scholarly journals EvidenceIn VivoShowing Increase of Baseline Nitric Oxide Generation and Impairment of Endothelium-Dependent Vasodilation in Normotensive Patients on Chronic Hemodialysis

2000 ◽  
Vol 11 (9) ◽  
pp. 1726-1734 ◽  
Author(s):  
JENS PASSAUER ◽  
ECKHART BÜSSEMAKER ◽  
URSULA RANGE ◽  
MARIA PLUG ◽  
PETER GROSS
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Forearm Blood Flow ◽  
Matched Control ◽  
Venous Occlusion ◽  
Chronic Hemodialysis ◽  
Invasive Technique ◽  
Vascular Effects ◽  
Control Subjects ◽  
Pharmacologic Agents

Abstract.Cardiovascular mortality is excessive in hemodialyzed patients. Observations in atherosclerosis suggest that endothelial dysfunction and impaired nitric oxide (NO) may be involved. However, the relation of endothelial NO to its vascular effects has not been studied conclusively in uremia. Therefore, to study these questions an invasive technique was used in normotensive patients who were on hemodialysis (HD;n= 11) and in matched control subjects (n= 11). Pharmacologic agents were infused into the brachial artery to test the chain of events from NO generation to smooth muscle cell relaxation, measuring forearm blood flow by venous occlusion plethysmography. Glyceroltrinitrate (GTN 1:2.2 nmol/min; GTN 2:4.4; GTN 3:8.8), infused to establish the reaction of the vessel wall to defined doses of NO, caused a reduced response in HD patients (control subjects: 183 ± 20 [SEM], 246 ± 26, and 338 ± 29%; HD patients: 161 ± 7, 206 ± 12, and 262 ± 24%; baseline = 100% for each group,P= 0.032 by ANOVA). All subsequent data were corrected for this decreased response to defined doses of NO in HD patients. L-arginine (10 mg/min), given to exclude substrate deficiency of NO synthase (NOS), caused no significant changes (control subjects: 108 ± 4%; HD patients: 103 ± 4%;P= NS). Acetylcholine (ACH 1:55 nmol/min; ACH 2:110; ACH 3:220), infused to stimulate endothelial NOS, had a significantly reduced effect in HD patients (control subjects: 246 ± 32, 340 ± 40, and 465 ± 52%; HD patients: 251 ± 55, 244 ± 36, and 318 ± 50%;P= 0.002).N-monomethyl-L-arginine (LMA 1:1 μmol/min; LMA 2:2; LMA 3:4), given to block baseline NO generation, showed an enhanced response in HD patients (control subjects: 90 ± 2, 83 ± 2, and 74 ± 4%; HD patients: 84 ± 3, 73 ± 3, and 64 ± 4%;P= 0.037). Vascular response to three doses of norepinephrine (60, 120, and 240 pmol/min) was comparable in both groups, which indicated similar endothelium-independent vasoconstriction. In summary, in normotensive HD patients, (1) vasodilation to defined doses of exogenous NO was reduced, (2) there was no evidence of substrate deficiency of NOS, and (3) stimulation of NOS was impaired; however, (4) baseline NO generation was increased. It is concluded that in HD patients, the NO system has a reduced capacity to regulate vascular tone and this impairment is most significant under conditions of NOS stimulation.

Vasoconstrictor Sensitivity to Noradrenaline and NG-monomethyl-l-arginine in Men and Women

1997 ◽  
Vol 93 (6) ◽  
pp. 513-518 ◽  
Author(s):  
Barry J. Kneale ◽  
Philip J. Chowienczyk ◽  
John R. Cockcroft ◽  
D. John Coltart ◽  
James M. Ritter
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Animal Studies ◽  
Vascular Tone ◽  
Forearm Blood Flow ◽  
Premenopausal Women ◽  
Relative Sensitivity ◽  
Venous Occlusion ◽  
Men And Women ◽  
Arterial Blood

