Contractile responses of helically-cut strips of the rabbit aorta to drugs, ions and transmural electrical stimulation were compared at different temperatures of the bathing medium, the response at 37 °C being taken as control. The dose-response curve of norepinephrine was moved to the right and downward by lowering the temperature from 37 to 25 °C and by raising temperature to 40 °C. Responses to transmural neural stimulation at frequencies of 5 and 20/sec were attenuated at 25 °C, the attenuation being greater in the response at the lower frequency. Concentrations of exogenous norepinephrine needed to produce the same magnitude of contraction as that with transmural stimulation were markedly increased by lowering the temperature to 25 °C. Contractile responses to norepinephrine (2 x 10-6 m), histamine (2 × 10-5 m) and angiotensin II (10-7 m) were attenuated by 32–44% at 25 °C, whereas the responses to K+ (25 mil) and Ba++ (2 mil) were dependent on temperatures between 25 and 37 °C and were attenuated by 69 and 92%, respectively, at 25 °C. Contractures induced by Ca++ in K+-depolarized preparations exposed to Ca++-free media and also by Ba++ in preparations exposed to Ca++-free media varied directly by raising temperatures. Interference with the influx of divalent cations, such as Ca++ and Ba++, may be involved in the cold inhibition of aortic contractility.
Isolated canine coronary arteries were contracted with prostaglandin F2α and the relaxing effects of dopamine, adenosine, isoproterenol and acetylcholine were compared. Relaxation induced by dopamine in phenoxybenzamine-treated arteries was not significantly influenced by propranolol and atropine in concentrations sufficient to shift dose-response curves of isoproterenol and acetylcholine, respectively, to the right. Dose-response curves of isoproterenol were shifted significantly to the left by 2 x 10–5 M aminophylline. In contrast, the relaxing effect of adenosine was significantly attenuated by aminophylline (5 × 10–6–10–4 M) in a dose-dependent manner. Kinetic analysis showed that aminophylline competitively antagonized the effect of adenosine, and the pA2 was 5.57. At these concentrations, aminophylline did not alter the relaxing action of dopamine and acetylcholine. It may be concluded that dopamine produces relaxation at a different site and with a different mechanism of action from those of isoproterenol, the effect of the latter being presumably mediated by cellular cyclic AMP, and that dopamine also does not share the site of action with adenosine and acetylcholine. It appears that receptive sites specific for adenosine are present in canine coronary arteries.
Recent study in this laboratory has demonstrated that 5-hydroxykynurenamine (5 HK) (1), converted from serotonin by trvptophan 2, 3 dioxygenase (2) and formamidase, causes contractions of isolated canine cerebral arteries as does serotonin, and also attenu ates the vascular response to serotonin (3). 5-Hydroxyindoleacetic acid (5-HIAA), a major metabolite of serotonin (4) via a catalysis of monoamine oxidase, has been shown to possess no or only slight serotonin-like activity in a variety of organs and tissues (5 7); however, little is known concerning interactions of this metabolite with serotonin ac
It has been demonstrated that prostaglandin E1 (PGE1) and E2 are structurally quite similar and share the same actions on the systemic blood pressure (1, 2), the isolated vascular smooth muscle (3) and the sympathetic neurotransmission (4). In contrast, the present study describes the different effects of PGE1 and E2 on isolated canine coronary arteries.Mongrel dogs were anesthetized with sodium pentobarbital and sacrificed by bleeding from carotid arteries. The interventricular branch of left coronary arteries of 0.5 to 0.8 mm outside diameter was isolated and helically cut into strips. The specimen was fixed under a resting tension of 1.5 g in a muscle bath containing the nutrient solution maintained at 37'C. Isometric contractions and relaxations were recorded. Details of the experimental procedures are described in an earlier report (5). Paired comparison of the effect of PGE1and E2 in 9 preparations from 9 dogs was made.
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