Effect of calculation stress on hemodynamics and plasma catecholamines before and after?-blockade with propranolol (inderal�) and mepindolol sulfate (CORINDOLAN�)

Bonelli, J; Hörtnagl, Heide; Brücke, T.; Magometschnigg, D; Lochs, Herbert; Kaik, G

doi:10.1007/bf00563551

Cited by 45 publications

(12 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is evidenced by the fact that plasma norepinephrine levels have been reported to increase,' decrease,' or not change 10 following beta-adrenergic blockade. Nonetheless, a number of studies in animals suggest that, in higher doses, propranolol exerts an additional antihypertensive action either through a decrease in sympathetic nerve activity via central mechanisms, 1113 or adrenergic nerve blockade.…”

Section: Hypertension Vol 3 No 1 January-february 1981mentioning

confidence: 96%

A possible antihypertensive mechanism of propranolol: antagonism of angiotensin II enhancement of sympathetic nerve transmission through prostaglandins.

Jackson¹,

Campbell²

1981

Hypertension

View full text Add to dashboard Cite

The effects of propranolol on angiotensin II (AH) enhancement of sympathetic nerve transmission were investigated in the in situ blood-perfused mesenteric vascular bed of the rat. Angiotensin II in sub-pressor concentrations (3 ng/ml) potentiated the vasoconstrictor responses to both sympathetic nerve stimulation (NS) and exogenous norepinephrine (NE). The dl-propranolol had no effect on the basal vasoconstrictor responses to NS and NE, yet inhibited the All-enhanced vasoconstrictor responses to NS by 47% (p < 0.0S) and 81% (p < 0.001) at 100 and 300 ng/ml respectively. In contrast, the potentiation of NE responses by AH was unaffected by propranolol. A similar blockade of All enhancement of NS was observed with the d-isomer of propranolol. Dibucaine (300 ng/ml), a local anesthetic, failed to alter the basal or AH-enhanced responses to either NS or NE. Indomethacin, a prostaglandin synthetase inhibitor (5 mg/kg, s.c), abolished the in-hibitory effect of dl-propranolol on AH enhancement of NS. Prostaglandin Ej (PGE,), but not prostaglandin Ii. (3 ng/ml) inhibited AH enhancement of NS without altering the basal response to NS or NE in indomethacin-pretreated animals. Intraarterial infusions of dl-propranolol, d-propranolol, AH, and dl-propranolol-plus-AII into the superior mesenteric artery increased mesenteric venous PGE, concentrations from 216 ± 33 to 355 i 33 (p < 0.01), 328 ± 44 (p < 0.05), 325 ± 27 (p < 0.02), and 407 ± 44 pg/ml (p < 0.01) respectively. We conclude that propranolol antagonizes AH enhancement of NS by increasing prostaglandin levels in vascular tissue. Furthermore, these findings suggest that propranolol may exert its an-tihypertensive effect through the release of prostaglandins when used in therapeutic doses in excess of those required for beta-adrenergic blockade. (Hypertension 3: 23-33, 1981) KEY WORDS • sympathetic nervous system • angiotensin II • vasoconstriction norepinephrine • propranolol • dibucaine • indomethacin • prostaglandins • antihypertensive activity P ROPRANOLOL, a beta-adrenergic antagonist , has gained wide acceptance as an antihy-pertensive drug. Despite this fact, the mechanism by which it exerts its antihypertensive effect still remains unclear. Michelakis and McAllister 1 were the first to report that propranolol lowered plasma renin activity (PRA) in hypertensive patients. Subsequently, Buhler and co-workers s reported that administration of propranolol to patients with low, normal, and high renin hyperten-sion resulted in a greater lowering of blood pressure From the (BP) in those patients with high renin hypertension. Furthermore, they noted that the fall in BP correlated with the suppression of renin release produced by the beta-adrenergic antagonist. From these studies they concluded that beta-adrenergic antagonists lowered BP through suppression of renin release. It should be mentioned, however, that other investigators have failed to find an association between suppression of renin release and the antihypertensive activity of propranolol. 3 In contrast, Pricha...

show abstract

Section: Hypertension Vol 3 No 1 January-february 1981mentioning

confidence: 96%

A possible antihypertensive mechanism of propranolol: antagonism of angiotensin II enhancement of sympathetic nerve transmission through prostaglandins.