1. Nitric oxide has potential anti-atherogenic actions as well as regulating vascular tone. Animal studies suggest that there are sex differences in basal nitric oxide biosynthesis, but it is not known whether such differences exist between men and women. 2. We have investigated this question by measuring forearm blood flow responses, using venous occlusion plethysmography, to brachial artery infusion of NG-monomethyl-l-arginine (an inhibitor of NO biosynthesis) and noradrenaline in 40 healthy subjects (20 men and 20 premenopausal women). Mean arterial blood pressure was 89 ± 10 mmHg (mean ± SD) in men and 87 ± 9 mmHg in women, and mean total cholesterol was 4.25 ± 0.99 mmol/l (mean ± SD) and 4.26 ± 0.80 mmol/l respectively. 3. In men, vasoconstrictor responses to NG-monomethyl-l-arginine, 1–4 μmol/min (15–28% mean reduction in blood flow), were consistently less than responses to noradrenaline, 60–240 pmol/min (26–37%), whereas in women, vasoconstrictor responses to NG-monomethyl-l-arginine (19–30%) were consistently greater than those to noradrenaline(11–17%). The sex difference in relative sensitivity to vasoconstrictors was significant (P < 0.001). 4. Our findings are consistent with either greater sensitivity to noradrenaline in men compared with premenopausal women, or a greater basal nitric oxide biosynthesis in premenopausal women compared with men.

scholarly journals Agonist-dependent variablity of contributions of nitric oxide and prostaglandins in human skeletal muscle

2005 ◽  
Vol 98 (4) ◽  
pp. 1251-1257 ◽  
Author(s):  
William G. Schrage ◽  
Niki M. Dietz ◽  
John H. Eisenach ◽  
Michael J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Animal Studies ◽  
Forearm Blood Flow ◽  
Feedback Inhibition ◽  
Venous Occlusion ◽  
No Synthase ◽  
Human Forearm ◽  
Independent Mechanism ◽  
Treatment Order

The relative contributions of endothelium-dependent dilators [nitric oxide (NO), prostaglandins (PGs), and endothelium-derived hyperpolarizing factor (EDHF)] in human limbs are poorly understood. We tested the hypothesis that relative contributions of NO and PGs differ between endothelial agonists acetylcholine (ACh; 1, 2, and 4 μg·dl−1·min−1) and bradykinin (BK; 6.25, 25, and 50 ng·dl−1·min−1). We measured forearm blood flow (FBF) using venous occlusion plethysmography in 50 healthy volunteers (27 ± 1 yr) in response to brachial artery infusion of ACh or BK in the absence and presence of inhibitors of NO synthase [NOS; with NG-monomethyl-l-arginine (l-NMMA)] and cyclooxygenase (COX; with ketorolac). Furthermore, we tested the idea that the NOS + COX-independent dilation (in the presence of l-NMMA + ketorolac, presumably EDHF) could be inhibited by exogenous NO administration, as reported in animal studies. FBF increased ∼10-fold in the ACh control; l-NMMA reduced baseline FBF and ACh dilation, whereas addition of ketorolac had no further effect. Ketorolac alone did not alter ACh dilation, but addition of l-NMMA reduced ACh dilation significantly. For BK infusion, FBF increased ∼10-fold in the control condition; l-NMMA tended to reduce BK dilation ( P < 0.1), and addition of ketorolac significantly reduced BK dilation. Similar to ACh, ketorolac alone did not alter BK dilation, but addition of l-NMMA reduced BK dilation. To test the idea that NO can inhibit the NOS + COX-independent portion of dilation, we infused a dose of sodium nitroprusside (NO-clamp technique) during ACh or BK that restored the reduction in baseline blood flow due to l-NMMA. Regardless of treatment order, the NO clamp restored baseline FBF but did not reduce the NOS + COX-independent dilation to ACh or BK. We conclude that the contribution of NO and PGs differs between ACh and BK, with ACh being more dependent on NO and BK being mostly dependent on a NOS + COX-independent mechanism (EDHF) in healthy young adults. The NOS + COX-independent dilation does not appear sensitive to feedback inhibition from NO in the human forearm.

