| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Physiology, University of Missouri, Columbia 65212.
1. Sodium nitroprusside (NP) caused both an inhibition of a noradrenaline (NA)-induced contraction and an elevation of cyclic guanosine 3',5'-monophosphate (cyclic GMP) in rat aorta. Both NP-induced responses were enhanced by the selective cyclic GMP phosphodiesterase inhibitor, M&B 22948 (2-o-propoxyphenyl-8-aza-purin-6-one, 30 microM). 2. The inhibition of a NA-induced contraction by NP was characterized by dissociating the intracellular Ca2+ release component from the extracellular Ca2+ influx component of the contraction. The transient contraction stimulated by NA in the absence of extracellular Ca2+ was inhibited by NP. Also, the slowly developed tension stimulated by NA in aortas depleted of stored Ca2+ and subsequently exposed to extracellular Ca2+ was inhibited by NP. Both components of contraction were equally sensitive to NP. 3. NA stimulated both unidirectional 45Ca2+ influx in the presence of extracellular Ca2+ and 45Ca2+ efflux into a 0 Ca2+ solution that contained 2 mM-ethyleneglycol-bis-(beta-aminoethylether)N,N'-tetraacetic acid (EGTA). The increased 45Ca2+ efflux is thought to reflect release of stored Ca2+ followed by membrane transport. NP greater than 10 nM inhibited both 45Ca2+ influx and release components whereas NP at 1-3 nM enhanced NA-stimulated 45Ca2+ efflux and relaxed the maintained tension caused by NA in 0 Ca2+, 2 mM-EGTA. 4. NP also inhibited the Ca2(+)-dependent 42K+ and 36Cl- effluxes from rat aorta stimulated either by NA or by high potassium. NP inhibited the contractile and flux responses to NA more effectively than the responses to high potassium. 5. These data indicate that: (1) NP reduces cytosolic Ca2+ by the combined inhibitory effects on Ca2+ influx and intracellular Ca2+ release, and by the stimulation of a Ca2(+)-ATPase; and (2) the differential sensitivity of the NA and high-potassium responses to NP may reflect underlying differences in Ca2+ handling induced by receptor occupancy and depolarization.
This article has been cited by other articles:
|
|
 |
|
  L. Michea, V. Irribarra, I. A. Goecke, and E. T. Marusic Reduced Na-K pump but increased Na-K-2Cl cotransporter in aorta of streptozotocin-induced diabetic rat Am J Physiol Heart Circ Physiol, February 1, 2001; 280(2): H851 - H858. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. L. Griffin, M. H. Laughlin, and J. L. Parker Exercise training improves endothelium-mediated vasorelaxation after chronic coronary occlusion J Appl Physiol, November 1, 1999; 87(5): 1948 - 1956. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Akar, E. Skinner, J. D. Klein, M. Jena, R. J. Paul, and W. C. O'Neill Vasoconstrictors and nitrovasodilators reciprocally regulate the Na+-K+-2Cl- cotransporter in rat aorta Am J Physiol Cell Physiol, June 1, 1999; 276(6): C1383 - C1390. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. KURIYAMA, K. KITAMURA, T. ITOH, and R. INOUE Physiological Features of Visceral Smooth Muscle Cells, With Special Reference to Receptors and Ion Channels Physiol Rev, July 1, 1998; 78(3): 811 - 920. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. L. Tepperman, T. D. Abrahamson, and B. D. Soper The Role of Cyclic Guanylate Monophosphate in Nitric Oxide-Induced Injury to Rat Small Intestinal Epithelial Cells J. Pharmacol. Exp. Ther., March 1, 1998; 284(3): 929 - 933. [Abstract] [Full Text]
|
|
|
|
 |
|
 C.-T. Ting, J.-W. Chen, M.-S. Chang, and F. C. P. Yin Arterial Hemodynamics in Human Hypertension : Effects of the Calcium Channel Antagonist Nifedipine Hypertension, June 1, 1995; 25(6): 1326 - 1332. [Abstract] [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
