Ca2+ entry blockers inhibit prostaglandin F2+-induced cerebrovascular contractile responses In goats

Salom, Juan B.; Torregrosa, Germán; Miranda, Francisco Javier Noya; Alabadí, JoséA.; Álvarez, Cristina; Alborch, Enrique

doi:10.1016/0014-2999(91)90787-q

Cited by 12 publications

(8 citation statements)

References 42 publications

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“…The research on the biological effects of latanoprost is continuing. In the many studies, the effects on vessels range from constriction to dilation depending on the selected subjects, drug dosage and vessel size [3, 4, 5, 6]. The research regarding the effects of latanoprost on the microvasculature of the eye has been mostly done in cynomolgus monkeys [7, 8, 9, 10, 11].…”

Section: Introductionmentioning

confidence: 99%

Effects of 0.005% Latanoprost on Optic Nerve Head and Peripapillary Retinal Blood Flow

Seong

Lee

Hong³

1999

Ophthalmologica

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Fifty-two eyes of 26 healthy volunteers were recruited for evaluating the effects of 0.005% latanoprost on optic nerve head (ONH) and peripapillary retinal blood flow. In a randomized double-blind design, one eye received one drop of 0.005% latanoprost and its fellow eye received one drop of a placebo eyedrop. Intraocular pressure (IOP), ONH and peripapillary retinal blood flow were measured with Heidelberg retinal flowmetry (HRF) before, 2 and 24 h after administration of eyedrops. IOP was decreased significantly in latanoprost-treated eyes at 2 and 24 h after administration (p < 0.05). In the volume, flow or velocity of ONH and peripapillary retina, there were no significant changes from the baseline values at 2 and 24 h after latanoprost administration in either latanoprost-treated eyes or their fellow eyes (p > 0.05). No significant differences were found in the measured quantities between latanoprost-treated eyes and their fellow eyes at each time point (p > 0.05). This result may suggest that 0.005% latanoprost in healthy subjects does not have any adverse effect on ONH and peripapillary retinal blood flow.

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Section: Introductionmentioning

confidence: 99%

Effects of 0.005% Latanoprost on Optic Nerve Head and Peripapillary Retinal Blood Flow

Seong

Lee

Hong³

1999

Ophthalmologica

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“…The vasorelaxing activity of nicardipine was more pronounced in cerebral arteries pre-constricted with K + than with PGF 2α , thromboxane A 2 , or hemolisate (11). In isolated preparations of human cerebral arteries, preconstricted with 5-HT or PGF 2α , the vasorelaxing effect of nicardipine concentrations between 0.1 and 10 μM was more pronounced than that of the dihydropyridine-type calcium antagonist nimodipine, and remarkably more potent than that of magnesium sulphate (22). These results collectively indicate that nicardipine is a powerful vasodilator primarily of cerebral arteries and probably represents one of the most effective inhibitors of vasoconstriction elicited by a variety of agents including K + , 5-HT, PGF 2α , thromboxane A 2 , or hemolisate.…”

Section: Effect On Preparations Of Cerebral Arteriesmentioning

confidence: 87%

“…In this species, the compound exerted transient decrease of mean arterial blood pressure accompanied by increased local CBF without changes in pH, Pco 2 , or Po 2 values (26). Moreover, in goats, nicardipine countered the decrease of maxillary artery blood flow caused by injection of PGF 2α (22). The administration of nicardipine in monkeys caused cerebral vasodilatation associated with an increase of internal carotid blood flow, fall of arterial pressure, and increase in heart rate (3).…”

Section: F Amenta Et Almentioning

confidence: 97%

“…Vasodilatation was determined in helical strips or rings of cerebral arteries by microelectrode or isometric tension recording methods. Vasoconstriction was generated by adding to the incubation medium K + , prostaglandin PGF 2α , tromboxane, or hemolisate (11,12,(17)(18)(19)(20)(21)(22)(23). In these investigations, nicardipine was shown to inhibit primarily extracellular calcium influx through the external cellular membrane.…”

Section: Effect On Preparations Of Cerebral Arteriesmentioning

confidence: 99%

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Nicardipine: A Hypotensive Dihydropyridine-Type Calcium Antagonist with a Peculiar Cerebrovascular Profile