Jackson¹,

Campbell²

1981

Hypertension

View full text Add to dashboard Cite

show abstract

“…The progressive fall in PNE from baseline to exercise to recovery that we observed with mental arithmetic parallels these changes, suggesting that a reduction in sympathetic discharge to muscle and an increase in norepinephrine clearance may obscure any increase in sympathetic activity elsewhere. Neither Bonelli et al 41 nor Hjemdahl and Eliasson 25 observed an increase in venous PNE during mental stress. The latter authors found that PNE was increased by tilting but not a color-word conflict test, although this test evoked greater increases in blood pressure and HR.…”

mentioning

confidence: 89%

“…Vasodilation occurs in skeletal muscles, and systemic vascular resistance falls. 41 ' *•** Sympathetic nerve discharge to muscle 33 and norepinephrine release from muscle 46 are reduced. The progressive fall in PNE from baseline to exercise to recovery that we observed with mental arithmetic parallels these changes, suggesting that a reduction in sympathetic discharge to muscle and an increase in norepinephrine clearance may obscure any increase in sympathetic activity elsewhere.…”

mentioning

confidence: 99%

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

Floras¹,

Jones²,

Hassan³

et al. 1986

Hypertension

View full text Add to dashboard Cite

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

show abstract

“…It is generally agreed that long-term treatment with ,Badrenoceptor blockers such as propranolol and labetalol causes an increase in the plasma concentration of adrenaline and noradrenaline (Christensen et al, , 1979Carlsen et al, 1980). Therefore it is of interest that Brecht et al (1976), Bonelli et al (1979) and Dominiak & Grobecker (1982) found that the plasma concentrations of catecholamines were reduced after treatment with pindolol, a nonselective 13-adrenoceptor blocker with ISA (Table 1).…”

mentioning

confidence: 99%

Beta‐adrenoceptor blockade and psychic stress in man. A comparison of the acute effects of labetalol, metoprolol, pindolol and propranolol on plasma levels of adrenaline and noradrenaline.

Trap‐Jensen¹,

Carlsen²,

Oj³

et al. 1982

Brit J Clinical Pharma

View full text Add to dashboard Cite

1 A random double-blind study was performed in healthy volunteers. The immediate effects of three different 3-adrenoceptor blocking agents, metoprolol, pindolol and propranolol, on the plasma concentrations of adrenaline and noradrenaline were compared in a situation of pleasant psychic stimulation during a television-game of tennis. The immediate effects of labetalol in a group of patients with arterial hypertension were studied in a similar experimental situation. 2 During psychic stress the plasma concentration of noradrenaline rose significantly by 85% after placebo, by 95% after labetalol, by 63% after metoprolol and by 55% after propranolol. After pindolol the noradrenaline concentration remained unchanged. 3 During psychic stress the plasma concentration of adrenaline rose significantly by 135% after labetalol, by 110% after metoprolol and by 83% after propranolol. After pindolol and placebo the adrenaline concentration remained unchanged. 4 The present results are taken to indicate that the intrinsic sympathomimetic activity possessed by pindolol prevents the rise in plasma noradrenaline normally seen during psychic stress. It is suggested that P-adrenoceptor blockers with strong intrinsic sympathomimetic effect reduce the release of catecholamines during psychic stress.

show abstract

Effect of calculation stress on hemodynamics and plasma catecholamines before and after?-blockade with propranolol (inderal�) and mepindolol sulfate (CORINDOLAN�)

Cited by 45 publications

References 11 publications

A possible antihypertensive mechanism of propranolol: antagonism of angiotensin II enhancement of sympathetic nerve transmission through prostaglandins.

A possible antihypertensive mechanism of propranolol: antagonism of angiotensin II enhancement of sympathetic nerve transmission through prostaglandins.

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

Beta‐adrenoceptor blockade and psychic stress in man. A comparison of the acute effects of labetalol, metoprolol, pindolol and propranolol on plasma levels of adrenaline and noradrenaline.

Contact Info

Product

Resources

About