Clinical pharmacology, physiology and pathophysiology of superficial veins‐1.

Aellig, W. H.

doi:10.1111/j.1365-2125.1994.tb04341.x

Cited by 72 publications

(55 citation statements)

References 3 publications

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“…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%

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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: 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%

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

et al. 2004

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“…The dorsal hand vein technique provides a sensitive, easy and reproducible means of assessing the effect of drugs on peripheral veins. The effects of oral drugs on venoconstrictor response caused by the infusion of a vasoconstricting agent can be detected without affecting systemic hemodynamics, 9 because the measurement is made within the vicinity of the infusion site, allowing the amount of the agent to be extremely small. The venoconstrictor response of dorsal hand veins to phenylephrine or noradrenaline is reported to reflect the responsiveness of the foot vein 29 and the overall vascular system.…”

Section: Discussionmentioning

confidence: 99%

“…24 Although measurements obtained with a laser Doppler flowmeter are of a relative nature, the method is particularly appropriate for the study of local skin vasomotor responses in human subjects. 9,25 Cold stimulation rapidly increases an endogenous noradrenaline concentration, which, in turn, causes -adrenoceptor-mediated vasoconstriction and a reduction in blood flow. 26 This method is used for the evaluation of autonomic failure, 25,27,28 including Shy-Drager syndrome, Parkinson's disease, amyloidosis and diabetic neuropathy.…”

Section: Discussionmentioning

confidence: 99%

“…7,8 Second, the venoconstrictor response to locally infused noradrenaline was examined using a linear variable differential transformer (LVDT), which provides a sensitive and easy reproducible means of assessing the effect of a drug on peripheral veins. 9 As the decrease in venous blood return to the heart is involved in the pathogenesis of orthostatic hypotension, 3 it is interesting to also examine the effect of these drugs on veins.…”

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Effect of Amezinium Metilsulfate on the Finger Skin Vasoconstrictor Response to Cold Stimulation and Venoconstrictor Response to Noradrenaline

et al. 1998

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hen a person assumes an upright posture, an increase of sympathetic outflow and an inhibition of parasympathetic activity occur reflexly, 1,2 which increases the heart rate and vascular resistance in order to maintain systemic blood pressure. Orthostatic hypotension may be caused by failure of these responses, 3,4 and for the treatment it is important to select a drug considering its pharmacological properties and the pathophysiology of the disease. At present, vasoconsticting agents are often used for the treatment of orthostatic hypotension. To understand the mechanism of these drugs, their effects not only on systemic blood pressure but also on the vasoconstrictor response to sympathetic stimulation should be examined. However, to our knowledge, such information is limited.Amezinium metilsulfate (amezinium) is one of the most popular drugs in Japan for the treatment of orthostatic hypotension. Amezinium has a unique mechanism of vasoconstriction; that is, it inhibits monoamine oxidase (MAO) activity and uptake of noradrenaline, 5,6 which prompted us to examine whether it influences the vasoconstrictor response to sympathetic stimulation and to -adrenoceptor stimulation by noradrenaline in humans.To examine the effects of the drug, the following 2 methods were thought to be suitable and were used in the present study, because they are sensitive and noninvasive and are used for the evaluation of autonomic disturbances or orthostatic hypotension. First, the finger-tip vasoconstrictor response to cold stimulation on the contralateral hand was examined using a laser Doppler flowmeter, which is an appropriate means for the study of the vasomotor response mediated by -adrenoceptor stimulation. 7,8 Second, the venoconstrictor response to locally infused noradrenaline was examined using a linear variable differential transformer (LVDT), which provides a sensitive and easy reproducible means of assessing the effect of a drug on peripheral veins. 9 As the decrease in venous blood return to the heart is involved in the pathogenesis of orthostatic hypotension, 3 it is interesting to also examine the effect of these drugs on veins.In the present study, we examined, using these methods, the effects of amezinium on the vasoconstrictor responses, and compared them in healthy subjects with those of midodrine hydrochloride (midodrine), an 1-adrenoceptor agonist, 10 which is also a popular drug for orthostatic hypotention. Methods SubjectsEight healthy Japanese males (21-26 years, 64-78 kg) were selected. They were normotensive and nonsmokers, without concomitant medication for at least 2 weeks before the study. The study was approved by the Ethical Committee of Jichi Medical School and all subjects gave their informed consent.Jpn Circ J 1998; 62: 824 -828 (Received April 10, 1998; revised manuscript received July 9, 1998; accepted July 14, 1998 Orthostatic hypotension can be caused by an inadequate vasoconstrictor response. The effects of amezinium on vasoconstrictor response to sympathetic stimulation and to exogenous noradre...

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No Evidence of a Direct Venodilatory Effect of Furosemide in Healthy Human Subjects

Harada

Ohmori

Fujimura

et al. 1996

The Journal of Clinical Pharma

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The present study was undertaken to examine whether furosemide, a loop diuretic, has a direct venodilatory effect in healthy male subjects. Furosemide, or amrinone, an inotropic agent with a vasodilatory action, was infused into a dorsal hand vein that had been preconstricted by phenylephrine. The diameter of the vein was measured by a linear variable differential transformer. Venodilation was observed during the infusion of amrinone, but such a response was not detected with furosemide. These findings do not support the hypothesis that furosemide has a direct venodilatory effect in healthy human subjects.

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Clinical pharmacology, physiology and pathophysiology of superficial veins‐1.

Cited by 72 publications

References 3 publications

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

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

Effect of Amezinium Metilsulfate on the Finger Skin Vasoconstrictor Response to Cold Stimulation and Venoconstrictor Response to Noradrenaline

No Evidence of a Direct Venodilatory Effect of Furosemide in Healthy Human Subjects

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Clinical pharmacology, physiology and pathophysiology of superficial veins‐1.

Cited by 72 publications

References 3 publications

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

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

Effect of Amezinium Metilsulfate on the Finger Skin Vasoconstrictor Response to Cold Stimulation and Venoconstrictor Response to Noradrenaline

No Evidence of a Direct Venodilatory Effect of Furosemide in Healthy Human Subjects

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

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