Amenta

Tomassoni

Traini

et al. 2008

Clinical and Experimental Hypertension

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Control of blood pressure protects against the development of cerebrovascular lesions, stroke, and vascular dementia (VaD). Cerebrovascular disease is increasingly recognized as a cause of cognitive impairment and dementia primarily in the elderly. Nicardipine is a dihydropyridine-type calcium channel blocker (CCB) with a peculiar cerebrovascular profile developed approximately 30 years ago. This study has reviewed the main controlled clinical studies investigating the use of nicardipine in pathologies associated with cerebrovascular injury, such as subarachnoid haemorrhage (SAH), acute stroke, and VaD. SAH is a main cerebrovascular indication of CCBs. In this indication, CCBs prevent vasospasm and improve clinical outcomes. Nimodipine represents the CCB more investigated in this indication. Former studies did not demonstrate a clear advantage of nicardipine versus nimodipine in SAH. A more recent approach using implants of nicardipine prolonged-release showed a decreased incidence of vasospasm, delayed ischemic deficits, and improved clinical outcome after severe SAH. Controlled trials have shown the effectiveness of the drug in preventing stroke. Increasing evidence suggests some benefit of some CCBs in VaD or mixed degenerative and vascular dementia. In this setting, nicardipine has been investigated in approximately 6,000 patients, with an improvement of cognitive deterioration in more than 60% of patients treated. The pronounced anti-hypertensive activity of nicardipine and its safety and effectiveness in cognitive domain suggest its reconsideration in the treatment of cognitive impairment of vascular origin as well as for reducing the risk of recurrent stroke in patients at high risk of it.

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“…Vasodilatation was determined in helical strips or rings of cerebral arteries by microelectrode or isometric tension recording methods. Vasoconstriction was generated by adding to the incubation medium K+, prostaglandin PGFzal thromboxane or hemolisate (20)(21)(22)(23)(24)(25)(26)(27)(28). These investigations have shown that nicardipine inhibits primarily extracellular Ca2+ influx through the external cellular membrane.…”

Section: A) In Vifro Studies Of Arterial Confracfilitymentioning

confidence: 99%

Nicardipine and Treatment of Cerebrovascular Diseases with Particular Reference to Hypertension-Related Disorders

Sabbatini¹,

Strocchi²,

Amenta³

1995

Clinical and Experimental Hypertension

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Nicardipine is a second generation dihydropyridine-type Ca2+ antagonist with high vascular selectivity and strong cerebral and coronary vasodilatory activity. The compound is used in the treatment of hypertension, primarily in the elderly. In this review the main evidence of the cerebrovascular activity of nicardipine in preclinical studies using in vitro and in vivo models is detailed. A particular physico-chemical property of nicardipine is the almost complete protonation in acid environment. This allows its accumulation in ischemic brain regions and makes it a candidate for the treatment of cerebrovascular disorders characterised by impaired brain perfusion. The main clinical data on the use of nicardipine in cerebral ischemia and related disorders, subarachnoid haemorrhage and stroke, are also reviewed. These studies included 5940 patients affected by chronic cerebrovascular insufficiency (cerebral ischemia, cerebral atherosclerosis mainly associated with hypertension, transient ischemic attacks, sequelae of cerebral infarction, thrombosis or embolia, hypertensive encephalopathy), 1540 patients affected by sequelae of subarachnoid haemorrhage and 206 patients affected by stroke. Both preclinical studies and clinical trials have shown that nicardipine is a safe Ca2+ antagonist with powerful cerebrovascular activity. This suggests its possible use in cerebrovascular disorders in which blockade of Ca2+ channels of the L-type and/or selective cerebral vasodilatation is desirable. Further studies are necessary to establish if modulation of neuronal Ca2+ channels of the L-type by nicardipine may have a neuroprotective effect independent by the cerebrovascular activity of the compound.

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Ca2+ entry blockers inhibit prostaglandin F2+-induced cerebrovascular contractile responses In goats

Cited by 12 publications

References 42 publications

Effects of 0.005% Latanoprost on Optic Nerve Head and Peripapillary Retinal Blood Flow

Effects of 0.005% Latanoprost on Optic Nerve Head and Peripapillary Retinal Blood Flow

Nicardipine: A Hypotensive Dihydropyridine-Type Calcium Antagonist with a Peculiar Cerebrovascular Profile

Nicardipine and Treatment of Cerebrovascular Diseases with Particular Reference to Hypertension-Related Disorders

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