<i>Work of Digital Vasoconstriction Produced by Infused Norepinephrine in Primary Hypertension</i>

Mendlowitz, Milton; Naftchi, Nosrat E.

doi:10.1152/jappl.1958.13.2.247

Cited by 67 publications

(19 citation statements)

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“…Contrariwise, Mendlowitz and Naftchi (14), Barany and James (7), and Doyle, Fraser and Marshall (15) reported increased reactivity in hypertension; Duff (16) reported no increased sensitivity to epinephrine in "benign hypertension" but increased reactivity in "progressive or malignant hypertension." Greisman (17) found that the capillary bed of the nailfold of patients with essential hypertension was hyperreactive to infused l-norepinephrine.…”

Section: Reactivity Of Renal and Systemic Circulations To Vasoconstrimentioning

confidence: 99%

Reactivity of Renal and Systemic Circulations to Vasoconstrictor Agents in Normotensive and Hypertensive Subjects*

Gombos¹,

Hulet²,

Bopp³

et al. 1962

J. Clin. Invest.

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Section: Reactivity Of Renal and Systemic Circulations To Vasoconstrimentioning

confidence: 99%

Reactivity of Renal and Systemic Circulations to Vasoconstrictor Agents in Normotensive and Hypertensive Subjects*

Gombos¹,

Hulet²,

Bopp³

et al. 1962

J. Clin. Invest.

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“…Moreover, no generalized defect in monamine oxidase (16) or catechol-O-methyltransferase (11, 14, 15) activity could be detected. The observations that these patients (13), as well as a relatively large number of their children (17), possessed abnormally high vascular reactivity to infused NE remained unexplained.…”

Section: Discussionmentioning

confidence: 99%

“…Since no clear-cut evidence of NE overproduction could be found (8)(9)(10), and since physiologic studies suggested that essential hypertension was associated with abnormally increased vascular reactivity to infused NE (13), it seemed possible that the disease might be causally related to abnormal metabolic handling of that NE produced in normal quantities by these patients. To evaluate the metabolism of a substance that underwent degradation within moments of its administration and which produced an intense physiologic effect in nanogram amounts, a tracer compound of high * Submitted for publication December 26, 1963; accepted July 1, 1964. Aided by grants from the U. S. Public Health Service, National Heart Institute, grant HE-06546 (CV), and the New York Heart Association.…”

mentioning

confidence: 99%

Plasma Clearance of dl-β-H3-Norepinephrine in Normal Human Subjects and Patients with Essential Hypertension*

Gitlow¹,

Mendlowitz²,

Wilk³

et al. 1964

J. Clin. Invest.

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In 1936 hemodynamic measurements in patients with essential hypertension suggested the presence of a functional increase in peripheral vasoconstriction producing an abnormally high peripheral resistance to blood flow (1). The concept that physiologic degrees of vasoconstriction were maintained by the adrenergic neurohumor, norepinephrine (NE), was proposed almost simultaneously (2), but it was nearly 10 years later that von Euler (3, 4), Holtz, Credner, and Kroneberg (5), and others demonstrated that NE was normally present in and released by mammalian sympathetic nerves. Within a year, Goldenberg and co-workers (6) suggested that essential hypertension might be caused by the simple overproduction of NE. This neurohumoral theory underwent repeated evaluation, first by the measurement of NE in urine (7, 8) and plasma (9), and later by the assay in urine of the major NE catabolites, vanillylmandelic acid (VMA) (10), normetanephrine (NM) (11), and 3-methoxy, 4-hydroxyphenyl glycol (NMG) (12).Since no clear-cut evidence of NE overproduction could be found (8-10), and since physiologic studies suggested that essential hypertension was associated with abnormally increased vascular reactivity to infused NE (13), it seemed possible that the disease might be causally related to abnormal metabolic handling of that NE produced in normal quantities by these patients. To evaluate the metabolism of a substance that underwent degradation within moments of its administration and which produced an intense physiologic effect in nanogram amounts, a tracer compound of high

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“…This change in relative responsiveness to the two dilators cannot be explained by structural changes in the vessels and must reflect a functional disturbance involving either the vascular smooth muscle itself or certain of the mechanisms by which its activity is controlled. The origin of this functional abnormality is, as yet, undetermined and it is not known if it is related to the increased responsiveness to noradrenaline that has previously been demonstrated in patients with hypertension (Doyle et al, 1959;Mendlowitz & Naftchi, 1958;Sivertsson, 1970). 327 In an attempt to gain further information as to the changes in resistance vessel function that occur in primary hypertension and also to investigate the mechanism of action of two widely used types of antihypertensive agent, we have examined the effect of treatment with chlorthalidone and atenolol on the responsiveness of the forearm resistance vessels to verapamil and sodium nitroprusside.…”

Section: Introductionmentioning

confidence: 99%

Effect of treatment with chlorthalidone and atenolol on response to dilator agents in the forearm resistance vessels of men with primary hypertension.

Robinson¹,

Dobbs²,

Phillips³

1983

Brit J Clinical Pharma

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1 The forearm resistance vessels of men with primary hypertension respond to verapamil with a greater than normal dilatation relative to that induced by sodium nitroprusside. 2 We have examined the effect on this functional abnormality of treatment with chlorthalidone (50 mg daily in 16 patients) and atenolol (100 mg daily in eight patients and 200 mg daily in two).3 The responsiveness of the forearm resistance vessels to local intra-arterial infusion of verapamil and sodium nitroprusside was assessed before treatment and again after a minimum of 1 month ofdrug therapy. Forearm blood flow was measured by venous occlusion plethysmography. 4 Chlorthalidone induced significant reductions in calculated mean arterial pressure, which fell from 135 ± 4 to 117 + 4 mm Hg, and the dilator response to verapamil at 5 ,ug/min, which was reduced from 2.4 ± 0.2 to 1.5 ± 0.2 ml min-' 100 ml-' forearm; the response to sodium nitroprusside at 3.2 ,ug/min was not significantly changed. 5 Atenolol induced significant reductions in mean arterial pressure, which fell from 134 + 6 to 123 ± 6 mm Hg, heart rate which fell from 72 + 3 to 55 + 2 beats/min, and response to verapamil at 5 ,ug/min which fell from 2.7 + 0.2 to 2.1 ± 0.2 ml min-I 100 ml-' forearm; the response to sodium nitroprusside was not significantly changed. 6 Both drugs caused reversion towards normal of the relative enhancement of responsiveness to verapamil that was present before treatment. Normalization of this aspect of resistance vessel function may be one component of the mechanism by which both diuretics and 18-adrenoceptor antagonists exert their antihypertensive effect.

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Work of Digital Vasoconstriction Produced by Infused Norepinephrine in Primary Hypertension

Cited by 67 publications

References 0 publications

Reactivity of Renal and Systemic Circulations to Vasoconstrictor Agents in Normotensive and Hypertensive Subjects*

Reactivity of Renal and Systemic Circulations to Vasoconstrictor Agents in Normotensive and Hypertensive Subjects*

Plasma Clearance of dl-β-H3-Norepinephrine in Normal Human Subjects and Patients with Essential Hypertension*

Effect of treatment with chlorthalidone and atenolol on response to dilator agents in the forearm resistance vessels of men with primary hypertension.

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