Relation between the rate of stimulation and the quantity of noradrenaline liberated from sympathetic nerve endings in the isolated perfused spleen of the cat.

Haefely, W.; Hürlimann, A.; Thoenen, H.

doi:10.1113/jphysiol.1965.sp007744

Cited by 61 publications

(21 citation statements)

References 9 publications

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“…As already shown for the inhibition of release induced by a-receptor agonists, there was a relationship between the frequency of nerve Gillespie, 1957;Kirpekar & Cervoni, 1963;Haefely, Hurlimann & Thoenen, 1965;Langer, 1970;Dubocovich & Langer, 1974;Langer et al, 1975a;Dubocovich & Langer, 1976). …”

Section: Introductionmentioning

confidence: 79%

Sixth Gaddum Memorial Lecture National Institute for Medical Research, Mill Hill, January 1977

Langer

1977

British J Pharmacology

917

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Section: Introductionmentioning

confidence: 79%

Sixth Gaddum Memorial Lecture National Institute for Medical Research, Mill Hill, January 1977

Langer

1977

British J Pharmacology

917

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“…Early reports of a relationship between resting PNE concentrations and blood pressure have not been confirmed consistently. 9 ' "~1 3 Several factors may account for this. Differences between subjects in norepinephrine reuptake, clearance, or conjugation make the interpretation of individual or group comparisons of PNE concentrations difficult.…”

mentioning

confidence: 99%

“…Norepinephrine concentration in the venous drainage of an organ is also proportional to the rate of stimulation of its nerves. 3 In humans, physical and emotional stimuli that increase blood pressure and heart rate (HR) also increase PNE. …”

mentioning

confidence: 99%

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Failure of plasma norepinephrine to consistently reflect sympathetic activity in humans.

Floras¹,

Jones²,

Hassan³

et al. 1986

Hypertension

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SUMMARY To determine whether venous plasma norepinephrine concentrations consistently reflect changes in sympathetic nervous activity, the influence of mental arithmetic, static handgrip, and submaximal bicycle exercise on infra-arterial blood pressure, heart rate, and plasma norepinephrine was studied in 51 subjects with untreated essential hypertension (mean age, 46 years; range, 16-69 years). At rest, plasma norepinephrine was unrelated to age or blood pressure. Mental arithmetic increased mean arterial pressure from 108 ± 18 to 127 ± 18 mm Hg (mean ± S.D.; p<0.001) and heart rate from 69 ± 7 to 93 ± 13 beats/min (p<0.001) but not plasma norepinephrine (547 ± 297 to 518 ± 250 pg/ml). Isometric exercise raised mean arterial pressure from 115 ± 18 to 148 ± 21 mm Hg (p<0.001) and heart rate from 76 ± 9 to 95 ± 13 beats/min (p<0.001) but not plasma norepinephrine (683 ± 253 to 741 ± 253 pg/ml). Bicycle exercise increased mean arterial pressure from 114 ± 20 to 146 ± 26 mm Hg (p< 0.001), heart rate from 77 ± 9 to 128 ± 19 beats/min (p< 0.001), and plasma norepinephrine from 645 ± 228 to 1151 ± 462 pg/ml (p<0.001). Both the maximum mean arterial pressure and the peak heart rate attained during bicycle exercise were related to the exercise plasma norepinephrine level (r = 0.33, p<0.02 and r=0.28, p<0.03, respectively). Increases in plasma norepinephrine with exercise were not greater in older or more hypertensive subjects. In fact, the relative rise in mean arterial pressure and the absolute increase in plasma norepinephrine during cycling were greater in those with lower resting blood pressures. As only bicycle exerdse increased plasma norepinephrine, and as there was no direct relationship between plasma norepinephrine and arterial blood pressure in subjects studied supine, seated, and during these three activities, we conclude that plasma norepinephrine concentrations do not consistently reflect variations in sympathetic neuronal activity and therefore are relatively insensitive measures of sympathetic tone in humans. Received March 25, 1985; accepted January 21, 1986. Norepinephrine concentration in the venous drainage of an organ is also proportional to the rate of stimulation of its nerves. 3 In humans, physical and emotional stimuli that increase blood pressure and heart rate (HR) also increase PNE. "7 Conversely, concentrations of this catecholamine may be reduced in subjects with autonomic nervous dysfunction 8 or lowered by drugs that interfere with the action of the sympathetic nervous system. 9 Watson et al., 6 who recorded PNE and blood pressure in hypertensive subjects while they slept, lay quietly, woke, stood, walked, and cycled, described a log-linear relationship between PNE and systolic blood pressure during these activities, which suggests that PNE concentrations indeed reflect changes in sympathetic activity.Although increases in PNE with exertion may be greater in some subjects with essential hypertension, 10

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“…Nearly the same ratio is arrived at when calculations are carried out for the cat spleen, using data from Haefely, Hurliman & Thoenen (1965). In the presence of phenoxybenzamine and cocaine, and with a frequency of stimulation of 4/sec, 5 ng transmitter were released per pulse, or 0-5 ng/g.…”

Section: Noradrenaline From Nictitating Membrane 169mentioning

confidence: 99%

Noradrenaline release from isolated muscles of the nictitating membrane of the cat

Langer¹,

Vogt²

1971

The Journal of Physiology

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SUMMARY1. When the splanchnic nerves were stimulated in the cat for periods of up to 2 hr, the amount of adrenaline taken up by the nictitating membrane was very small; the highest figure was 0 37 ,tg/g, corrected for losses.2. The noradrenaline (NA) stores of the isolated medial muscle of the nictitating membrane were labelled with [3H]NA, and field stimulation of single muscles was carried out in a small organ bath. A stimulation period of 5 min with supramaximal shocks delivered at a frequency of 25/sec produced a mean release of NA into the bath fluid of 0 46 + 0413 ,ug/g (uncorrected). Phenoxybenzamine, 10 jug/ml., increased this figure by a factor of 2-3*6. When corrections were made for the amount of transmitter metabolized before it could be collected, 47 % of the tissue content of NA were shown to be released during the 5 min stimulation of the normal membrane, and about 55 % in the presence of phenoxybenzamine.

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Relation between the rate of stimulation and the quantity of noradrenaline liberated from sympathetic nerve endings in the isolated perfused spleen of the cat.

Cited by 61 publications

References 9 publications

Sixth Gaddum Memorial Lecture National Institute for Medical Research, Mill Hill, January 1977

Sixth Gaddum Memorial Lecture National Institute for Medical Research, Mill Hill, January 1977

Failure of plasma norepinephrine to consistently reflect sympathetic activity in humans.

Noradrenaline release from isolated muscles of the nictitating membrane of the cat

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