Clinical pharmacology, physiology and pathophysiology of superficial veins‐2.

Aellig, W. H.

doi:10.1111/j.1365-2125.1994.tb04357.x

Cited by 51 publications

(49 citation statements)

References 183 publications

(116 reference statements)

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“…There was wide interindividual variability in response, with the range of the ED 50 spanning several log units, as occurs with other agonists. 18 The ED 50 ranged from 0.08 ng/min to 256 ng/min, and the geometric mean (95% CI) was 1.91 ng/min (0.042 to 87.1 ng/min), with an E max of 74.5Ϯ17.72% (nϭ37).…”

Section: Hand Vein Response To Dexmedetomidinementioning

confidence: 99%

“…26 The hand vein model, however, is useful in defining agonist-receptor relations in vivo while minimizing the effects of systemic exposure to agonists and the potentially confounding reflex responses. 18,20 In addition, ␣ 2 -AR venous response is important in its own right, since as the chief capacitance compartment, the venous bed has profound effects on cardiac filling, which in turn is an important determinant of cardiac output, especially in patients with heart failure.…”

Section: Muszkat Et Al Ethnicity and Vascular ␣ 2 -Adrenoceptor Responsementioning

confidence: 99%

“…including adrenergic vasodilators and vasoconstrictors, 18,20 but study of the ␣ 2 -AR in vivo has been hampered by the lack of an potent and selective agonist. Several investigators have used clonidine to study human vascular ␣ 2 -AR responses.…”

Section: Muszkat Et Al Ethnicity and Vascular ␣ 2 -Adrenoceptor Responsementioning

confidence: 99%

“…18 This instrument, when mounted on the hand, measures and records changes in the diameter of the vein. Subjects rested on a comfortable bed and remained supine throughout the study.…”

Section: Measurement Of Vascular Responsesmentioning

confidence: 99%

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Alpha ₂ -Adrenergic Receptor–Induced Vascular Constriction in Blacks and Whites

et al. 2004

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Abstract-Black Americans have a reduced hypotensive response to the ␣ 2 -adrenergic receptor agonist clonidine compared with whites, despite similar central sympathoinhibition. This reduced hypotensive response might be explained by greater postsynaptic vascular ␣ 2 -adrenergic receptor vasoconstrictive response. However, clonidine has a low ␣ 2 /␣ 1 selectivity ratio. Therefore, to determine the role of altered ␣ 2 -adrenergic receptor vascular sensitivity in ethnic differences in vascular response, we compared local vascular responses with the highly selective ␣ 2 -adrenergic receptor agonist dexmedetomidine in healthy black (nϭ18) and white (nϭ19) subjects. Increasing doses of dexmedetomidine (0.001 to 1000 ng/min) were infused into a dorsal hand vein, and the local response was measured with a linear variable differential transformer. Dexmedetomidine caused pronounced venoconstriction, with an average (ϮSD) maximum response of 74.5Ϯ17.72% but with no difference between blacks and whites. There was substantial intersubject variability in the sensitivity to dexmedetomidine; the dose resulting in 50% (ED 50 ) of maximum vasoconstriction ranged from 0.08 ng/min to 256 ng/min. The geometric mean ED 50 was 2.28 ng/min (95% CI, 0.02 to 271.6 ng/min) in blacks and 1.58 ng/min (95% CI, 0.11 to 24.55 ng/min) in whites (Pϭ0.59). Our data indicate that ␣ 2 -adrenergic receptor-induced venoconstriction is similar in blacks and whites. These findings do not support the hypothesis that altered ␣ 2 -adrenergic receptor sensitivity is the explanation for the decreased blood pressure response to systemic administration of clonidine in blacks. The response to dexmedetomidine provides a model that will allow further study of the regulation of Key Words: adrenergic receptor agonists Ⅲ ethnicity Ⅲ human Ⅲ receptors, adrenergic, alpha Ⅲ vasoconstriction Ⅲ veins H ypertension is more prevalent and more severe in black Americans and is associated with greater morbidity and mortality rates. 1 Several environmental and genetic factors have been suggested to contribute. 2 Many investigators have observed that blood pressure responses to stress are higher in normotensive black than white subjects. [3][4][5] This finding suggests that ethnic differences exist, either in regulation of sympathetic activity or in vascular response to the same degree of sympathetic activation. In keeping with this possibility is the observation that the decrease in blood pressure in response to antihypertensive drugs acting through adrenergic mechanisms is smaller in blacks. 6,7 We and others have previously examined the hypothesis that there are ethnic differences in sympathetic activation and vascular response. On balance, there do not appear to be differences between well-matched black and white subjects in sympathetic activity, either at rest or after stimulation, measured by means of two complementary techniques, norepinephrine spillover and muscle sympathetic nerve activity. 8 -10 However, several different groups have reported ethnic differences in ...

