Potassium depolarization of adrenergic varicosities in resistance arteries from SHR and WKY rats.

We characterized the function of adrenergic nerve varicosities in mesenteric resistance arteries from spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats by observing contractile responses to depolarization with a high potassium solution (HiK). Intact rings of resistance arteries were mounted in a specialized muscle chamber for measurement of circumferential contractile forces. Contractile responses to exogenous norepinephrine (NE), to HiK, and to the combination of NE plus HiK were significantly greater in SHR compared to WKY vessels. Using either phentolamine or 6-hydroxydopamine-treated vessels to eliminate a neurogenic adrenergic response, we determined that a part of the HiK-induced contraction was due to NE released from nerve varicosities (i.e., the adrenergic component). In order to compare these adrenergic components for possible nerve-related differences, they were first normalized to their maximum exogenous NE responses. This normalized adrenergic component of SHR vessels (52 and 58% for phentolamine and 6-hydroxydopamine treatment, respectively) was significantly greater than that of the WKY vessels (35 and 37%). This greater adrenergic component could reflect either a greater vascular smooth muscle sensitivity to NE in arteries from SHR or an increase in NE concentration, or both.