VASCULAR GROWTH-RESPONSES IN SHR AND WKY DURING DEVELOPMENT OF RENAL (1K1C) HYPERTENSION

Intrinsic differences between vascular smooth muscle cells (VSMC) in n ormotension and genetic hypertension may account for the exaggerated g rowth response often observed in the hypertensive vasculature. To test this hypothesis, in this study we compared the vascular growth respon se of the spontaneously hypertensive rat (SHR) and Wistar-Kyoto rat (W KY) following induction of one kidney, one clip (1K1C) renal hypertens ion. SHR and WKY rats were uninephrectomized and renal hypertension (R H) induced using silver clips of 0.22 and 0.24 mm width. Four weeks la ter, vessel and VSMC growth were assessed in small mesenteric arteries . The systolic blood pressure (SEP) in the RH animals was significantl y higher than in uninephrectomised controls, in RH-SHR with a 0.24 mm clip SEP averaged 215 +/- 4 mm Hg and in RH-WKY with a 0.22 or 0.24 mm clip the SBPs averaged 214 +/- 5 mm Hg and 190 +/- 2 mm Hg, respectiv ely. For the same SEP, there were no differences in medial cross-secti onal areas of the small mesenteric arteries between RH-SHR and RH(0.22 )-WKY, which averaged 1.73 +/- 0.19 x 10(4) mu m(2) and 1.66 +/- 0.15 x 10(4) mu m2, respectively. Likewise, the number of VSMCs (within a p recise anatomical site of the mesenteric vasculature) were not differe nt between the RH-SHR and the RH(0.22)-WKY with VSMC number 7.6 +/- 0. 8 x 10(4) cells and 6.9 +/- 0.4 x 10(4) cells, respectively. In the RH (0.22)-WKY vascular growth responses were generally unchanged compared with the RH(0.24)-WKY except for a further increase in the incidence of polyploid cells. In conclusion, the results of this study demonstra te that smooth muscle cells of the SHR are not hyperresponsive to all growth-promoting stimuli. Taken together with previous observations, i t appears that sustained activity of the renin-angiotensin system may be required for exaggerated vascular growth responses in SHR. (C) 1997 American Journal of Hypertension, Ltd.