Forearm Vascular Response to Nitric Oxide and Calcitonin Gene- Related Peptide: Comparison between Migraine Patients and Control Subjects

Cephalalgia ◽  
2006 ◽  
Vol 26 (1) ◽  
pp. 56-63 ◽  
Author(s):  
JNJM de Hoon ◽  
P Smits ◽  
J Troost ◽  
HAJ Struijker-Boudier ◽  
LMAB Van Bortel
Keyword(s):  
Nitric Oxide ◽  
Vascular Function ◽  
Venous Occlusion ◽  
Calcitonin Gene Related Peptide ◽  
Vascular Response ◽  
No Donor ◽  
Related Peptide ◽  
Control Subjects ◽  
Calcitonin Gene ◽  
Endogenous Release

The forearm vascular response to nitric oxide (NO) and calcitonin gene-related peptide (CGRP) was investigated in 10 migraine patients and 10 matched control subjects. Changes in forearm blood flow (FBF) during intrabrachial infusion of: (i) serotonin (releasing endogenous NO), (ii) sodium nitroprusside (SNP, exogenous NO-donor), and (iii) CGRP were measured using venous occlusion plethysmography. Flow-mediated dilation (FMD) of the brachial artery, a measure for the endogenous release of NO reactive to occlusion, was measured using ultrasound and expressed as percentage change vs. baseline diameter. FBF ratio (i.e. FBF in the infused over the control arm) at baseline (1.1 ± 0.1) did not differ between both populations. Serotonin, SNP and CGRP induced a dose-dependent increase ( P < 0.001) in FBF ratio in controls (to 2.8 ± 0.3, 6.7 ± 1.4 and 6.9 ± 1.2 at the highest dose, respectively) and migraineurs (2.5 ± 0.4, 5.6 ± 0.8 and 6.5 ± 1.3, respectively); these ratios did not differ between both groups. FMD was comparable in control subjects (5.8 ± 1%) and migraine patients (5.2 ± 1%). Based on the forearm vascular response to NO and CGRP, migraine patients do not display generalized changes in vascular function.

Rho kinase contributes to basal vascular tone in humans: role of endothelium-derived nitric oxide

2007 ◽  
Vol 293 (1) ◽  
pp. H541-H547 ◽  
Author(s):  
E. Büssemaker ◽  
Frank Pistrosch ◽  
Sarah Förster ◽  
Kay Herbrig ◽  
Peter Gross ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Rho Kinase ◽  
Calcium Sensitivity ◽  
Venous Occlusion ◽  
Dependent Manner ◽  
Endothelin 1 ◽  
Mlc Phosphorylation ◽  
Constrictor Response

Our objective was to determine the role of the Rho-associated kinase (ROK) for the regulation of FBF (FBF) and to unmask a potential role of ROK for the regulation of endothelium-derived nitric oxide (NO). Moreover, the effect of fasudil on the constrictor response to endothelin-1 was recorded. Regarding background, phosphorylation of the myosin light chain (MLC) determines the calcium sensitivity of the contractile apparatus. MLC phosphorylation depends on the activity of the MLC kinase and the MLC phosphatase. The latter enzyme is inhibited through phosphorylation by ROK. ROK has been suggested to inhibit NO generation, possibly via the inhibition of the Akt pathway. In this study, the effect of intra-arterial infusion of the ROK inhibitor fasudil on FBF in 12 healthy volunteers was examined by venous occlusion plethysmography. To unmask the role of NO, fasudil was infused during NO clamp. As a result, fasudil markedly increased FBF in a dose-dependent manner from 2.34 ± 0.21 to 6.96 ± 0.93 ml/100 ml forearm volume at 80 μg/min ( P < 0.001). At 1,600 μg/min, fasudil reduced systolic, diastolic, and mean arterial pressure while increasing heart rate. Fasudil abolished the vasoconstrictor effect of endothelin-1. The vascular response to fasudil (80 μmol/min) was blunted during NO clamp (104 ± 18% vs. 244 ± 48% for NO clamp + fasudil vs. fasudil alone; data as ratio between infused and noninfused arm with baseline = 0%, P < 0.05). In conclusion, 1) basal peripheral and systemic vascular tone depends on ROK; 2) a significant portion of fasudil-induced vasodilation is mediated by NO, suggesting that vascular bioavailable NO is negatively regulated by ROK; and 3) the constrictor response to endothelin involves the activation of ROK.

