Cardiovascular effects of anatoxin-A in the conscious rat

Sirén, Anna‐Leena; Feuerstein, Giora

doi:10.1016/0041-008x(90)90086-a

Cited by 29 publications

(12 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, involvement of the cyclooxygenase pathway has not been verified in in vivo rat experiments [25,26]. In parallel to these latter findings, we did not observe any contribution of prostaglandins to CGRPinduced dilation in in vitro rat kidney vasculature, since indomethacin had no effect on the responses.…”

Section: Discussionsupporting

confidence: 74%

Mechanism of CGRP-Induced Vasodilation in the Rat Isolated Perfused Kidney

Tuncer

2004

Pharmacology

View full text Add to dashboard Cite

We investigated the intracellular mechanisms involved in calcitonin gene-related peptide (CGRP)-induced vasodilation in rat isolated perfused kidney. CGRP-1 receptor antagonist, CGRP-8-37, abolished the responses. Endothelial denudation by Triton X-100 or nitric oxide (NO) synthase inhibition by N^G-nitro-L-arginine attenuated the maximum dilation by about 63 and 55%, respectively. Protein kinase A inhibitor, KT-5720, caused an about 72% inhibition in CGRP-induced maximum dilation. Soluble guanylate cyclase inhibitor, ODQ, and ATP-sensitive potassium channel blocker, glibenclamide, inhibited the CGRP-induced maximum responses by 75 and 55%, respectively. Cyclooxygenase inhibitor, indomethacin, had no effect. Our data suggest that CGRP-1 receptors, endothelium, NO synthase, protein kinase A, soluble guanylate cyclase, and ATP-sensitive potassium channels, but not the cyclooxygenase pathway, may play a role in CGRP-induced vasodilation in rat isolated perfused kidney.

show abstract

Section: Discussionsupporting

confidence: 74%

Mechanism of CGRP-Induced Vasodilation in the Rat Isolated Perfused Kidney

Tuncer

2004

Pharmacology

View full text Add to dashboard Cite

show abstract

“…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: Discussioncontrasting

confidence: 34%

“…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. However, Lappe et al (1987) recorded I Author for correspondence.…”

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

View full text Add to dashboard Cite

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.

show abstract

“…In con scious rats, intracerebroventricularly administered CGRP increased (6) or induced no change (21) in arterial blood pressure. In the present study performed under urethane anesthesia, intracerebroventricularly administered a CGRP induced a marked decrease in arterial blood pres sure.…”

Section: Discussionmentioning

confidence: 99%

“…However, after desensitization of peripheral CGRP receptors by repeated intravenous bolus administration of a-CGRP, intracerebroventricular administration of this peptide did not induce any significant decrease or rather induced an increase in arterial blood pressure. Peripheral ly administered a-CGRP has intense hypotensive and vasodilator actions (6,(21)(22)(23)(24). Furthermore, 8% leakage of a-CGRP from the lateral brain ventricle to the peripheral circulation was demonstrated in rats (25).…”

Section: Discussionmentioning

confidence: 99%