Comparison of non‐invasive methods for the assessment of haemodynamic drug effects in healthy male and female volunteers: sex differences in cardiovascular responsiveness.

Wolzt, Michael; Schmetterer, Leopold; Rheinberger, A.; Salomon, Alexander K.; Unfried, C; Breiteneder, Helene; Ehringer, H; Eichler, H.-G.; Fercher, Adolf Friedrich

doi:10.1111/j.1365-2125.1995.tb04462.x

Cited by 43 publications

(28 citation statements)

References 28 publications

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“…Thus, premenopausal women seem to be protected against noradrenaline-induced vasoconstriction by counterregulatory beta 2 adrenoceptor-induced vasodilation. This corroborates experiments in the forearm vasculature [3][4][5] and is in good agreement with our previous results using the alpha adrenoceptor agonist phenylephrine, where no gender differences were seen 8 and the same experiments could also not reveal sex differences to nonspecific beta adrenoceptor stimulation by small doses of isoprenaline.…”

supporting

confidence: 81%

“…Again, these results are in accordance with previous studies. 8,9 These functional experiments also demonstrate that the vascular response caused by elevated luminal concentrations of noradrenaline is different from that released neuronally. 10 An increase in systemic plasma concentrations of noradrenaline by exogenous infusion by approximately nine-fold as compared to tyramine did only translate into a three-fold increased blood pressure response.…”

mentioning

confidence: 71%

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Endogenously and exogenously increased noradrenaline exerts sex-different responses in humans

et al. 2002

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confidence: 81%

mentioning

confidence: 71%

Endogenously and exogenously increased noradrenaline exerts sex-different responses in humans

et al. 2002

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“…Systemic hemodynamics. Blood pressure was measured by an automated oscillometric device on the upper arm at 15-min intervals during the study periods, and the pulse rate was monitored continuously by a finger pulseoxymetric device (CMS patient monitor; Hewlett Packard, Palo Alto, CA) (29). Statistical analysis.…”

Section: Methodsmentioning

confidence: 99%

Plasma Ghrelin Concentrations Are Not Regulated by Glucose or Insulin

Schaller¹,

Schmidt

Pleiner³

et al. 2003

Diabetes

185

117

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Ghrelin plasma concentrations increase during fasting and fall rapidly after nutrient ingestion. We hypothesized that insulin or glucose could regulate ghrelin secretion by a feedback mechanism. In this randomized, double-blind, placebo-controlled crossover study, three different study days were carried out in nine healthy volunteers (age 26 ؎ 6 years). On each day, stepwise increasing systemic glucose concentrations of 5.0, 8.3, and 11.1 mmol/l were attained by intravenous infusion of glucose, representing fasting and postprandial conditions. Ghrelin plasma concentration was studied during concomitant exogenous hyperinsulinemia, inhibition of endogenous insulin production by somatostatin infusion, and placebo time control, respectively. Elevated glucose concentrations increased circulating insulin to 612 ؎ 85 pmol/l (P < 0.01), but they did not affect ghrelin concentrations. Prolonged hyperinsulinemia by exogenous infusion resulted in circulating insulin of 1,602 ؎ 261 pmol/l (P < 0.01) and suppressed plasma ghrelin to 49.6% of baseline (P < 0.01). During administration of somatostatin, insulin concentration remained constant, but an even greater decrease in ghrelin to 39.5% of baseline was noted (P < 0.01). Hyperglycemia does not decrease ghrelin, and a reduction in ghrelin is only seen at supraphysiological insulin concentrations. In contrast, systemic ghrelin concentrations are decreased by somatostatin. The meal-related suppression of ghrelin appears not directly regulated by glucose or insulin.