Abstract 1286: Neuronal Nitric Oxide Synthase Regulates Basal Vascular Tone in the Healthy Human Forearm in vivo.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Mike Seddon ◽  
Phil Chowienczyk ◽  
Barbara Casadei ◽  
Ajay Shah
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Vascular Tone ◽  
Venous Occlusion ◽  
No Synthase ◽  
Healthy Human ◽  
Vasodilator Response ◽  
Nos Inhibitors ◽  
Human Forearm

Nitric oxide (NO) has an established role in the maintenance of vascular tone, generally assumed to be mediated by endothelial NO synthase (eNOS). Previous studies using the non-selective NOS inhibitor N G monomethyl-L-arginine (L-NMMA) in humans confirmed the in vivo importance of NO but the contribution of neuronal NO synthase (nNOS) is unknown due to the lack of available selective NOS inhibitors for human use. In this study, we investigated for the first time in humans the effects of S-methyl-L-thiocitrulline (SMTC), a competitive nNOS-selective inhibitor with 17-fold selectivity over eNOS. SMTC or L-NMMA were infused into the brachial artery of healthy male volunteers and forearm blood flow was measured by venous occlusion plethysmography. SMTC 0.025, 0.05, 0.1 and 0.2 μmol/min caused a dose-dependent reduction in basal blood flow in the infused arm of 9.2±1.9, 16.2±2.9, 22.9±3.9 and 30.1±3.8% respectively (n=10; mean±SE; all P<0.01). Substantially higher doses of L-NMMA of 0.5, 1, 2 and 4 μmol/min were required to reduce basal flow by 11.5±3.0, 25.1±3.0, 33.7±3.0 and 37.4±3.1% respectively (n=10). The highest dose of SMTC (ie, 0.2 μmol/min) tested had no significant effect on the vasodilator response to acetylcholine (ACh): Ach 40 and 80nmol/min increased blood flow by 3.93±0.64 and 5.54±0.69 ml/min/100mls tissue above baseline during saline co-infusion versus 3.95±0.69 and 4.90±0.71 ml/min/100mls tissue during SMTC co-infusion (n=10; P=NS). In contrast, L-NMMA significantly reduced the response to these doses of ACh by 64±9.9 and 60±10% (n=10; both P<0.01). The effect of SMTC on basal blood flow was completely abolished in the presence of the NOS substrate L-arginine (n=6; P<0.001) but was unaffected by the stereoisomer D-arginine (n=6). SMTC had no effect on the vasodilator response to sodium nitroprusside (n=5). In conclusion , SMTC reduced basal blood flow by stereospecific inhibition of the L-arginine:NO pathway but did not affect the eNOS-mediated vasodilator response to ACh. These results indicate that nNOS has a crucial role in the regulation of basal vascular tone in the human forearm in vivo .

Ageing is associated with impairment of nitric oxide and prostanoid dilator pathways in the human forearm

2002 ◽  
Vol 102 (5) ◽  
pp. 595-600 ◽  
Author(s):  
Nivedita SINGH ◽  
Sanjay PRASAD ◽  
Donald R.J. SINGER ◽  
Raymond J. Mac ALLISTER
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Area Under The Curve ◽  
Venous Occlusion ◽  
Response Curves ◽  
Age Related ◽  
Older Subjects ◽  
Synthase Inhibitor ◽  
Dose Dependent

Ageing is associated with endothelial dysfunction and increased cardiovascular risk. We assessed the activity of nitric oxide (NO) and prostaglandin pathways in older subjects. Bilateral venous occlusion plethysmography was used to measure forearm blood flow during intra-arterial infusion of the NO synthase inhibitor, NG-monomethyl-l-arginine (l-NMMA; 1, 2 and 4μmol/min), the cyclo-oxygenase inhibitor, aspirin (3, 9 and 30μmol/min), and the smooth muscle constrictor, noradrenaline (60, 120 and 240pmol/min); each dose infused for 5min. Eighteen young and 15 healthy older subjects (mean age±S.E.M., 32±1 and 65±1 years respectively) were studied. Effects of treatment were calculated from the ratio of blood flow in the infused to control arm, expressed as a percentage. Dose-response curves were compared by analysis of the area under the curve (AUC) using independent samples t test. All agents caused dose-dependent decreases in basal forearm blood flow. AUC values for noradrenaline, aspirin and l-NMMA in younger and older subjects were 162±24, 173±24 and 170±17, and 138±22, 70±22 and 89±22 respectively. Effects of aspirin and l-NMMA, but not noradrenaline, were reduced in older subjects (P = 0.004, 0.007 and 0.461 respectively). Our findings suggest a generalized abnormality of basal endothelial function in older people, with similar impairment of NO and prostanoid dilator pathways. Defects in both pathways could contribute to the development of age-related cardiovascular disease.