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Section: Hand Vein Response To Dexmedetomidinementioning

confidence: 99%

Section: Muszkat Et Al Ethnicity and Vascular ␣ 2 -Adrenoceptor Responsementioning

confidence: 99%

Section: Muszkat Et Al Ethnicity and Vascular ␣ 2 -Adrenoceptor Responsementioning

confidence: 99%

“…18 This instrument, when mounted on the hand, measures and records changes in the diameter of the vein. Subjects rested on a comfortable bed and remained supine throughout the study.…”

Section: Measurement Of Vascular Responsesmentioning

confidence: 99%

See 2 more Smart Citations

Alpha ₂ -Adrenergic Receptor–Induced Vascular Constriction in Blacks and Whites

et al. 2004

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“…Should Fls considerably enhance the action of norepinephrine or otherwise cause vasoconstriction, it would probably elevate blood pressure in arterial hypertension. Although some degree of venous tone does exist in vivo [17,18], there is no convincing evidence that it can be significantly influenced by Fls.…”

Section: Sirmentioning

confidence: 99%

The potential use of flavonoids as venoactive drugs and the role of citrus fruits

Jargin¹

2018

J Intercult Ethnopharmacol

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Effects of different congestion pressures on the diameter of the dorsal hand vein and on its apparent sensitivity to noradrenaline

Abdelmawla

Langley

Szabadi

et al. 1996

Naunyn-Schmiedeberg's Arch Pharmacol

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We have measured the diameter of the human dorsal hand vein (DHV) in situ and compared the venoconstrictor dose-response curves to locally infused noradrenaline at different venous congestion pressures using the DHV compliance technique. Congestion pressure was defined as the inflation pressure of a sphygmomanometer cuff on the ipsilateral upper arm. Male healthy volunteers (20-45 years) participated in two experimental sessions. In Session I, DHV diameter was measured at congestion pressures of 20, 25, 30, 35, 40, 45, 50, 55, 60, 65, 70 mmHg. In Session II, venoconstrictor dose-response curves to six doses (0.1-33.33 ng min-1) of (-)noradrenaline acid tartrate were established at congestion pressures 30 and 45 mmHg. DHV diameter increased as a function of congestion pressure. The rate of increase in DHV diameter (mm/5 mmHg) declined at higher values of congestion pressure (e.g. 0.14 mm/5 mmHg between 20 and 45 mmHg, and 0.04 mm/5 mmHg between 45 and 70 mmHg). Noradrenaline was less potent at 45 mmHg than at 30 mmHg. Mean log ED50 was significantly greater at 45 mmHg than at 30 mmHg congestion pressure, while mean E(max) did not differ at the two congestion pressures. The geometric mean ED50 was approximately 195% greater at 45 mmHg than at 30 mmHg. These results show that DHV diameter is positively related to congestion pressure, and that as the congestion pressure increases, the apparent sensitivity of the vein to the venoconstrictor effect of noradrenaline decreases. This latter finding is consistent with the physiological antagonism between congestion-induced venodilatation and noradrenaline-evoked venoconstriction. It is recommended that a standard congestion pressure is used in order to facilitate the comparison of results obtained in different laboratories.

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Clinical pharmacology, physiology and pathophysiology of superficial veins‐2.

Cited by 51 publications

References 183 publications

Alpha ₂ -Adrenergic Receptor–Induced Vascular Constriction in Blacks and Whites

Alpha ₂ -Adrenergic Receptor–Induced Vascular Constriction in Blacks and Whites

The potential use of flavonoids as venoactive drugs and the role of citrus fruits

Effects of different congestion pressures on the diameter of the dorsal hand vein and on its apparent sensitivity to noradrenaline

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Clinical pharmacology, physiology and pathophysiology of superficial veins‐2.

Cited by 51 publications

References 183 publications

Alpha 2 -Adrenergic Receptor–Induced Vascular Constriction in Blacks and Whites

Alpha 2 -Adrenergic Receptor–Induced Vascular Constriction in Blacks and Whites

The potential use of flavonoids as venoactive drugs and the role of citrus fruits

Effects of different congestion pressures on the diameter of the dorsal hand vein and on its apparent sensitivity to noradrenaline

Contact Info

Product

Resources

About

Alpha ₂ -Adrenergic Receptor–Induced Vascular Constriction in Blacks and Whites

Alpha ₂ -Adrenergic Receptor–Induced Vascular Constriction in Blacks and Whites