Unterschiedliche Temperaturabh�ngigkeit der Gef��muskelkontraktion nach Aktivierung durch Kalium-Depolarisation bzw. Noradrenalin

Peiper, U.; Griebel, L.; Wende, W.

doi:10.1007/bf00587797

Cited by 23 publications

(5 citation statements)

References 24 publications

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“…The present study revealed that in isolated rabbit aortas, lowering the temperature of bathing medium from 37 to 25 °C shifted the doseresponse curve of norepinephrine to the right and downward, as was demonstrated with isolated rat aortas [9]. Transmural electrical stimu lation caused a transient contraction of isolated ascending aortas possibly by releasing norepinephrine from adrenergic nerve terminals, since tetrodotoxin abolished the response to the stimulation.…”

Section: Discussionmentioning

confidence: 75%

Modification by Temperature of the Response of Isolated Aorta to Stimulatory Agents and Transmural Stimulation

Toda¹,

Hojo²,

Sakae³

1976

J Vasc Res

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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.

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Section: Discussionmentioning

confidence: 75%

Modification by Temperature of the Response of Isolated Aorta to Stimulatory Agents and Transmural Stimulation

Toda¹,

Hojo²,

Sakae³

1976

J Vasc Res

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“…6) (Bohr & Webb, 1978;Godfraind & Morel, 1978). The depressant effect of cooling on K+-evoked responses is not specific for cutaneous vessels but has also been observed in other systemic vessels (Keatinge, 1964;Vanhoutte & Shepherd, 1970;Peiper, Griebel & Wende, 1971, Andersson, Hellstrand, Johansson & Ringberg, 1972;Godfraind & Kaba, 1972;Janssens & Vanhoutte, 1978); an important component of this depression is a decrease in membrane permeability for Ca2+ (see Vanhoutte, 1980). At 5 IC, high concentrations of K+ still cause significant increases in tension of the canine saphenous vein confirming this observation on isolated arteries (Keatinge, 1964).…”

Section: Unstimulated Preparationsmentioning

confidence: 97%

The effect of profound cooling on adrenergic neurotransmission in canine cutaneous veins.

Rusch¹,

Shepherd²,

Vanhoutte³

1981

The Journal of Physiology

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1. Experiments were performed to investigate how profound cooling affects adrenergic neurotransmission and vascular smooth muscle reactivity in isolated saphenous veins of the dog. 2. Cooling from 37 to 5 degrees C caused progressive depression of the contractile responses to high K+ solutions, illustrating the direct inhibitory effect of cooling on depolarization‐induced contraction of the venous smooth muscle cells. 3. During prolonged cooling to 20, 15 and 10 degrees C, the contractile response to exogenous norepinephrine (10(‐8)‐10(‐6) M) was augmented compared to that at 37 degrees C. At 5 degrees C responses up to 10(‐7) M were also augmented, but those at higher concentrations were depressed. When veins contracted with 2 x 10(‐6) M‐norepinephrine were cooled to 20, 15, 10 and 5 degrees C, there was a further increase in tension; this increase slowly subsided to control values at 5 degrees C but was sustained at the other temperatures. 4. Cooling to 20 and 15 degrees C augmented the contraction caused by low but not high frequencies of electrical stimulation of the adrenergic nerve endings. Further cooling to 10 degrees C depressed, and at 5 degrees C abolished the response, demonstrating that profound cooling interrupted adrenergic neurotransmission. 5. In rings stimulated electrically at a low frequency (0.5 Hz), warming from 7 to 9 degrees C or from 9 to 11 degrees C, caused marked increases in tension. This may be explained by the combination of resumption of adrenergic neurotransmission and the increased responsiveness of the cutaneous venous smooth muscle cells to adrenaline. 6. The combination of enhanced affinity for noradrenaline combined with inhibition of neurotransmitter disposition probably permits the cutaneous veins to remain constricted during exposure to severe cold.

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“…Perfusion temperature affected vascular responsiveness to norepinephrine in chicken hind-limb blood vessels In the rabbit ear artery the immediate, rapid vasoconstrictor response to norepinephrine shows a small increase when the temperature is reduced from 37 to 25 °C [Glover et al, 1968] but in other mammalian blood vessels responsiveness to nor epinephrine decreases as temperature is reduced [Glover et al, 1968;Malik, 1969;Vanhoutte and Lorenz, 1970;Peiper et al, 1971].…”

Section: Discussionmentioning

confidence: 99%

Development of Vascular Reactivity in Chickens: Responses of Mesenteric and Hind-Limb Blood Vessels to Norepinephrine and Acetylcholine

Knight¹,

McGregor²

1974

J Vasc Res

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Mesenteric arteries and the hind-limb vasculature supplied by the sciatic artery were isolated from chickens 0–25 vity days after hatching and perfused with physiological saline. Mesenteric arteries gave only small responses to norepinephrine until the 2nd week after hatching when there was a striking increase in their reactivity. Hind-limb blood vessels were much more responsive to norepinephrine from the 1st day. The height of vasoconstrictor responses in hind-limbs showed no marked change with age but the duration of responses decreased as chickens grew older. The duration of responses to norepinephrine increased when perfusion temperature was lowered from 40 to 20 °C. Acetylcholine produced vasodilatation in mesenteric and hind-limb blood vessels. It is concluded that the receptor mechanisms for adrenergic and cholinergic control of hind-limb blood flow are functional at or before hatching. The increase in vascular reactivity to norepinephrine in mesenteric arteries coincides with reported increases in blood pressure and thermoregulatory ability of chickens and may contribute to these increases.

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Unterschiedliche Temperaturabh�ngigkeit der Gef��muskelkontraktion nach Aktivierung durch Kalium-Depolarisation bzw. Noradrenalin

Cited by 23 publications

References 24 publications

Modification by Temperature of the Response of Isolated Aorta to Stimulatory Agents and Transmural Stimulation

Modification by Temperature of the Response of Isolated Aorta to Stimulatory Agents and Transmural Stimulation

The effect of profound cooling on adrenergic neurotransmission in canine cutaneous veins.

Development of Vascular Reactivity in Chickens: Responses of Mesenteric and Hind-Limb Blood Vessels to Norepinephrine and Acetylcholine

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