Inhibition of adrenergic neurotransmission in isolated veins of the dog by potassium ions.

Lorenz, Robert R.; Vanhoutte, Paul M.

doi:10.1113/jphysiol.1975.sp010900

Cited by 76 publications

(19 citation statements)

References 39 publications

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“…This conclusion is supported by three sets of observations: (1) the high concentration of 5-HT caused an increase in the release of norepinephrine and its metabolites; (2) the pattern of radioactive compounds released is similar to that released by tyramine 27 but differs from the release by nerve depolarization in that there was a greater proportion of deaminated metabolites; and (3) the increased release of norepinephrine was inhibited by cocaine. This indirect sympathomimetic action of 5-HT has been observed previously in other tissues including rabbit heart, 10 guinea pig vas deferens," and cat spleen capsule.…”

mentioning

confidence: 63%

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

McGrath¹

1977

Circulation Research

112

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mentioning

confidence: 63%

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

McGrath¹

1977

Circulation Research

112

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“…The hyperpolarization observed was smaller than 2 mV and this hyperpolarization was not reproducible twice on the same tissue (data not shown) which is in contrast to the hyperpolarization produced by acetylcholine being often larger than 18 mV and reproducible in the same artery . As the eect of potassium could have been aected by the unwanted alteration in neurotransmitters release by depolarized axons (Lorenz & Vanhoutte, 1975), the same experiments were performed in the presence of tetrodotoxin. In these conditions, potassium only depolarized the guinea-pig carotid artery smooth muscle cells.…”

Section: Discussionmentioning

confidence: 99%

Potassium ions and endothelium‐derived hyperpolarizing factor in guinea‐pig carotid and porcine coronary arteries

Quignard

Félétou

Thollon

et al. 1999

British J Pharmacology

104

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1 Experiments were designed to determine in two arteries (the guinea-pig carotid and the porcine coronary arteries) whether or not the endothelium-derived hyperpolarizing factor (EDHF) can be identi®ed as potassium ions, and to determine whether or not the inwardly rectifying potassium current and the Na 3 In vascular smooth muscle cells of guinea-pig carotid and porcine coronary arteries, acetylcholine and bradykinin induced endothelium-dependent hyperpolarizations (718+1 mV, n=39 and 719+1 mV, n=7, respectively). The hyperpolarizations were not aected signi®cantly by ouabain (1 mM), barium chloride (up to 100 mM) or the combination of ouabain plus barium. 4 In both arteries, increasing extracellular potassium concentration by 5 or 10 mM induced either depolarization or in a very few cases small hyperpolarizations which never exceeded 2 mV. 5 In isolated smooth muscle cells of the guinea-pig carotid artery, patch-clamp experiments shows that only 20% of the vascular smooth muscle cells expressed inwardly rectifying potassium channels. The current density recorded was low (0.5+0.1 pA pF 71 , n=8). 6 These results indicate that, in two dierent vascular preparations, barium sensitive-inwardly rectifying potassium conductance and the ouabain sensitive-Na + /K + pump are not involved in the EDHF-mediated hyperpolarization. Furthermore, potassium did not mimic the eect of EDHF pointing out that potassium and EDHF are not the same entity in those arteries.

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“…15 Also, the increased extracellular K concentration could decrease the nerve-evoked release of norepinephrine from the nerve ending, in vitro. 30 Finally, KC1 supplementation could decrease plasma norepinephrine concentration in NaCl-loaded stroke-prone spontaneously hypertensive rats. 14 The present observation with respect to hemodynamics is in keeping with our previous report, 5 namely, that the increase in blood pressure with NaCl loads in hypertensive patients might be attributed to the increase in cardiac output.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic and endocrine changes associated with potassium supplementation in sodium-loaded hypertensives.

Fujita¹,

Ando²

1984

Hypertension

108

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SUMMARY To clarify the mechanism by which potassium (KC1) protects against the blood pressure rising action of sodium (NaCl), we studied the effects of KC1 loading in patients with idiopathic hypertension who, after a period of NaCl restriction, partook of a high NaCl diet. Eleven patients who had taken the KC1 supplement (96 mEq/day) during the high NaCl period showed lesser mean blood pressure (MAP) rise with changes in NaCl intake from 25 to 250 mEq/day than 12 patients who had not taken the KCI supplement (p < 0.001). With a high NaCl diet, the KCl-supplemented patients retained less NaCl, gained less weight, and showed a lesser increase in plasma volume and cardiac output than the non-KCl-supplemented ones. Overall, the increase in blood pressure levels during the high Na diet correlated directly either with changes in plasma volume (p < 0.05) or with changes in cardiac output (p < 0.01). The results suggest that KCI may prevent a rise in blood pressure with NaCl loads in hypertensive patients by attenuating the increase in cardiac output, mainly as a result of the natriuresis. Furthermore, plasma norepinephrine was measured to estimate the sympathetic activity, since the sympathetic nervous system is known to control urinary NaCl excretion. From the low NaCl diet to Day 3 of the high NaCl diet, plasma norepinephrine was significantly (p < 0.01) decreased in the KCl-supplemented patients, whereas it remained unchanged in the non-KCl-supplemented ones. Concomitantly, urinary Na excretion was significantly greater in the early period of NaCl loading in the KCl-supplemented group as compared to the other group. Taken together, these results suggest that lower levels of norepinephrine measured in the plasma of the KCl-supplemented patients in the early NaCI-loading phases of the study are indicative of reduced adrenergic neural activity, which might be involved not only in the attenuation of increased cardiac output, but also in the responses of the kidney to shift the pressure-natriuresis relationship toward normal, leading to the natriuresis. (Hypertension 6: 184-192, 1984) KEY WORDS • sodium • potassium • norepinephrine • cardiac output N UMEROUS animal studies have presented evidence that the mechanisms by which excess salt (NaCl) intake increases blood pressure may include augmentation of sympathetic nerve activity and release of norepinephrine from adrenergic nerve endings.1 : Studies in humans also suggest that an excess of dietary NaCl may augment not only the vascular responsiveness to catecholamines,-1 but also the sympathetic nerve activity in hypertensive patients. 4 Recently, several investigators found hyperactivity of the sympathetic nervous system in hypertensive patients, who showed a considerable increase in blood pressure with NaCl loads.5 -6 Since sympathetic nerve activity is known to influence urinary Na

show abstract

Inhibition of adrenergic neurotransmission in isolated veins of the dog by potassium ions.

Cited by 76 publications

References 39 publications

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

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

Potassium ions and endothelium‐derived hyperpolarizing factor in guinea‐pig carotid and porcine coronary arteries

Hemodynamic and endocrine changes associated with potassium supplementation in sodium-loaded hypertensives.

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