Key result
Platelet alpha 2-adrenoceptor density correlates positively with resting plasma norepinephrine and negatively with postural changes.
Why the study?
Does treatment with sympatholytic agents alter platelet alpha 2-adrenoceptor density in relation to sympathetic nerve activity?
Observational (n=45)
Does treatment with sympatholytic agents alter platelet alpha 2-adrenoceptor density in relation to sympathetic nerve activity?
Effect estimate: r = 0.471
p-value: p=<0.01
Platelet alpha 2-adrenoceptor density appears to be functionally regulated in parallel with sympathetic nerve activity rather than by plasma norepinephrine levels alone.
May reflect parallel regulation of platelet alpha 2-adrenoceptors with sympathetic activity; leaves open effects of sympatholytic agents.
Functional relationships between platelet alpha 2-adrenoceptors and sympathetic nerve activity were studied in patients with essential hypertension (n = 23), primary aldosteronism (n = 10), and normal subjects (n = 12). The maximum number of binding sites (Bmax) and the dissociation constant (Kd) of 3H-yohimbine on platelet membranes and resting plasma norepinephrine (NE) were similar among these groups of subjects. In all subjects combined, Bmax values were correlated positively (r = 0.471, p less than 0.01) to resting plasma NE and negatively (r = -0.531, p less than 0.01) to the changes in plasma NE when subjects were moved from lying to standing. A 2-4 week treatment with guanabenz or bethanidine induced a parallel fall of both Bmax and plasma NE, whereas administration of reserpine caused a similar fall of plasma NE but Bmax remained unchanged. Kd values were not changed after any of these treatments. The results support the view that platelet alpha 2-adrenoceptor density is functionally regulated in parallel with sympathetic nerve activity rather than plasma NE per se. This hypothesis seems quite reasonable when it is extended to the presynaptic alpha 2-adrenoceptors; otherwise, the negative feedback function on NE release should be lessened and contradictory to its physiological role.
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Noshiro et al. (1989) conducted an observational in Essential hypertension and primary aldosteronism (n=45). Sympathetic nerve activity was evaluated on Correlation between maximum number of binding sites (Bmax) and plasma norepinephrine (NE) (r = 0.471, p=<0.01). Platelet alpha 2-adrenoceptor density was positively correlated with resting plasma norepinephrine (r=0.471, p<0.01) and negatively correlated with postural changes in plasma norepinephrine (p<0.01).
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