Influences of extracellular calcium ions, verapamil, and calcium antagonistic cations on the positive inotropic effects mediated by α- and β-adrenoceptors in the left atria of rats

Contractile effects of the cardiac neuropeptides vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI), neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP), and neurotensin (NT) were compared with those of l-isoproterenol (ISO) in isolated canine atrial and ventricular trabeculae muscles stimulated to contract at 1 Hz. In ventricular muscles, ISO, VIP, and PHI augmented developed isometric force by approximately 100%. VIP and PHI were three times and 1/10, respectively, as potent as ISO. VIP also exhibited positive inotropic effects in atrial trabeculae. The contractile responses to VIP were unchanged after beta-adrenergic blockade with nadolol at a concentration (10 microM) that shifted the ISO dose-response curve two to three orders of magnitude to the right. In atrial and ventricular trabeculae, NPY (1 microM) attenuated contractile force by 36 +/- 8 and 30 +/- 4%, respectively. Each peptide also caused comparable increases or decreases in the rate of development of force and the rate of relaxation. CGRP and NT caused no significant changes in developed force in either atrial or ventricular muscles in concentrations up to 1 microM. Our results indicate a potential positive inotropic action of endogenous VIP and PHI and a cardiodepressant effect of endogenous NPY in the canine heart.

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Failure of dibutyryl and 8-bromo-cyclic gmp to mimic the antagonistic action of carbachol on the positive inotropic effects of sympathomimetic amines in the canine isolated ventricular myocardium

The Japanese Journal of Pharmacology ◽

10.1254/jjp.29.423 ◽

1979 ◽

Vol 29 (3) ◽

pp. 423-433 ◽

Cited By ~ 14

Author(s):

Masaso Endoh ◽

Tetsuo Shimizu

Keyword(s):

Cyclic Gmp ◽

Ventricular Myocardium ◽

Antagonistic Action ◽

Inotropic Effects ◽

Sympathomimetic Amines ◽

Positive Inotropic Effects

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Coronary vasodilation and positive inotropism by urocortin in the isolated rat heart

Journal of Endocrinology ◽

10.1677/joe.0.1690177 ◽

2001 ◽

Vol 169 (1) ◽

pp. 177-183 ◽

Cited By ~ 64

Author(s):

K Terui ◽

A Higashiyama ◽

N Horiba ◽

KI Furukawa ◽

S Motomura ◽

...

Keyword(s):

Rat Heart ◽

Isolated Rat Heart ◽

Coronary Vasodilation ◽

Duration Of Action ◽

Inotropic Effects ◽

Vasodilator Effect ◽

Cardiac Effects ◽

Positive Inotropic Effects ◽

Isolated Rat

Corticotropin-releasing factor (CRF) has a coronary vasodilator effect and a positive inotropic effect on the isolated rat heart. Recently, expression of CRF receptor type 2 (CRF-R2) has been demonstrated in the heart. In addition, urocortin (Ucn), a new member of the CRF family, has been reported to have much greater affinity for CRF-R2 than CRF. It is suggested that the cardiac effects of Ucn may be more potent than those of CRF. We compared the effect of Ucn with that of CRF on isolated rat heart. The effects of Ucn were then analyzed to determine whether these effects were mediated by CRF receptors and/or any other mediators under the following conditions: perfusion buffer containing (1) alpha-helical CRF 9-41, (2) indomethacin, (3) N(G)-nitro-l -arginine methylester and (4) propranolol. Ucn exhibited a greater effect with a longer duration of action than CRF. Indomethacin significantly attenuated the vasodilator effects of Ucn (P<0.05). CRF receptor antagonist diminished both coronary vasodilation and the positive inotropic effects of Ucn (P<0.05). These results suggest that the cardiac effects of Ucn may be mediated by a CRF receptor, and prostaglandins may be involved in the vasodilator effect.

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Nitrendipine blocks high potassium contractures but not twitches in rat skeletal muscle

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y88-199 ◽

1988 ◽

Vol 66 (9) ◽

pp. 1210-1213 ◽

Cited By ~ 4

Author(s):

G. B. Frank ◽

L. Konya ◽

T. Subrahmanyam Sudha

Keyword(s):

Skeletal Muscle ◽

Calcium Ions ◽

Calcium Uptake ◽

Channel Blocker ◽

Mechanical Response ◽

Extracellular Calcium ◽

The Other ◽

Rat Skeletal Muscle ◽

Potassium Depolarization ◽

High Potassium

The effects of the organic calcium channel blocker nitrendipine was tested on electrically evoked twitches and on potassium depolarization-induced contractures of rat lumbricalis muscles. Nitrendipine (10−7 to 5 × 10−5 M) blocked only the potassium contractures. It was concluded that blocking calcium uptake through the slow voltage-senstitive calcium channels during potassium depolarization blocks the mechanical response of the muscle. Thus extracellular calcium ions are required for the excitation–contraction (E–C) coupling during depolarization contractures. On the other hand, electrically evoked twitches were not affected by nitrendipine; therefore, extracellular calcium ions entering via the slow voltage-sensitive channels are not required for E–C coupling during the twitch.

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