Human and rat α-CGRP but not calcitonin cause mesenteric vasodilatation in rats

Marshall, Ian; Al-Kazwini, Susan J.; Holman, Jennifer J.; Craig, Roger K.

doi:10.1016/0014-2999(86)90662-x

Cited by 110 publications

(27 citation statements)

References 17 publications

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“…This is in accord with studies on isolated mesenteric vascular prepara tions from rat and rabbit in which human and salmon calcitonin evoked only very weak dilator responses (Marshall et aI., 1986a). CGRP, sub stance P, and neurokinin A lower mean arterial blood pressure in the guinea pig (Lundberg et al , 1985).…”

Section: Discussionsupporting

confidence: 86%

Calcitonin Gene-Related Peptide and Cerebral Blood Vessels: Distribution and Vasomotor Effects

Edvinsson

Ekman

Jansen

et al. 1987

J Cereb Blood Flow Metab

287

141

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Summary: The innervation of cerebral blood vessels by nerve fibers containing calcitonin gene-related peptide (CGRP) and the vasomotor effects of this peptide are de scribed for a number of different mammalian species. CGRP-immunoreactive nerve fibers were present in the adventitia of cerebral arteries in all species examined (guinea pig, cat, rabbit, rat, and mouse). Numerous peri karya containing CGRP immunoreactivity are demon strable in the trigeminal ganglion of all species. In the cerebral perivascular nerve fibers and in trigeminal peri karya, CGRP is often colocalized with substance P and neurokinin A. Marked interspecies differences exist both in the density of CGRP-immunoreactive nerve fibers and in the cerebrovascular levels measured with radioimmu noassay. The highest concentrations were observed in ce rebral vessels from guinea pigs, the lowest concentration in rabbit vessels, and intermediate levels in the feline and human cerebral vasculature. CGRP is a potent dilator of Calcitonin gene-related peptide (CGRP) is a 37 amino acid peptide recently identified from struc tural analysis of the products of calcitonin gene ex pression (Amara et al., 1982;Rosenfeld et al. , 1983). CGRP-immunoreactive fibers are abundant in the sensory receiving areas of the spinal cord and to a lesser extent in the sympathetic and parasym pathetic centers. CGRP-containing terminals are also present in sensory nuclei of the lower brain stem, for example, the nucleus tractus solitarius (Gibson et aI. , 1984; Kawai et aI., 1985;Skofitsch and Jacobowitz, 1985). Immunocytochemical studies have revealed that CGRP coexists with sub stance P and neurokinin A in nerve cell bodies of 720cerebral arteries in all species examined (human pial, fe line middle cerebral, rabbit, guinea pig and rat basilar ar teries). The concentration of CGRP eliciting half-max imal responses ranged from 0.4 nM (human pial artery) to 3 nM (rat and rabbit basilar arteries). Pretreatment of ce rebral arteries with low concentrations of either sub stance P (0.1 nM) or neurokinin A (3 nM) attenuated slightly the CGRP-induced relaxations of guinea pig bas ilar arteries. Calcitonin was found to be a very weak di lator of cerebral arteries from human and guinea pig. Thus, cardiovascular nerve fibers containing CGRP ap pear to be present in all mammalian species (although to varying degrees) and CGRP is invariably a potent dilator of the cerebral arteries for all species.

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Section: Discussionsupporting

confidence: 86%

Calcitonin Gene-Related Peptide and Cerebral Blood Vessels: Distribution and Vasomotor Effects

Edvinsson

Ekman

Jansen

et al. 1987

J Cereb Blood Flow Metab

287

141

View full text Add to dashboard Cite

show abstract

“…In addition, although a recent investigation by Howden et al, (1988) showed that bolus doses of human a-CGRP in conscious human volunteers caused increases in HR with no statistically significant effect on systolic or diastolic BP, the data indicate that 00 120 some subjects probably did show a fall, particularly 110 in diastolic, BP. Struthers et al, (1986) (Marshall et al, 1986a;Kawasaki et al, 1988). This about central conclusion is consistent with the finding that mesen-teric vasodilatation can be elicited by bolus administration of rat a-CGRP (Gardiner et al, 1988) where the rapidity of onset of vasodilator effect may outstrip 'on-line' baroreflex compensation.…”

Section: Discussionsupporting

confidence: 79%

“…There were vasodilatations in renal, hindquarters and common carotid vascular beds, although only in the latter two regional circulations were flows increased above baseline, and the effect in the common carotid vascular bed was about double that in the hindquarters. In spite of direct evidence for a vasodilator effect of CGRP on the superior mesenteric vascular bed in vitro (Marshall et al, 1986a), hypotensive doses of rat a-CGRP caused clear-cut superior mesenteric vasoconstriction, with the increase in vascular resistance being associated with a significant reduction in flow below baseline. The magnitude of the heart rate (HR) responses to rat a-CGRP indicated a possible direct cardiac effect of the peptide in addition to baroreflex-mediated influences.…”

Section: Introductionmentioning

confidence: 88%

Regional haemodynamic effects of human α‐ and β‐calcitonin gene‐related peptide in conscious Wistar rats

Gardiner

Compton

Bennett

1989

British J Pharmacology

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“…At higher doses it does not appear to exert a selective dilator effect on the mesenteric vascular bed (Marshall et al, 1986a), but its effects may be particularly marked in the hindquarters.…”

Section: Effects Ofcalcitonin Gene-related Peptidementioning

confidence: 88%

Regional haemodynamic effects of depressor neuropeptides in conscious, unrestrained, Long Evans and Brattleboro rats

Gardiner

Compton

Bennett

1988

British J Pharmacology

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Human and rat α-CGRP but not calcitonin cause mesenteric vasodilatation in rats

Cited by 110 publications

References 17 publications

Calcitonin Gene-Related Peptide and Cerebral Blood Vessels: Distribution and Vasomotor Effects

Calcitonin Gene-Related Peptide and Cerebral Blood Vessels: Distribution and Vasomotor Effects

Regional haemodynamic effects of human α‐ and β‐calcitonin gene‐related peptide in conscious Wistar rats

Regional haemodynamic effects of depressor neuropeptides in conscious, unrestrained, Long Evans and Brattleboro rats

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