Showing papers by "Sverre E. Kjeldsen published in 1998"

Whole-blood viscosity and the insulin-resistance syndrome.

Abstract: BackgroundIn a previous study we found that elevated blood viscosity was linked to the insulin resistance syndrome, and we proposed that high blood viscosity may increase insulin resistance. That study was based on calculated viscosity.ObjectiveTo determine whether directly measured whole-blood visc

Hypertension Optimal Treatment (HOT) Study : Home blood pressure in treated hypertensive subjects

Abstract: —The Hypertension Optimal Treatment Study is a prospective trial conducted in 26 countries. The aims are to (1) evaluate the relationship between three levels of target office diastolic blo...

Relationship Between Insulin Sensitivity and Maximal Forearm Blood Flow in Young Men

Abstract: Insulin resistance is a part of the metabolic cardiovascular syndrome. We aimed to test the hemodynamic hypothesis of insulin resistance, which suggests that a decreased skeletal muscle blood supply with subsequent reduced nutritional flow causes insulin resistance in skeletal muscle. We assessed determinants of peripheral blood flow such as maximal forearm blood flow (MFBF), minimal forearm vascular resistance (MFVR), and whole blood viscosity (WBV) in 27 young men with borderline elevation of blood pressure. Insulin sensitivity measured as glucose disposal rate (GDR) correlated with MFBF (r=0.55, P=0.003), MFVR (r=-0.58, P=0. 002), and WBV (r=-0.39, P=0.046 at shear rate 201 s-1). There was no correlation between GDR and myocardial thickness or left ventricular mass. In a stepwise multiple regression analysis, MFVR and WBV explained 54% of the variation in GDR. The relative increase in mean arterial blood pressure during a mental stress test, as a marker of reactivity or an alert reaction, was correlated with MFVR (r=0.56, P=0.002) and inversely with GDR (r=-0.45, P=0.018) and MFBF (r=-0.49, P=0.01) but not with cardiac dimensions. In a stepwise multiple regression analysis, 48% of the increase in blood pressure during a mental stress test was explained by MFVR and WBV. Fasting insulin correlated with MFVR (r=0.41, P=0.036) and GDR (r=-0.62, P=0.001). These data show a positive association between the appearance of peripheral structural vascular changes as quantified through a hemodynamic technique and insulin resistance in young men with borderline elevation of blood pressure. The cause-effect relationship of this finding needs further evaluations.

Clustering of coronary risk factors with increasing blood pressure at rest and during exercise

Abstract: BackgroundThe metabolic cardiovascular syndrome is the label given to the clustering of unfavourable levels of a number of coronary risk factors in subjects with high resting blood pressures We found recently that exercise blood pressure had a strong independent prognostic valueObjectiveTo search

Circulating levels of endothelin-1 during acute hyperinsulinemia in patients with essential hypertension treated with type 1 angiotensin receptor antagonist or placebo

Abstract: Insulin and angiotensin II (Ang II) are involved in the regulation of endothelin-1 (ET-1). This study investigates their possible influence on plasma levels of ET-1 in humans. Twenty patients with essential hypertension were included in a randomized, double-blind, placebo-controlled crossover study of 4 weeks' treatment with losartan, a selective type 1 angiotensin (AT1) receptor antagonist. The effect was evaluated in the fasting state and during acute hyperinsulinemia physiologically induced by oral glucose ingestion (OGTT) and by euglycemic glucose clamp. Losartan lowered blood pressure significantly, but did not influence plasma levels of ET-1 in the fasting condition (5.2 +/- 0.2 fmol/mL on placebo and 5.6 +/- 0.3 fmol/mL after losartan treatment). During both models of acute hyperinsulinemia, there was a significant decrease in plasma ET-1. In the OGTT the mean values after placebo treatment decreased from 5.2 +/- 0.2 fmol/mL at time 0 to 4.7 +/- 0.4 (P = .001) and 4.0 +/- 0.5 (P = .001) at 60 and 120 minutes, respectively. During the clamp the mean ET-1 values decreased from 5.7 +/- 0.4 fmol/mL at time 0 to 4.6 +/- 0.2 (P < .001) and 4.3 +/- 0.3 (P = .006) at 60 and 120 minutes, respectively. No differences in these profiles occurred after losartan treatment. Significant inverse correlation between fasting levels of ET-1 and insulin sensitivity index was found, r = -.51, P = .003. In conclusion, losartan did not influence the circulating levels of ET-1 in basal condition or during acute hyperinsulinemia, whereas a significant decrease in plasma ET-1 occurred during acute hyperinsulinemia. A significant inverse correlation demonstrated between basal levels of plasma ET-1 and the insulin-stimulated glucose uptake could point to a possible regulatory influence of ET-1 production on glucose metabolism or vice versa.

Insulin modifies the glucose response to mental stress independently of forearm blood flow.

Abstract: In the present study we aimed to reproduce and extend our recent finding that insulin infusion modifies the glucose response to mental stress and to determine whether the altered glucose response, i.e. glucose uptake, may be explained by a rise in forearm blood flow (FBF). The subjects were borderline hypertensive; there was one former blood pressure measurement > or =140/90 mm Hg, but otherwise they were healthy 21-year-old men. In the first series (n = 18) the subjects were exposed to a 5-min mental arithmetic stress test prior to (MST-1) and at the end of (MST-2) 120 min of hyperinsulinemic glucose clamp. Blood glucose was unchanged (0.067+/-0.05 mmol/l, p = 0.24) during MST-1 and decreased (-0.37+/-0.09 mmol/l, p = 0.001) during MST-2. Blood glucose also decreased in a second series (n = 28) in which the subjects were exposed to MST after 120 min of glucose clamp (-0.33+/-0.09 mmol/l , p = 0.001), and FBF increased from 4.4+/-0.4 to 7.7+/-1.1 ml/min/100 ml (p<0.0001). Glucose was unchanged (p = 0.48) in response to MST in a saline time control group (n = 8). However, FBF increased in response to MST from 3.7+/-0.5 to 7.0+/-1.2 ml/min/100 ml (p<0.01). The increase in FBF averaged 3.3 ml/min/100 ml in both groups. Serum insulin remained unchanged in response to MST in controls, but decreased in response to MST during insulin infusion in both series (p = 0.04 and p = 0.004, respectively). The fall in glucose in response to MST during insulin infusion correlated with glucose disposal rate (GDR) (r = -0.40, p = 0.034, n = 28) and inversely with fasting insulin (r = 0.52, p = 0.004, n = 28). Thus, insulin infusion alters the glucose response to mental stress, i.e. there is a decrease in blood glucose concentration concomitant with an increased uptake. This glucose uptake is unrelated to FBF, but related to higher skeletal muscle insulin sensitivity and inversely to the fasting insulin level. Our data therefore suggest that infused insulin modifies the stress response through a mechanism at the tissue level. It may be speculated whether insulin counteracts unfavourable effects of mental stress and sympathetic activation on glucose metabolism.