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      Cellular Signalling by Lipoproteins in Cultured Smooth Muscle Cells from Spontaneously Hypertensive Rats

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          Abstract

          We investigated pivotal signalling responses of cultured aortic smooth muscle cells (VSMC) from the spontaneously hypertensive rat (SHR) and the normotensive Wistar Kyoto rat (WKY) to lipoproteins. Low-density lipoprotein (LDL) and high-density lipoprotein (HDL<sub>3</sub>) stimulated a time- and dose-dependent accumulation of inositol phosphates in VSMC. SHR and WKY VSMC exhibited comparable half-maximal dose requirements (≈13 µg/ml for LDL and ≈14 µg/ml for HDL<sub>3</sub>), although, at any given dose, the response of SHR VSMC was significantly greater than WKY VSMC. Simultaneous addition of LDL and HDL<sub>3</sub> to VSMC resulted in additive stimulatory effects on phosphoinositide catabolism. Pertussis toxin pretreatment of VSMC completely negated the stimulatory effects of LDL and HDL<sub>3</sub> on IP accumulation. [<sup>32</sup>P]-ADP ribosylation and immunoblotting studies revealed the guanine nucleotide-binding (G protein) substrate(s) for pertussis toxin to be a G<sub>i</sub> protein(s). SHR and WKY VSMC did not differ with respect to levels of G<sub>iα</sub> or G<sub>β</sub>, and, thus, the amplified responsiveness in SHR VSMC cannot be attributed to alterations in levels of pertussis toxin-sensitive G protein. The spectrum of signalling responses elicited by LDL and HDL<sub>3</sub> are similar to those elicited by vasoactive hormones, and thus lipoproteins may, via stimulation of phosphoinositide catabolism, <sup>45</sup>Ca<sup>2+</sup> uptake and Na<sup>+</sup>/H<sup>+</sup>-exchange, directly regulate smooth muscle cell growth and contraction.

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          Author and article information

          Journal
          JVR
          J Vasc Res
          10.1159/issn.1018-1172
          Journal of Vascular Research
          S. Karger AG
          1018-1172
          1423-0135
          1993
          1993
          23 September 2008
          : 30
          : 3
          : 169-180
          Affiliations
          aDepartment of Research, Basel University Hospital, Basel, Switzerland; bInstitute of Experimental Cardiology, Academy of Medical Sciences, Moscow, Russia
          Article
          158992 J Vasc Res 1993;30:169–180
          10.1159/000158992
          8390863
          © 1993 S. Karger AG, Basel

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          Page count
          Pages: 12
          Categories
          Research Paper

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