Kyoto University rules for the care and use of laboratory animals.After the administration of atropine sulfate (50 µg/ kg, i.p.), the rats were anesthetized with pentobarbital sodium (40 mg / kg, i.p.). As soon as autologous blood (0.3 ml) was withdrawn from a femoral artery, the rat was held in a vertical position at 20°. After a 26-gauge needle was carefully inserted into the cisterna magna, the blood was injected in a 3-min time frame. In the present study, we used experimental SAH rats 1 day after the hemorrhage-induction, because the vasospasm was observed 1 -2 days after hemorrhage-induction, as described in our previous study (1).Rats were anesthetized with pentobarbital sodium (40 mg/ kg, i.p.) and sacrificed by bleeding the abdominal aorta. The brain was rapidly removed and put into Krebs-Henseleit solution. The solution consisted of 120 mM NaCl, 4.7 mM KCl, 1.2 mM MgSO 4 ⋅ 7H 2 O, 1.2 mM KH 2 PO 4 , 2.5 mM CaCl 2 ⋅ 2H 2 O, 25 mM NaHCO 3 , and 10 mM glucose; the pH of the solution was 7.4. The basilar artery was dissected free ...

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Enhanced reactivity to vasopressin in rat basilar arteries during vasospasm after subarachnoid hemorrhage

Cited by 18 publications

References 32 publications

Vasopressin-induced vasoconstriction: two concentration-dependent signaling pathways

Vasopressin-induced vasoconstriction: two concentration-dependent signaling pathways

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Hypersensitivity to Hydroxyl Radicals in Rat Basilar Artery After Subarachnoid Hemorrhage

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