Hemodynamic effects of calcitonin gene-related peptide in spontaneously hypertensive rats

Ando, Katsuyuki; Pegram, Barbara L.; Fröhlich, Edward D.

doi:10.1152/ajpregu.1990.258.2.r425

Cited by 30 publications

(29 citation statements)

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“…This finding was compatible with the previous report that AM and CGRP exerted a potent vasodilator action via cAMP (7). Although HR was increased by both peptides, implying that reflexive sympathetic activation occurs as a result of both treatments, CI was increased by AM (23,24) but not by CGRP (15,16), in agreement with previous reports. This finding was probably due to the difference in cardiac-afterload reduction between the AM and CGRP groups.…”

Section: Discussionsupporting

confidence: 92%

Regional Hemodynamic Effects of Adrenomedullin in Wistar Rats: A Comparison with Calcitonin Gene-Related Peptide.

et al. 2002

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Section: Discussionsupporting

confidence: 92%

Regional Hemodynamic Effects of Adrenomedullin in Wistar Rats: A Comparison with Calcitonin Gene-Related Peptide.

et al. 2002

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“…It is likely the latter was due to a venodilator action of human a-CGRP (Tornebrandt et al, 1987;Crossman et al, 1987; but see Al-Kazwini et al, 1987;Marshall et al, 1988). The present results, therefore, provide some explanation for the conflicting data in the literature regarding the cardiac haemodynamic effects of CGRP (DiPette et al, 1987;Lappe et al, 1987;Siren & Feuerstein, 1988;Ando et al, 1990) (see Introduction), since it is apparent that the effects of the peptide depend on the dose used. Moreover, it may be that the cardiac haemodynamic responses to bolus injections of CGRP would give a less clear picture of the interrelated changes that were seen in the present study, particularly with the infusion of the higher dose of human a-CGRP.…”

Section: Discussionmentioning

confidence: 51%

“…However, results of experiments in rats are less clearcut, possibly because of limitations with the methodology used. Thus, there have been two studies (DiPette et al, 1987;Ando et al, 1990) using the radiolabelled microsphere technique in acutely prepared rats (3 h post surgery), in which single measurements of cardiac output were made at a fixed time point after bolus injections of CGRP. Using this approach DiPette et al (1987) observed a small increase, while Ando et al (1990) found no change, in cardiac output after administration of rat and human a-CGRP, respectively.…”

Section: Introductionmentioning

confidence: 99%

“…Thus, there have been two studies (DiPette et al, 1987;Ando et al, 1990) using the radiolabelled microsphere technique in acutely prepared rats (3 h post surgery), in which single measurements of cardiac output were made at a fixed time point after bolus injections of CGRP. Using this approach DiPette et al (1987) observed a small increase, while Ando et al (1990) found no change, in cardiac output after administration of rat and human a-CGRP, respectively. In contrast, Siren & Feuerstein (1988) measured cardiac output intermittently with the thermodilution technique in conscious rats and reported an increase of 95 + 16mlmin--kg1' in cardiac index in response to a bolus dose of 1.0 nmol kg-l rat CGRP, but found doses of 0.1 and 10nmol kg-I were without significant effect.…”

Section: Introductionmentioning

confidence: 99%

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Differential effects of (±)‐dobutamine and human α‐CGRP on cardiac and on regional haemodynamics in conscious Long Evans rats

