Role of β 2- and β 3 -adrenoceptors in arterial stiffness in a state of hypertension.

An increase in arterial stiffness is associated with a high risk for morbidity and mortality in a state of elevated systemic pressure. The sympathetic nervous system plays an important role in the regulation of vascular tone via activation of β-adrenoceptors. The aim of this investigation was to determine the involvement of β-adrenoceptors in the control of arterial stiffness in a state of hypertension versus normotension. Pulse wave velocity (PWV), an index of vascular stiffness, was assessed in isoflurane-anaesthetized 13-14-week-old male spontaneously hypertensive (SH) and Wistar-Kyoto (WKY) rats. At baseline, PWV was significantly higher in SH (9.2±0.9m/s) compared to WKY rats (6.7±0.4m/s). The stimulation of β2 - but not β3 -adrenoceptors significantly reduced PWV in SH rats despite comparable reductions in blood pressure. Stimulation of β2 - or β3 -adrenoceptors did not reduce PWV in WKY rats. The administration of sodium nitroprusside (SNP) also significantly reduced PWV in SH but not WKY rats. Immunofluorescence revealed the expression of β2 - and β3 -adrenoceptors in endothelial cells and vascular smooth muscle cells of the abdominal aorta. There were no significant differences in the distribution of the expression of β2 - and β3 -adrenoceptors in endothelial and/or smooth muscle cells in blood vessels of SH compared to WKY rats. The evidence suggests that β2 -adrenoceptor stimulation and SNP infusion reduce PWV independently from reduction in blood pressure in a state of high systemic arterial pressure. A reduction in vascular tone of the central arteries may play a key role in decreasing PWV that is elevated due to stiffer arterial wall.