Size-dependent heterogeneity of contractile Ca2+ sensitization in rat arterial smooth muscle

J Physiol. 2012 Nov 1;590(21):5401-23. doi: 10.1113/jphysiol.2012.241315. Epub 2012 Aug 28.

Abstract

Each segment along arterial vessels adapts to different circumstances, including blood pressure and sympathetic innervation. PKC and Rho-associated kinase (ROCK) Ca(2+)-sensitizing pathways leading to myosin phosphatase inhibition are critically involved in α(1)-adrenoceptor-mediated vascular smooth muscle contraction in distinctive time-dependent manners. We tested whether the amplitude and time course of each pathway varies dynamically between arterial segments. Using pharmacological approaches, we determined the time-dependent roles of Ca(2+) release, Ca(2+) influx, PKC and ROCK in α(1)-agonist-induced contraction and phosphorylation of key proteins in denuded rat small mesenteric artery, midsized caudal artery and thoracic aorta. SR Ca(2+) release and voltage-dependent Ca(2+) influx were essential for the initial rising and late sustained phases, respectively, of phenylephrine-induced contraction, regardless of arterial size. In small mesenteric arteries, α(1A)-subtype-specific antagonists and inhibitors of PKC, but not ROCK, markedly reduced the initial and late phases of contraction in a non-additive manner and suppressed phosphorylation of myosin light chain (MLC) and CPI-17, but not myosin targeting subunit of myosin light chain phosphatase (MYPT1). In aorta, an α(1D)-specific antagonist reduced both the initial and late phases of contraction with a significant decrease in MLC but not CPI-17 or MYPT1 phosphorylation. ROCK inhibitors, but not PKC inhibitors, suppressed the sustained phase of contraction with a decrease in MLC and MYPT1 phosphorylation in the aorta. The effect of ROCK inhibitors was additive with the α(1D)-antagonist. The results for midsized arteries were intermediate. Thus, the PKC-CPI-17 Ca(2+)-sensitizing pathway, which is dependent on PKC subtype and a Ca(2+)-handling mechanism, and is downstream of α(1A) receptors, plays a major role in α(1)-agonist-induced contraction of small resistance arteries in the splanchnic vascular beds. The effect of PKC and ROCK increases and decreases, respectively, with decreasing arterial size.

MeSH terms

  • Amides / pharmacology
  • Animals
  • Arteries / drug effects
  • Arteries / physiology*
  • Calcium / physiology*
  • Enzyme Inhibitors / pharmacology
  • Female
  • In Vitro Techniques
  • Male
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / physiology*
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / physiology*
  • Pyridines / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Adrenergic, alpha-1 / physiology*
  • Signal Transduction / drug effects
  • Vasoconstriction / drug effects
  • rho-Associated Kinases / antagonists & inhibitors
  • rho-Associated Kinases / physiology*

Substances

  • Amides
  • Enzyme Inhibitors
  • Pyridines
  • Receptors, Adrenergic, alpha-1
  • Y 27632
  • rho-Associated Kinases
  • Protein Kinase C
  • Calcium