Gardiner

Compton

Kemp

et al. 1991

British J Pharmacology

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1 Comparisons were made of the full haemodynamic profiles of the known cardiostimulant, (± )-dobutamine, and the putative inotropic peptide, human a-calcitonin gene-related peptide (human a-CGRP), in conscious, chronically-instrumented Long Evans rats. Both substances were administered continuously i.v. for 60min at two doses ((±)-dobutamine, 2 and lOpmolkgr'h-i; human a-CGRP, 0.15 and 1.5 nmol kg1 h 1). 2 In spite of their similar (small) effects on mean arterial blood pressure, the low doses of (±)-dobutamine and human a-CGRP influenced cardiac haemodynamics differently. Thus, (±)-dobutamine caused an increase in cardiac index (due to a tachycardia), accompanied by rises in peak aortic flow, maximum rate of rise of aortic flow (dF/dtmai) and total peripheral conductance. However, the latter waned during the infusion, and after the infusion there was a significant systemic vasoconstriction and reductions in peak aortic flow, dF/dtmax and stroke index. Such 'off' effects following dobutamine infusion have not been described previously. The infusion of the lower dose of human cx-CGRP caused only a transient fall in central venous pressure.3 The rise in total peripheral conductance during infusion of the lower dose of (±)-dobutamine was associated with increases in hindquarters and common and internal carotid vascular conductances. The fall in total peripheral conductance after infusion was associated with renal vasoconstriction. Although there was no significant change in total peripheral conductance during the infusion of the lower dose of human a-CGRP there were hindquarters and carotid vasodilatations together with mesenteric vasoconstriction. 4 Infusion of the higher dose of ( )-dobutamine had greater effects than the lower dose on all cardiac haemodynamic variables and additionally, increased stroke index. However, the negative cardiac haemodynamic effects following the offset of infusion were also enhanced in association with marked renal and mesenteric vasoconstrictions. While infusion of the higher dose of human a-CGRP increased cardiac index, peak aortic flow, dF/dtmax and total peripheral conductance, stroke index fell together with central venous pressure. 5 (±)-Dobutamine caused greater cardiostimulation and increases in hindquarters blood flow than did human a-CGRP. However, the latter at the higher dose caused substantially greater common and internal carotid hyperaemia than did (±)-dobutamine, possibly indicating a selective and additional effect of human a-CGRP on cranial blood flow. Furthermore, there were no adverse cardiovascular effects following infusion of human a-CGRP.

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“…All CGRP family peptides exhibit cardiovascular actions, although relative potency differs among the members, CGRPOAMRAM2[amylin (Ando et al 1990, Charles et al 1997, Hall & Brain 1999, Fujisawa et al 2004. CGRP is a neuropeptide in the brain and periphery, which is released from axon terminals innervating the vascular smooth muscles (see Brain & Grant 2004 for review).…”

Section: Introductionmentioning

confidence: 99%

Central and peripheral cardiovascular actions of adrenomedullin 5, a novel member of the calcitonin gene-related peptide family, in mammals

Takei¹,

Hashimoto

Inoue³

et al. 2008

Journal of Endocrinology

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Adrenomedullin 5 (AM5) is a new member of the calcitonin gene-related peptide (CGRP) family identified in teleost fish. Although its presence was suggested in the genome database of mammals, molecular identity and biological function of AM5 have not been examined yet. In this study, we cloned a cDNA encoding AM5 in the pig and examined its cardiovascular and renal effects. Putative mature AM5 was localized in the middle of prohormone and had potential signals for intermolecular ring formation and C-terminal amidation. The AM5 gene was expressed most abundantly in the spleen and thymus. Several AM5 genes were newly identified in the database of mammals, which revealed that the AM5 gene exists in primates, carnivores, and undulates but could not be identified in rodents. In primates, nucleotide deletion occurred in the mature AM5 sequence in anthropoids (human and chimp) during transition from the rhesus monkey. Synthetic mature AM5 injected intravenously into rats induced dose-dependent decreases in arterial pressure at 0 . 1-1 nmol/kg without apparent changes in heart rate. The decrease was maximal in 1 min and AM5 was approximately half as potent as AM. AM5 did not cause significant changes in urine flow and urine Na C concentration at any dose. In contrast to the peripheral vasodepressor action, AM5 injected into the cerebral ventricle dose-dependently increased arterial pressure and heart rate at 0 . 1-1 nmol. The increase reached maximum more quickly after AM5 (5 min) than AM (15-20 min). AM5 added to the culture cells expressing calcitonin receptor-like receptor (CLR) or calcitonin receptor (CTR) together with one of the receptor activitymodifying proteins (RAMPs), the combination of which forms major receptors for the CGRP family, did not induce appreciable increases in cAMP production in any combination, although AM increased it at 10 K10 -10 K9 M when added to the CLR and RAMP2/3 combination. These data indicate that AM5 seems to act on as yet unknown receptor(s) for AM5, other than CLR/CTRCRAMP, to exert central and peripheral cardiovascular actions in mammals.

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Hemodynamic effects of calcitonin gene-related peptide in spontaneously hypertensive rats

Cited by 30 publications

References 0 publications

Regional Hemodynamic Effects of Adrenomedullin in Wistar Rats: A Comparison with Calcitonin Gene-Related Peptide.

Regional Hemodynamic Effects of Adrenomedullin in Wistar Rats: A Comparison with Calcitonin Gene-Related Peptide.

Differential effects of (±)‐dobutamine and human α‐CGRP on cardiac and on regional haemodynamics in conscious Long Evans rats

Central and peripheral cardiovascular actions of adrenomedullin 5, a novel member of the calcitonin gene-related peptide family, in mammals

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