© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
Increased Ca2+ sensitivity of contractile elements via protein kinase C in 
-toxin permeabilized SMA from young spontaneously hypertensive rats
Division of Cardiology, Department of Medicine, Wakayama Medical College 27,7-Bancho, Wakayama 640, Japan
* Corresponding author. Present address: c/o Prof. Cornelis van Breemen, Head, Department of Pharmacology and Therapeutics, Faculty of Medicine, The University of British Columbia, 2176 Health Sciences Mall, Vancouver, B.C., Canada V6T 1Z3. Tel.: +1 (604) 822-2447; fax: +1 (604) 822-2281; e-mail: hisashi@unixg.ubc.ca
Objective: The purpose of the present investigation was to examine the Ca2+ sensitivity of the contractile elements via protein kinase C (PKC) in superior mesenteric artery (SMA) from young (5–6 weeks old) spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Methods: Staphylococcal aureus 
-toxin, which produces pores in the plasma membrane too small to allow passage of proteins such as PKC, was used to investigate the signal transduction system in vascular smooth muscle cells. We investigated the Ca2+ sensitivity of the contractile apparatus via PKC in intact and -toxin skinned SMA from young SHR and WKY. Results: In intact SMA, high K+ responses were not different between SHR and WKY. However, phorbol 12,13-dibutyrate (PDBu, a PKC activator) augmented high K+-evoked contractions and PKC inhibitors, such as 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) and calphostin C, suppressed them more in SHR as compared with WKY. In -toxin skinned SMA, the [Ca2+]i–force relationship curve was not significantly different between SHR and WKY. However, PDBu augmented [Ca2+]i-evoked contractions and PKC inhibitors suppressed them more in SHR than in WKY. Conclusion: These results suggest that the Ca2+ sensitivity of the contractile elements via PKC is significantly greater in prehypertensive SHR than in age-matched WKY. This abnormality in small muscular arteries may be involved in the pathogenesis of hypertension in SHR.
KEYWORDS Protein kinase C; Vascular smooth muscle; Spontaneously hypertensive rat; Wistar-Kyoto rat; Calcium sensitivity; Contractile elements
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