Extracellular calcium, contractile activity and membrane potential in tail arteries from genetically hypertensive rats

Objective and design: This study compares the effect of extracellular calcium on contractile responsiveness and membrane potential (E_m) in arteries from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto normotensive (WKY) rats. Methods: Isometric force and E_m were measured in isolated tail artery strips using standard muscle bath and microelectrode techniques, respectively. Results: The resting contractile force in SHRSP and WKY arteries was not influenced by the extracellular calcium concentration. However, the rate of force development in response to norepinephrine (3 × 10−8mol/l) was slowed when calcium was elevated and increased when calcium was reduced. Compared with WKY rats, this stabilizing action of calcium on contractions to norepinephrine was reduced in SHRSP. In 1.6 mmol/l calcium, resting E_m in SHRSP did not differ from that in WKY rats. Calcium-free buffer caused depolarization in SHRSP and WKY rats. Reductions in calcium below physiological levels resulted in depolarization, whereas elevations in calcium caused hyperpolarization. Regardless of the calcium concentration, E_m values in SHRSP did not differ from those in WKY rats. Norepinephrine (3 × 10−8mol/l) caused a depolarization in WKY rat and SHRSP arteries, and the magnitude of this depolarization was not influenced by calcium. Endothelium removal did not alter the stabilizing effects of calcium on the membrane potential or contractile activity in WKY rats or SHRSP. Conclusions: The reduced stabilizing effect of calcium on the contractile activity in SHRSP arteries is not due to an alteration in the general effect of the cation on the membrane potential.