Comparison of Forearm Vasodilatation to Substance P and Acetylcholine: Contribution of Nitric Oxide

1997 ◽  
Vol 92 (2) ◽  
pp. 133-138 ◽  
Author(s):  
David E. Newby ◽  
Nicholas A. Boon ◽  
David J. Webb
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Substance P ◽  
Cell Function ◽  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Nitric Oxide Synthase Inhibitor ◽  
Endothelial Cell Function ◽  
Synthase Inhibitor ◽  
Oxide Synthase

1. Forearm blood flow responses to incremental challenges of acetylcholine and substance P, administered via the brachial artery, were measured by venous occlusion plethysmography in eight subjects in the presence of saline, the nitric oxide synthase inhibitor, NG-monomethyl-l-arginine, and a control vasoconstrictor, noradrenaline. 2. Substance P and acetylcholine caused dose-dependent increases in forearm blood flow (P < 0.001). When separated by 30 min saline infusions, repeated responses did not undergo tachyphylaxis. 3. Noradrenaline caused a mean reduction in basal blood flow of 34–51% (P < 0.001), and augmented the percentage increases in blood flow with both substance P (P = 0.05) and acetylcholine (P = 0.03) infusions. 4. NG-Monomethyl-l-arginine caused a mean reduction in basal blood flow of 42–45% (P < 0.001) and significantly inhibited the responses to both substance P (P < 0.001) and acetylcholine (P = 0.05). 5. In comparison with saline responses, NG-monomethyl-l-arginine caused a mean inhibition of 69 ± 8% for substance P-induced vasodilatation and 40 ± 5% for acetylcholine-induced vasodilatation. However, comparing responses with those to the control vasoconstrictor noradrenaline, NG-monomethyl-l-arginine caused a mean inhibition of 81 ± 5% for substance P responses and 58 ± 3% for acetylcholine responses. Inhibition by NG-monomethyl-l-arginine of the response to substance P was significantly greater than inhibition of the response to acetylcholine (P = 0.02). 6. Hence, in healthy men, a greater proportion of the forearm vasodilatation to substance P than to acetylcholine appears to be nitric oxide-mediated. Given its greater stability, substance P may be more suitable as a pharmacological tool in the investigation of stimulated nitric oxide production and endothelial cell function.

Direct effect of ethanol on human vascular function

2004 ◽  
Vol 286 (6) ◽  
pp. H2468-H2473 ◽  
Author(s):  
Ahmed Tawakol ◽  
Torbjørn Omland ◽  
Mark A. Creager
Keyword(s):  
Nitric Oxide ◽  
Dose Response ◽  
Vascular Function ◽  
Human Subjects ◽  
Venous Occlusion ◽  
Response Curves ◽  
Vascular Effects ◽  
Healthy Human ◽  
Ethanol Infusion ◽  
Healthy Human Subjects

