Acute effects of insulin on cardiovascular function and noradrenaline uptake and release

Christensen, N. J.

doi:10.1007/bf00282513

Cited by 64 publications

(29 citation statements)

References 34 publications

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“…First, MSNA increased during the low insulin dose when blood glucose values remained constant. Second, Berne et al (13) have reported that intravenous administration of D-glucose does not markedly increase MSNA in humans.…”

Section: Discussionmentioning

confidence: 98%

“…Elevated plasma norepinephrine during insulin infusion could reflect increased sympathetic nerve activity, facilitated norepinephrine release from nerve terminals, decreased neuronal reuptake, or altered peripheral metabolism of norepinephrine (13). Experiments in animals demonstrate that insulin can increase sympathetic neural outflow by altering glucose metabolism in ventromedial hypothalamic neurons (14).…”

Section: Introductionmentioning

confidence: 99%

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Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans.

Anderson¹,

Hoffman²,

Balon³

et al. 1991

J. Clin. Invest.

1,033

608

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Hyperinsulinemia may contribute to hypertension by increasing sympathetic activity and vascular resistance. We sought to determine if insulin increases central sympathetic neural outflow and vascular resistance in humans. We recorded muscle sympathetic nerve activity (MSNA; microneurography, peroneal nerve), forearm blood flow (plethysmography), heart rate, and blood pressure in 14 normotensive males during 1-h infusions of low (38 mU/m2/min) and high (76 mU/m2/min) doses of insulin while holding blood glucose constant. Plasma insulin rose from 8±1 uU/ml during control, to 72±8 and 144±13 MtU/ml during the low and high insulin doses, respectively, and fell to 15±6 gU/ml 1 h after insulin infusion was stopped.MSNA, which averaged 21.5±1.5 bursts/min in control, increased significantly (P < 0.001) during both the low and high doses of insulin (±5.4 and ±9.3 bursts/min, respectively) and further increased during 1-h recovery (+15.2 bursts/min). Plasma norepinephrine levels (119±19 pg/ml during control) rose during both low (258±25; P < 0.02) and high (285±95; P < 0.01) doses of insulin and recovery (316±23; P < 0.01). Plasma epinephrine levels did not change during insulin infusion. Despite the increased MSNA and plasma norepinephrine, there were significant (P < 0.001) increases in forearm blood flow and decreases in forearm vascular resistance during both doses of insulin. Systolic pressure did not change significantly during infusion of insulin and diastolic pressure fell -4-5 mmHg (P < 0.01). This study suggests that acute increases in plasma insulin within the physiological range elevate sympathetic neural outflow but produce forearm vasodilation and do not elevate arterial pressure in normal humans. (J. Clin. Invest.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans.

Anderson¹,

Hoffman²,

Balon³

et al. 1991

J. Clin. Invest.

1,033

608

View full text Add to dashboard Cite

show abstract

“…15 - 17 The lack of a significant insulin-blood pressure relation in clipped animals indicates that hypertension was maintained by mechanisms that neither involved nor impacted on the insulin-glucose axis. This finding suggests that neither blood pressure elevation per se nor mechanisms similar to those involved in the development of short-term renovascular hypertension (e.g., activation of the renin-angiotensin system) can be invoked to explain the insulin-blood pressure relation in normal animals.…”

Section: Discussionmentioning

confidence: 99%

Glucose tolerance and insulin action in rats with renovascular hypertension.

