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Impaired arterial β‐adrenergic receptor function in DOCA‐salt hypertension

Vascular tone is regulated by constrictor α1‐adrenergic receptors (ARs) and β‐AR‐mediated dilation. Increased constrictor reactivity for norepinephrine (NE) in mesenteric arteries (MA) contributes to increased vascular tone in DOCA‐salt hypertension. These studies examined if these alterations are due to reduced β‐AR function. The MA from sham and DOCA‐salt hypertensive rats were pressurized at 80 mmHg, α1‐ and β‐AR function was tested using computer‐assisted video‐microscopy to measure agonist induced changes in diameter in vitro. Constrictor activity of NE was similar in sham and DOCA‐salt MA, but EC50s for NE were reduced in sham, but not DOCA‐salt MA after blockade of β‐ARs by propranolol. β‐AR dilator function was tested in serotonin‐preconstricted MA, α1‐ARs were blocked by prazosin. Agonist‐induced relaxation was normalized to that caused by papaverine. In DOCA‐salt MA, EC50s for NE, epinephrine, and isoproterenol were similar to sham MA; but Emax for all agonists was reduced. Western blot and immunohistochemical studies in isolated smooth muscle cells revealed similar expression of β1‐ and β2‐AR in MA from sham and DOCA‐salt rats. Our results indicate that there is reducedβ‐AR vasodilator activity in DOCA‐salt hypertension. Reduced β‐AR function is not due to reduced β‐AR expression. Reduced β‐AR dilator function may contribute to increased sympathetic vasoconstrictor tone known to occur in DOCA‐salt hypertension.