5-hydroxytryptamine and neurotransmitter release in canine blood vessels. Inhibition by low and augmentation by high concentrations.

McGrath, Michael A.

doi:10.1161/01.res.41.4.428

Cited by 112 publications

(40 citation statements)

References 27 publications

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“…To exclude adrenerglc effects of serotonin (9), all experiments were conducted in the presence ofpropranolol (10-6 M) and prazosin (5 X 10-' M). Apyrase (0.67 U/ml) was added to the bath immediately before the addition of platelets; the concentration used here has little or no direct effect on the tension of the rings.…”

Section: Methodsmentioning

confidence: 99%

Aggregating human platelets cause direct contraction and endothelium-dependent relaxation of isolated canine coronary arteries. Role of serotonin, thromboxane A2, and adenine nucleotides.

Houston¹,

Shepherd²,

Vanhoutte³

1986

J. Clin. Invest.

169

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Aggregating human platelets contract isolated rings of canine coronary artery without endothelium, but relax rings with intact endothelium. We performed experiments to identify the substances released from platelets responsible for these effects. The contraction in rings without endothelium was reduced by treating the platelets with the thromboxane synthetase inhibitor, dazoxiben, or treating the vessels with the thromboxane-receptor antagonist, SQ 29548. The serotonergic antagonist, methiothepin, also reduced the platelet-induced contraction. The combination of methiothepin plus dazoxiben or SQ 29548 caused a further inhibition. The endothelium-dependent relaxation to platelets during contractions evoked by prostaglandin F2. was nearly abolished by the ADP-and ATP-scavenger, apyrase. It was not inhibited by methiothepin, which antagonizes endothelium-dependent relaxations to serotonin. Thus, both serotonin and thromboxane A2 contribute to the direct activation of coronary smooth muscle by aggregating human platelets, whereas adenine nucleotides are the principal mediators of the endothelium-dependent relaxation.

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Section: Methodsmentioning

confidence: 99%

Aggregating human platelets cause direct contraction and endothelium-dependent relaxation of isolated canine coronary arteries. Role of serotonin, thromboxane A2, and adenine nucleotides.

Houston¹,

Shepherd²,

Vanhoutte³

1986

J. Clin. Invest.

169

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“…However, there is evidence both of an increased renal norepinephrine content and of a larger area of catecholamine fluorescence around the arterioles in the young SHR. 18 -17 This could be due to an enhanced norepinephrine synthesis by each nerve terminal or to a larger number of adrenergic nerve varicosities in the SHR. Either of these alterations could cause an increased release of norepinephrine in response to electrical stimulation of the renal sympathetic nerves.…”

Section: Renal Sympathetic Nerresmentioning

confidence: 99%

“…18 When the sympathetic nerves of the SHR and the control rats were severely damaged by treatment with 6-hydroxydopamine, the increased reactivity of the SHR kidney to submaximal doses of this agonist was abolished. This implies that increased reactivity to 5-hydroxytryptamine in the young SHR is due mainly to an altered interaction of the amine with the sympathetic nerve terminal, rather than with the vascular smooth muscle cell.…”

Section: -Hydroxytryptaminementioning

confidence: 99%

Renal vascular reactivity in the young spontaneously hypertensive rat.

Collis¹,

DeMey²,

Vanhoutte³

1980

Hypertension

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SUMMARYThe renal resistance vessels of the mature spontaneously hypertensive rat (SHR) exhibit increased reactivity to vasoconstrictor agonists. This could be a cause or consequence of hypertension. We have compared vascular reactivity in isolated perfused kidneys from 46-day-old SHR and from normotensive control rats. The amplitude of responses in kidneys from the SHR to angiotensin II, barium chloride, or norepinephrine was not different from the control. Therefore, increased reactivity of the renal vascular smooth muscle cannot be an early pathogenic mechanism in spontaneous hypertension. Responses evoked by 5-hydroxytryptamine (serotonin) were of a greater amplitude in the SHR than in the control kidney. However, this difference was due to an interaction of serotonin with the sympathetic nerves, as it was abolished by treatment of the rats with 6-hydroxydopamine. Responses induced by electrical stimulation of the renal sympathetic nerves were also of greater amplitude in SHR than in control kidneys, both before and after the blockade of norepinephrine disposition mechanisms. Nerve stimulation evoked a greater efflux of endogenous norepinephrine from kidneys of the SHR than from those of control rats. Thus, the increased reactivity of the SHR kidney to renal nerve stimulation is due to an augmented release of endogenous norepinephrine. This could be an important factor in the early development of hypertension.

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“…It is known that when most adrenergically innervated blood vessels are exposed during electrical stimulation to 5-HT, the release of norepinephrine and, consequently, the response of the tissue are inhibited (19,20). The coronary arteries in this study were washed repeatedly after exposure to aggregating platelets and 5-HT; this was done to remove from the tissue free vasoactive substances that could have direct effects on neurotransmission.…”

Section: Discussionmentioning

confidence: 99%

Platelet-induced neurogenic coronary contractions due to accumulation of the false neurotransmitter, 5-hydroxytryptamine.

Cohen¹

1985

J. Clin. Invest.

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5-hydroxytryptamine and neurotransmitter release in canine blood vessels. Inhibition by low and augmentation by high concentrations.

Cited by 112 publications

References 27 publications

Aggregating human platelets cause direct contraction and endothelium-dependent relaxation of isolated canine coronary arteries. Role of serotonin, thromboxane A2, and adenine nucleotides.

Aggregating human platelets cause direct contraction and endothelium-dependent relaxation of isolated canine coronary arteries. Role of serotonin, thromboxane A2, and adenine nucleotides.

Renal vascular reactivity in the young spontaneously hypertensive rat.

Platelet-induced neurogenic coronary contractions due to accumulation of the false neurotransmitter, 5-hydroxytryptamine.

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