title: Vascular growth responses in SHR and WKY during development of renal (1K1C) hypertension.
abstract: Intrinsic differences between vascular smooth muscle cells (VSMC) in normotension and genetic hypertension may account for the exaggerated growth response often observed in the hypertensive vasculature. To test this hypothesis, in this study we compared the vascular growth response of the spontaneously hypertensive rat (SHR) and Wistar-Kyoto rat (WKY) following induction of one kidney, one clip (1KlC) renal hypertension. SHR and WKY rats were uninephrectomized and renal hypertension (RH) induced using silver clips of 0.22 and 0.24 mm width. Four weeks later, vessel and VSMC growth were assessed in small mesenteric arteries. The systolic blood pressure (SBP) in the RH animals was significantly higher than in uninephrectomised controls, in RH-SHR with a 0.24 mm clip SBP 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, respectively. For the same SBP, there were no differences in medial cross-sectional areas of the small mesenteric arteries between RH-SHR and RH0.22-WKY, which averaged 1.73 +/- 0.19 x 10(4) microm2 and 1.66 +/- 0.15 x 10(4) microm2, respectively. Likewise, the number of VSMCs (within a precise anatomical site of the mesenteric vasculature) were not different between the RH-SHR and the RH0.22-WKY with VSMC number 7.6 +/- 0.8 x 10(4) cells and 6.9 +/- 0.4 x 10(4) cells, respectively. In the RH0.22-WKY vascular growth responses were generally unchanged compared with the RH0.24-WKY except for a further increase in the incidence of polyploid cells. In conclusion, the results of this study demonstrate that smooth muscle cells of the SHR are not hyperresponsive to all growth-promoting stimuli. Taken together with previous observations, it appears that sustained activity of the renin-angiotensin system may be required for exaggerated vascular growth responses in SHR.
authors.affiliation: Baker Medical Research Institute, The University of Melbourne, Victoria, Australia.
authors.forename: M J
authors.initials: MJ
authors.lastname: Black
authors.forename: A
authors.initials: A
authors.lastname: Niklaus
authors.forename: J F
authors.initials: JF
authors.lastname: Bertram
authors.forename: R
authors.initials: R
authors.lastname: Dilley
authors.forename: A
authors.initials: A
authors.lastname: Bobik
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002455:Cell Division; D048429:Cell Size; D006978:Hypertension, Renovascular / Q000473:pathology* / Q000503:physiopathology; D008638:Mesenteric Arteries / Q000473:pathology*; D009131:Muscle, Smooth, Vascular / Q000473:pathology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY