In vitro perfusion studies of human resistance artery function in essential hypertension.

Falloon, B. J.; Heagerty, Anthony M.

doi:10.1161/01.hyp.24.1.16

Cited by 62 publications

(31 citation statements)

References 32 publications

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“…In established essential hypertension there is evidence of an increased pressor response to vasoconstrictors 34 ; however, sensitivity to vasoconstrictors seems to be unchanged. 35 Eliasson et al 36 found borderline hypertension to be associated with enhanced cardiovascular reactivity revealed by MST but not by orthostatic testing or cold pressor test in their comparison of groups of established and borderline hypertensives with normotensives. Jern 22 found a correlation between stress-induced increase in forearm blood flow and increased forearm glucose extraction during MST in nonobese normotensive men.…”

Section: Discussionmentioning

confidence: 97%

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

et al. 1998

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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 (rϭ0.55, Pϭ0.003), MFVR (rϭϪ0.58, Pϭ0.002), and WBV (rϭϪ0.39, Pϭ0.046 at shear rate 201 s Ϫ1 ). 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 (rϭ0.56, Pϭ0.002) and inversely with GDR (rϭϪ0.45, Pϭ0.018) and MFBF (rϭϪ0.49, Pϭ0.01) 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 (rϭ0.41, Pϭ0.036) and GDR (rϭϪ0.62, Pϭ0.001). 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. (Hypertension. 1998;32:838-843.)

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Section: Discussionmentioning

confidence: 97%

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

et al. 1998

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“…23 Small arteries 65 m to 230 m were isolated and carefully cleaned under a dissecting microscope. Vessels were transferred to an arteriograph bath chamber (Living Systems Instruments, Burlington, Vt), 23 cannulated, 24,25 and examined as described previously. 15 …”

Section: Pressure Arteriographymentioning

confidence: 99%

Effects of Angiotensin Type-1 Receptor Antagonism on Small Artery Function in Patients With Type 2 Diabetes Mellitus

Malik

Schofield²,

Izzard³

et al. 2005

Hypertension

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Abstract-Endothelial dysfunction has been demonstrated to occur in small arteries from patients with type 2 diabetes and hypertension. The effects of angiotensin II receptor blockade on vessel function were examined using pressure myography in a randomized 12-week double-blind placebo-controlled parallel group study using candesartan cilexitil. The maximal vascular response to acetylcholine (Ach) was impaired at baseline and improved with candesartan. This improvement was primarily caused by an effect in the nitric oxide component of Ach-mediated dilatation. The degree of endothelial dysfunction directly correlated with serum low-density lipoprotein cholesterol levels. Sodium nitroprusside-induced endothelium-independent dilatation was reduced in diabetic patients and intervention with candesartan lead to an improvement in EC50 with no change in maximal response.

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“…medium-sized conduit arteries 8 and in resistance arteries. 9,10 Nonhypertensive patients with symptoms of angina pectoris, but with normal coronary angiograms, have decreased flow-mediated dilatation (FMD) in the brachial artery during reactive hyperaemia, 11 as well as increased minimal forearm vascular resistance (FVR), 12 suggesting parallel vascular dysfunction in the coronary and peripheral vasculature. This parallel vascular dysfunction has also been identified by Leschke et al, 13 who found increased minimal FVR in hypertensive patients with reduced MFR.…”

Section: Introductionmentioning

confidence: 99%

Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension: a LIFE substudy

et al. 2004

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Impaired myocardial flow reserve (MFR) has been demonstrated in hypertension, and has been associated with peripheral vascular changes. We investigated whether MFR was impaired and associated with structural and/or functional vascular changes in hypertensive patients without evidence of coronary artery disease (CAD). We measured left ventricular (LV) mass index by echocardiography and MFR by positron emission tomography in 33 unmedicated, hypertensive patients with electrocardiographic LV hypertrophy without CAD, and 15 age-and gender-matched normotensive subjects. We also measured 24-h ambulatory blood pressure, minimal forearm vascular resistance (MFVR) by plethysmography, media:lumen ratio in isolated, subcutaneous resistance arteries by myography, intima-media crosssectional area of the common carotid artery, and flow-mediated (FMD) and nitroglycerin-induced dilatation (NID) of the brachial artery by ultrasound. Compared to the controls, the patients had impaired MFR (2.4 (95% CI 1.95-2.8) vs 3.4 (2.7-4.2), Po0.01) due to increased resting myocardial blood flow (MBF) (0.82 (0.73-0.91) vs 0.65 (0.56-0.75) ml/g min), and decreased dipyridamole-stimulated MBF (1.80 (1.55-2.1) vs 2.3 (1.80-2.8) ml/g min, both Po0.05). The difference in resting MBF disappeared (80 (74-87) vs 86 (74-97) ll/ kg mmHg, NS) when normalized for blood pressure and heart rate. MFR correlated negatively to median 24-h systolic blood pressure (r ¼ À0.50, Po0.01) as well as to LV mass index (r ¼ À0.45, Po0.05) and MFVR in men (r ¼ À0.47, Po0.05), and positively to FMD (r ¼ 0.44, Po0.05) and NID (r ¼ 0.40, Po0.05). Hypertensive patients with electrocardiographic LV hypertrophy without CAD had impaired MFR associated with cardiovascular hypertrophy and vasodilatory dysfunction. This suggests that MFR is impaired by LV hypertrophy and structural/functional vascular damage in the coronary and noncoronary circulation.

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In vitro perfusion studies of human resistance artery function in essential hypertension.

Cited by 62 publications

References 32 publications

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

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

Effects of Angiotensin Type-1 Receptor Antagonism on Small Artery Function in Patients With Type 2 Diabetes Mellitus

Association between vascular dysfunction and reduced myocardial flow reserve in patients with hypertension: a LIFE substudy

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