Increased function of the voltage-dependent calcium channels, without increase of Ca2+ release from the sarcoplasmic reticulum in the arterioles of spontaneous hypertensive rats

It has been reported that the increased function of the voltage-dependent c alcium channels (VDCC) in the artery is involved in the increase of periphe ral resistance in hypertension, and that the sarcoplasmic reticulum (SR) in the artery plays an important role in preventing the development of hypert ension via a buffering effect. However, no reports have described the role of VDCC and SR in resistance arterioles in the development or maintenance o f hypertension. We investigated the function of VDCC and of SR in the crema ster arterioles of spontaneous hypertensive rats (SHR) and age-matched Wist ar Kyoto rats (WKY). The changes in diameter and the intracellular calcium ion concentration ([Ca2+](i)) in the microdissected arterioles, using fluor escent dyes, were measured with videomicroscopy. The KCl concentration-resp onse curves were analyzed in 4- to 5- and 7- to 8-week-old SHR and WKY. The changes in the vascular diameter and [Ca2+](i) in response to ryanodine, a n alpha-1 adrenoceptor, and angiotensin-II stimulation were compared betwee n the 7- to 8-week-old SHR and WKY. We found an increase in the Ca2+ influx by VDCC in the early hypertensive stage, but not in prehypertensive SHR. H owever, after the onset of hypertension, there were no significant differen ces from WKY in the SR function mediated by Ca2+-induced Ca2+ release or in ositol 1,4,5-trisphosphate-induced Ca2+ release. In conclusion, an increase d influx of Ca2+ in the cell membrane, without a buffering effect of SR, wa s associated with progression of hypertension in the cremaster arterioles o f SHR. Am J Hypertens 1999;12:1236-1242 (C) 1999 American Journal of Hypert ension, Ltd.