Cardiovascular effects of calcitonin gene-related peptide in conscious dogs

Wang, B. C.; Bie, Peter; Leadley, Robert J.; Goetz, K. L.

doi:10.1152/ajpregu.1989.257.4.r726

Cited by 11 publications

(7 citation statements)

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“…This is in contrast to the observed tachycardia during pentobarbital anesthesia in the present study as well as in those reported previously [10,11,16,17]. The increases in HR elicited by CGRP during pentobarbital anesthesia may be the results of two major mechanisms: one is the direct positive chronotropic action of CGRP on the heart [18], and the other is a reflex-mediated action on sympathetic tone in response to hypotension [10,11,19].…”

Section: Discussioncontrasting

confidence: 71%

Halothane anesthesia suppresses reflex tachycardia caused by calcitonin gene-related peptide in dogs

et al. 1996

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Calcitonin gene-related peptide (CGRP) is known to produce vasodilation, hypotension, and tachycardia. To investigate the interaction between CGRP and anesthetics, the hemodynamic response to infusions of CGRP was studied in dogs anesthetized with halothane or pentobarbital. In halothane-anesthetized dogs given 0.4 μg·kg(-1) of CGRP, mean arterial pressure (MAP) did not change significantly. However, there was a significant reduction in systemic vascular resistance (SVR) associated with significant increases in cardiac index (CI) and stroke volume index (SVI). Higher doses (4 and 40 μg·kg(-1)) of CGRP produced dose-dependent decreases in MAP accompanied by a reduction in SVR. Further, both CI and SVI significantly increased at 4 μg·kg(-1) CGRP but remained unchanged at the 40 μg·kg(-1) infusion rate. Heart rate (HR) was not increased at all doses but was decreased at 40 μg·kg(-1). In pentobarbital-anesthetized dogs, CGRP at doses of 4 μg·kg(-1) produced a qualitatively similar cardiovascular responses as that observed in halothane-anesthetized dogs, but with one exception: HR was significantly increased. The results show that the hemodynamic profiles induced by CGRP during halothane or pentobarbital anesthesia are a decrease in MAP accompanied by a reduction in SVR and no consistent alterations in CI. However, CGRP effects on HR showed in a different way. The results also show that HR response differs depending on the anesthetics used: HR increases during pentobarbital anesthesia, while it does not increase during halothane anesthesia.

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Section: Discussioncontrasting

confidence: 71%

Halothane anesthesia suppresses reflex tachycardia caused by calcitonin gene-related peptide in dogs

et al. 1996

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“…administration of drugs a catheter was placed in a jugular vein through which saline (0.9% NaCl, wt/wt) was continuously infused at a rate of 1.5mlh-' to avoid dehydration. In some experiments the drugs were administered close arterially to the stomach, in which case the abdominal aorta was cannulated with a catheter in a retrograde direction so that the tip of the catheter lay just above the branching of the coeliac artery (Lippe et al, 1989 (Burton & Gorewit, 1984;Wang et al, 1989 (model T106,Transonic).…”

Section: Methodsmentioning

confidence: 99%

Nitric oxide‐dependent and ‐independent hyperaemia due to calcitonin gene‐related peptide in the rat stomach

Holzer

Lippe

Jocič

et al. 1993

British J Pharmacology

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1 Calcitonin gene-related peptide (CGRP) potently enhances mucosal blood flow in the rat stomach. The aim of this study was to examine whether CGRP also dilates extramural arteries supplying the stomach and whether the vasodilator action of CGRP involves nitric oxide (NO). 2 Rat CGRP-x (0.03-1 nmol kg-', i.v.) produced a dose-dependent increase in blood flow through the left gastric artery (LGA) as determined by an ultrasonic transit time technique in urethane-anaesthetized rats. Blockade of NO synthesis by NG-nitro-L-arginine methyl ester (L-NAME, 20 and 60 ymol kg-', i.v.) significantly reduced basal blood flow (BF) in the LGA and attenuated the hyperaemic activity of CGRP by a factor of 2.8-4. D-NAME tended to enhance basal BF in the LGA but had no influence on the dilator activity of CGRP. The ability of vasoactive intestinal polypeptide to increase left gastric arterial blood flow remained unaltered by L-NAME. 3 L-NAME (20 and 60 ymol kg-', i.v.) evoked a prompt and sustained rise of mean arterial blood pressure (MAP) and caused a slight decrease in the hypotensive activity of CGRP. In contrast, D-NAME induced a delayed and moderate increase in MAP and did not influence the hypotensive activity of CGRP. 4 Rat CGRP-o dilated the isolated perfused bed of the rat LGA precontracted with methoxamine and was 3 times more potent in this respect than rat CGRP-P. The dilator action of rat CGRP-x in this preparation was not affected by L-NAME or D-NAME (40 pM).5 L-NAME (601tmol kg-', i.v.) reduced gastric mucosal blood flow as assessed by laser Doppler flowmetry and diminished the hyperaemic activity of rat CGRP-a in the gastric mucosa by a factor of 4.5, whereas D-NAME was without effect. 6 These data show that CGRP is a potent dilator of mucosal and extramural resistance vessels in the rat stomach. Its dilator action involves both NO-dependent and NO-independent mechanisms.

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“…In vivo studies in conscious dogs (Wang et al, 1989) and man (Gennari et al, 1989; indicate that human a-calcitonin gene-related peptide (human a-CGRP) can increase cardiac output. However, results of experiments in rats are less clearcut, possibly because of limitations with the methodology used.…”

Section: Introductionmentioning

confidence: 99%

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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Cardiovascular effects of calcitonin gene-related peptide in conscious dogs

Cited by 11 publications

References 0 publications

Halothane anesthesia suppresses reflex tachycardia caused by calcitonin gene-related peptide in dogs

Halothane anesthesia suppresses reflex tachycardia caused by calcitonin gene-related peptide in dogs

Nitric oxide‐dependent and ‐independent hyperaemia due to calcitonin gene‐related peptide in the rat stomach

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

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