Epidemiological studies indicate that moderate ethanol consumption reduces cardiovascular mortality. Cellular and animal data suggest that ethanol confers beneficial effects on the vascular endothelium and increases the bioavailability of nitric oxide. The purpose of this study was to assess the effect of ethanol on endothelium-dependent, nitric oxide-mediated vasodilation in healthy human subjects. Forearm blood flow (FBF) was determined by venous occlusion plethysmography in healthy human subjects during intra-arterial infusions of either methacholine (0.3, 1.0, 3.0, and 10.0 mcg/min, n = 9), nitroprusside (0.3, 1.0, 3.0, and 10.0 mcg/min, n = 9), or verapamil (10, 30, 100, and 300 mcg/min, n = 8) before and during the concomitant intra-arterial infusions of ethanol (10% ethanol in 5% dextrose). Additionally, a time control experiment was conducted, during which the methacholine dose-response curve was measured twice during vehicle infusions ( n = 5). During ethanol infusion, mean forearm and systemic alcohol levels were 227 ± 30 and 6 ± 0 mg/dl, respectively. Ethanol infusion alone reduced FBF (2.5 ± 0.1 to 1.9 ± 0.1 ml·dl−1·min−1, P < 0.05). Despite initial vasoconstriction, ethanol augmented the FBF dose-response curves to methacholine, nitroprusside, and verapamil ( P < 0.01 by ANOVA for each). To determine whether this augmented FBF response was related to shear-stress-induced release of nitric oxide, FBF was measured during the coinfusion of ethanol and NG-nitro-l-arginine (l-NAME; n = 8) at rest and during verapamil-induced vasodilation. The addition of l-NAME did not block the ability of ethanol to augment verapamil-induced vasodilation. Ethanol has complex direct vascular effects, which include basal vasoconstriction as well as potentiation of both endothelium-dependent and -independent vasodilation. None of these effects appear to be mediated by an increase in nitric oxide bioavailability, thus disputing findings from preclinical models.

Basal nitric oxide production is impaired in offspring of patients with essential hypertension

1999 ◽  
Vol 97 (2) ◽  
pp. 141-147 ◽  
Author(s):  
A. S. McALLISTER ◽  
A. B. ATKINSON ◽  
G. D. JOHNSTON ◽  
D.R. HADDEN ◽  
P. M. BELL ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Essential Hypertension ◽  
Endothelial Dysfunction ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Competitive Inhibitor ◽  
Venous Occlusion ◽  
Limited Data ◽  
Vasoconstrictor Response ◽  
Normotensive Subjects

There is considerable evidence that endothelium-dependent nitric oxide (NO)-mediated vasodilatation in response to acetylcholine is impaired in essential hypertension, whereas the endothelium-independent response to sodium nitroprusside is normal. More limited data have suggested that there is also reduced vasoconstriction in response to NG-monomethyl-⌊-arginine (⌊-NMMA), a competitive inhibitor of basal NO release. As it is not known whether endothelial dysfunction in hypertension, if indeed present, is a cause or consequence of the condition, we have studied the normotensive offspring of parents with essential hypertension. Both basal and stimulated vascular responses were examined in 12 normotensive offspring [mean age (°S.E.M.) 26.1°1.4 years] of parents with essential hypertension and compared with those in 12 age-matched offspring (mean age 25.6°1.1 years) of normotensive subjects. Forearm blood flow was measured simultaneously in both arms by venous occlusion plethysmography, both at baseline and during intra-arterial brachial infusion of increasing doses of acetylcholine, sodium nitroprusside, noradrenaline and ⌊-NMMA. There were no significant differences between the groups in the responses to acetylcholine, sodium nitroprusside or noradrenaline. In contrast, the vasoconstrictor response to l-NMMA was significantly blunted in the offspring of hypertensive parents compared with that in the offspring of normotensive parents (P = 0.005). Thus endothelial dysfunction, as demonstrated by impaired basal production of NO, is present in subjects at high risk of essential hypertension, and does not occur simply as a consequence of the condition.

Calf and forearm blood flow in patients with primary hyperparathyroidism and in control subjects

1991 ◽  
Vol 124 (5) ◽  
pp. 553-555
Author(s):  
P. D. Broulik ◽  
J. Spáĉil
Keyword(s):  
Blood Flow ◽  
Clinical Study ◽  
Primary Hyperparathyroidism ◽  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Ionized Calcium ◽  
Control Subjects ◽  
And Control ◽  
Peak Blood

Abstract. Using a venous occlusion air-filled plethysmograph we measured the blood flow in the limbs in 10 patients with established primary hyperparathyroidism and control subjects. The patients had highly raised ionized calcium and immunoreactive parathormone levels, and the diagnosis was verified at operation. In all patients resting blood flow values in the limbs were increased compared with control subjects. Peak blood flow after 5 min of ischemia was also increased, however, not significantly. This clinical study supports previous studies on a vasoactive effect of parathormone.

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