Adrenergic Receptor Function is Different in Male and Female Patients with Essential Hypertension

Kafka, Marian S.; Lake, C. Raymond; Güllner, Hans-Georg; Tallman, John F.; Bartter, Frederic C.; Fujita, Toshiro

doi:10.3109/10641967909068628

Cited by 31 publications

(13 citation statements)

References 21 publications

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“…It has been reported that the number of platelet a 2 -adrenergic receptors from hypertensive women was greater than that from normotensive women 28 and that estrogens or progesterone or both altered the a 2 -adrenergic receptor density in human platelets. 29 However, others have found no alteration in the number of VOL 7, No 6, NOVEMBER-DECEMBER 1985 platelet a 2 -adrenergic receptors in hypertensive subjects.…”

Section: Discussionmentioning

confidence: 99%

Effect of dietary sodium on platelet alpha 2-adrenergic receptors in essential hypertension.

Ashida¹,

Tanaka²,

Yokouchi³

et al. 1985

Hypertension

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SUMMARY To study the aggregation, adhesion, and specific binding of an a 2 -antagonist, [ 3 H]rauwolscine, to the platelet membrane fractions, platelets were obtained from 30 patients with essential hypertension and nine normotensive subjects fed a high sodium diet (NaCl, 16-18 g/day) for 7 days and thereafter a low sodium diet (NaCl, 1-3 g/day) for 7 days. The patients with essential hypertension were classified as either salt responders (all those who had > 7% decrease in mean arterial pressure from the high to low sodium period) or salt nonresponders (all others). In salt responders, the number of a 2 -adrenergic receptors on platelet membrane fraction was increased from 523.4 ± 55.4 fmol/mg of protein in the high sodium period to 669.4 ± 84.0 fmol/mg of protein in the low sodium period (p < 0.01), whereas it did not change in salt nonresponders. In contrast, the epinephrine-induced platelet aggregation through a 2 -adrenergic receptors was decreased in nonresponders, from 47.3 ± 7.4% in the high sodium period to 24.5 ± 9.3% in the low sodium period (p < 0.05), while it did not change in responders. No significant change in the number of c* 2 -adrenergic receptors or epinephrine-induced platelet aggregation was observed in the normotensive subjects.

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Section: Discussionmentioning

confidence: 99%

Effect of dietary sodium on platelet alpha 2-adrenergic receptors in essential hypertension.

Ashida¹,

Tanaka²,

Yokouchi³

et al. 1985

Hypertension

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“…Finally, Jones et al 67 found a lower number of platelet a 2 -adrenergic receptors in 19 hypertensive patients compared with 19 age-and sex-matched control subjects. Additionally, some studies' with small patient numbers have been published that generally did not detect significant differences in platelet a 2 -adrenergic receptor density between normotensive and hypertensive subjects 68 -72 ; Kafka et al 73 found an increased receptor number in 12'female hypertensive patients compared with 10 female normotensive subjects but could not reproduce' that difference in a male population of a similar size. The statistical power of these small studies, however, is weak.…”

Section: Human Platelet a R Adrenergic Receptorsmentioning

confidence: 99%

“…- 153 One study with poorly defined methods 73 and another study in a small population of borderline hypertensive patients 154 failed to detect significant differences between hypertensive and normotensive subjects.…”

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confidence: 99%

Peripheral adrenergic receptors in hypertension.

1990

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Increased sympathoadrenal activity appears to play an important role in the development or maintenance of elevated blood pressure in hypertensive patients and various annual models of hypertension. Alterations of adrenergic receptor number or responsiveness might contribute to this increased activity. We therefore reviewed the data on adrenergic receptor alterations in hypertension with special emphasis on several key cardiovascular tissues (i.e., heart, vascular smooth muscle, and kidney) and on lymphocytes and platelets as human tissues available for such studies. The data suggest that the number of o-adrenergic receptors in hypertension is regulated by catecholamines, dietary salt intake, and genetic factors. Increases in renal cv-adrenergic receptor number may be etiologic in genetic forms of essential hypertension. ^Adrenergic receptor alterations in states of elevated blood pressure do not appear to be specific for genetic hypertension. Desensitization of ^-adrenergic receptor function in hyper-tensive animals and patients contrasts with reports of decreased, unchanged, and increased /3-adrenergic receptor number, suggesting that signal transduction of /3-adrenergic (and possibly other) receptors that stimulate adenylyl cyclase is disturbed in hypertension. The mechanisms of such heterologous desensitization in states of elevated blood pressure remain to be elucidated. (Hypertension 1990;16:107-120)

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“…Franco-Morselli et al 12 Franco-Morselli et al 13 Geffen et al 14 Henry et al 15 Hjemdahl and Eliasson" Hofman et al 17 Jones et al 18 Kafka et al 19 Kiowski et al 80 Kobayashi et al 21 Lake et al 22 Lake 23 Louis et al 2 * Miura et al 26 Miura et al 26 Pedersen and Christensen 27 Philipp et al 28 Robertson et al 29 Sever et al 30 Sever et al 3 '…”

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confidence: 99%

Plasma norepinephrine in essential hypertension. A study of the studies.

Goldstein¹

1981

Hypertension

189

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SUMMARY Of 32 studies comparing plasma norepinephrine concentrations in hypertensive and normotensive groups, 28 (88%) reported higher levels in the hypertensive group. However, only 13 (41%) of the studies reported statistically significant hypertensive-nonnotensive differences in norepinephrine, leading the present attempt to identify factors differentiating "positive" studies (those reporting significant hypertensivenormotensive differences) from "negative" studies (those reporting nonsignificant differences). Hypertensive norepinephrine levels were similar in positive and negative studies (281 vs 288 pg/ml), but normotensive levels were lower in the positive studies (177 vs 269 pg/ml). When compared with the fluorimetric technique, the radioenzymatic type of assay was associated both with a lower frequency of positive results (25% vs 100%) and greater intrastudy standard deviations (152 vs 72 pg/ml). Hypertensive-normotensive differences varied inversely with age (> = -0.37). Resolution of the persisting controversy about norepinephrine levels in essential hypertension will require more attention to the causes of variability associated with the assay technique, to the sources, characteristics, and treatment of the normotensive controls, and to the age of the patient population. (Hypertension 3: 48-52, 1981) KEY WORDS • norepinephrine • catecholamines • hypertensionT HE introduction about a decade ago of sensitive techniques for measuring plasma norepinephrine,'• a and indications that those levels reflect sympathetic neural activity,' promised to help answer a perennial question in hypertension research: Does sympathetic hyperactivity cause essential hypertension? Despite the subsequent publication of more than 30 comparative studies in hypertensives and normotensive controls,*"" controversy persists about whether patients with hypertension exhibit elevated levels of norepinephrine. This report reexamines these studies in an attempt to identify the causes of the inconsistencies in results. MethodsThe studies considered in this review satisfied the following criteria: 1) they were published since 1973, in English; 2) they were not merely abstracts, but were

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Adrenergic Receptor Function is Different in Male and Female Patients with Essential Hypertension

Cited by 31 publications

References 21 publications

Effect of dietary sodium on platelet alpha 2-adrenergic receptors in essential hypertension.

Effect of dietary sodium on platelet alpha 2-adrenergic receptors in essential hypertension.

Peripheral adrenergic receptors in hypertension.

Plasma norepinephrine in essential hypertension. A study of the studies.

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