Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

In human hypertension there is an impairment of beta-adrenergic responsiveness, which parallels an increase in lymphocyte G-protein receptor kinase-2 (GRK-2) protein expression. However, whether changes in lymphocyte GRK-2 parallel alterations in vascular GRK-2 and whether this increase is due to regulation at the level of translation was unknown. To determine if increased GRK-2 protein expression in hypertensive subjects paralleled increased GRK-2 mRNA we studied lymphocytes from young borderline hypertensive (H, n=7) and young normotensive subjects (N, n=14). Immunodetectable lymphocyte GRK-2 protein expression in H was increased (155+/-7% of N, p < 0.05) and was inversely correlated with beta-adrenergic-mediated adenylyl cyclase activity and positively correlated with blood pressure. However, lymphocyte GRK-2 mRNA content was not altered in H (110+/-13% of N). To determine if lymphocyte GRK-2 protein expression paralleled alterations in vascular GRK-2 we studied lymphocytes and aortae obtained from normotensive Wistar (W) and WKY rat controls versus spontaneously hypertensive rats (SHR), which also demonstrate impaired beta-adrenergic responsiveness. Immunodetectable lymphocyte GRK-2 protein expression was increased in SHR (143+/-10% of the expression in W and 131+/-11% of WKY). Immunodetectable vascular myocyte GRK-2 was comparably increased in SHR (169+/-14% of expression in W and 183+/-8% of the expression in WKY). These studies indicate that GRK-2 protein expression is increased in both hypertensive subjects and SHR. This increase in lymphocyte GRK-2 parallels increased vascular GRK-2 protein expression, but was not associated with altered lymphocyte GRK-2 mRNA content.

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Poster Number PAgros0775
Keywords: Hypertension, adenylyl cyclase, adrenoceptors, GRK