et al. 1991

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To test whether hypertension can cause hyperinsulinemia or insulin resistance, we performed intravenous glucose tolerance tests at 1 month and euglycemic clamps at 3 months after induction of two-kidney, one clip renovascular hypertension in rats. At 1 month, systolic pressure was higher in 21 clipped than in 12 control animals (161 ±5 mm Hg, range 134-187 mm Hg versus 119±3 mm Hg, range 108-146 mm Hg;p<0.001). Glucose tolerance, assessed as the glucose fractional disappearance rate between 3 and 11 minutes after the glucose injection, was similar in the clipped and sham groups (0.059±0.002 versus 0.056±0.002 min" 1 , respectively,p>0.4). The total area under the insulin curve during glucose tolerance tests was also similar in the clipped and sham groups (926 ±95 versus 869 ±126 microunits/mlxmin; p>0.4). There was no significant relation between systolic blood pressure and insulin area during glucose tolerance tests in the clipped group, but there was a positive rectilinear relation in the control group (r=0.66;p=0.01). Fourteen animals had euglycemic clamps 2 months after glucose tolerance tests. At that time, systolic pressure (direct femoral measurement) was higher in the seven clipped animals (189±13 mm Hg versus 122±5 mm Hg in controls; p<0.001). Insulin infusions of 1 and 4 milliunits/min/kg body wt effected similar plasma insulin levels in the two groups. Glucose requirements during 1 milliunit/min/kg insulin were higher in the clipped than the control group (6.1 ±0.7 versus 2.4±0.6 mg/min/kg, respectively; p<0.001). Glucose requirements during 4 milliunits/min/kg insulin were similar in the two groups (28.4±1.1 versus 26.8±2.8 mg/min/kg; p>0.5). Our data indicate that neither mechanisms leading to renovascular hypertension nor elevated blood pressure per se caused sustained hyperinsulinemia or insulin resistance in this rat model. (Hypertension 1991;18:341-347)

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“…Tolbutamide in doses inducing hypoglycaemia has increased islet blood flow [16], whereas mild hypoglycaemia induced by starvation decreased islet blood perfusion [2]. Some of these discrepancies can be explained by the vasodilatory properties of insulin [17,18,19] and tolbutamide [20,21]. We investigated the effects of insulin-induced hypoglycaemia and of 2-deoxy glucose, which inhibits neuronal uptake of glucose and thereby induces a neuronal glucopenia [22,23] on islet blood flow.…”

mentioning

confidence: 99%

Hypoglycaemia induces decreased islet blood perfusion mediated by the central nervous system in normal and Type 2 diabetic GK rats

et al. 2003

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Aims/hypothesis. The aim of this study was to evaluate the effects of induced hypoglycaemia on pancreatic-islet blood flow in normal rats and in the GK rat, an animal model of Type 2 diabetes which normally has an increased islet blood perfusion. Methods. A 50% reduction in blood glucose concentrations was achieved by intravenous administration of a rapidly acting insulin (15 IU/kg body weight). Blood flows were measured by a non-radioactive microsphere technique. Results. A pronounced decrease in islet blood flow was observed in all animals, but preferentially in the Type 2 diabetic GK rats. When a similar dose of insulin was given to whole-pancreas transplanted rats only islet blood flow in the native pancreas was decreased, whereas that of the transplanted, i.e. denervated, pancreas was unchanged. Administration of 2-deoxy-Dglucose, which induces intracellular glucopenia especially in neurons, also decreased islet blood flow despite a systemic hyperglycaemia. Conclusion/interpretation. Hypoglycaemia leads to a preferential decrease in pancreatic-islet blood perfusion. The effect is probably mediated by the central nervous system, since 2-deoxy D-glucose-induced neuronal glucopenia caused a similar decrease in blood flow. The effects of islet blood flow are not likely to be mediated by nervous stimulation of the adrenal glands, with an associated release of catecholamines, because the transplanted pancreas was not affected by hypoglycaemia. The decreased islet blood perfusion could possibly diminish the output of insulin from the islets, thereby preventing a further decrease in blood glucose concentrations. [Diabetologia (2003[Diabetologia ( ) 46:1124[Diabetologia ( -1130

show abstract

Acute effects of insulin on cardiovascular function and noradrenaline uptake and release

Cited by 64 publications

References 34 publications

Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans.

Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans.

Glucose tolerance and insulin action in rats with renovascular hypertension.

Hypoglycaemia induces decreased islet blood perfusion mediated by the central nervous system in normal and Type 2 diabetic GK rats

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