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“…Systolic and diastolic blood pressures were measured on the upper arm by an automated oscillometric device. Pulse rate was automatically recorded from a finger pulseoxymetric device (HP-CMS patient monitor; Hewlett Packard, Palo Alto, CA) (Wolzt et al, 1995).…”

Section: Methodsmentioning

confidence: 99%

Specific Endothelin ET_A Receptor Antagonism Does Not Modulate Insulin-Induced Hemodynamic Effects in the Human Kidney, Eye, or Forearm

Rab

Dallinger²,

Polak³

et al. 2004

J Pharmacol Exp Ther

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There is evidence that hyperinsulinemia may stimulate endothelin-1 (ET-1) generation or release, which may affect diabetic vascular complications. BQ-123, a specific ET A receptor antagonist, was used to investigate if insulin-induced vascular effects are influenced by an acute ET-1 release. Two randomized, placebo-controlled, double-blind, cross-over studies were performed. In protocol 1, 12 healthy subjects received, on separate study days, infusions of BQ-123 (60 g/min for 30 min) during placebo clamp conditions, BQ-123 during euglycemic hyperinsulinemia (3 mU/kg/min for 390 min), or placebo during euglycemic hyperinsulinemia. Fundus pulsation amplitude (FPA) was measured to assess pulsatile choroidal blood flow, and mean flow velocity (MFV) of the ophtalmic artery was measured by color Doppler imaging. In protocol 2, eight healthy subjects received, on separate study days, intra-arterial infusions of BQ-123 (32 g/min for 120 min) during placebo or insulin clamp. Forearm blood flow was measured with bilateral plethysmography, expressing the ratio of responses in the intervention arm and in the control arm. Insulin alone increased FPA (ϩ10%, p Ͻ 0.001) and forearm blood flow (ϩ19%). BQ-123 increased FPA, MFV, and forearm blood flow ratio in the absence and presence of exogenous insulin, but this effect was not different between normo-and hyperinsulinemic conditions. ET-1 plasma concentrations were not affected by insulin. In conclusion, these data do not support the concept that hyperinsulinemia increases ET-1 generation in healthy subjects. Our results, however, cannot necessarily be extrapolated to diabetic and obese subjects.It has been reported that plasma endothelin-1 (ET-1) concentrations are significantly increased in some patients with type I (Takahashi et al., 1990) and type II diabetes mellitus (Laurenti et al., 1997), which may contribute to the vascular complications in diabetes. Several studies demonstrated that insulin can stimulate ET-1 release in endothelial cell cultures (Metsä rinne et al., 1994;. In addition, hyperinsulinemia elevates plasma ET-1 levels in rats (Hokanson et al., 1975), suggesting increased production and/or secretion of ET-1. This effect of insulin on circulating ET-1 levels was confirmed in obese patients (Wolpert et al., 1993) and type II diabetic patients but was not seen in healthy subjects during a standard glucose tolerance test (Leyva et al., 1997) or during mild hyperinsulinemia (Metsä rinne et al., 1994).We decided to rechallenge the question of whether insulin may stimulate ET-1 release in healthy subjects for several reasons. On the one hand, studies of the effect of hyperinsulinemia on circulating ET-1 levels may be of limited value since ET-1 is predominantly a paracrine modulator of vascular tone (Webb, 1997). Hence, ET-1 plasma concentrations do not necessarily predict the level of vascular ET-1 activity. Furthermore, ET-1 concentrations are subject to considerable within-subject variability (Jilma et al., 1997). Thus, determination of ET-1 plasma lev...

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Comparison of non‐invasive methods for the assessment of haemodynamic drug effects in healthy male and female volunteers: sex differences in cardiovascular responsiveness.

Cited by 43 publications

References 28 publications

Endogenously and exogenously increased noradrenaline exerts sex-different responses in humans

Endogenously and exogenously increased noradrenaline exerts sex-different responses in humans

Plasma Ghrelin Concentrations Are Not Regulated by Glucose or Insulin

Specific Endothelin ET_A Receptor Antagonism Does Not Modulate Insulin-Induced Hemodynamic Effects in the Human Kidney, Eye, or Forearm

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Comparison of non‐invasive methods for the assessment of haemodynamic drug effects in healthy male and female volunteers: sex differences in cardiovascular responsiveness.

Cited by 43 publications

References 28 publications

Endogenously and exogenously increased noradrenaline exerts sex-different responses in humans

Endogenously and exogenously increased noradrenaline exerts sex-different responses in humans

Plasma Ghrelin Concentrations Are Not Regulated by Glucose or Insulin

Specific Endothelin ETA Receptor Antagonism Does Not Modulate Insulin-Induced Hemodynamic Effects in the Human Kidney, Eye, or Forearm

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Specific Endothelin ET_A Receptor Antagonism Does Not Modulate Insulin-Induced Hemodynamic Effects in the Human Kidney, Eye, or Forearm