![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Vol. 294, Issue 3, 948-954, September 2000
Sezione di Anatomia Umana, Dipartimento di Scienze Farmacologiche e
Medicina Sperimentale (M.S., F.A.) and Dipartimento di Scienze
Morfologiche e Biochimiche Comparate (L.V., E.B.), Università of
Camerino, Camerino, Italy
The influence of hypertension and of treatment with some
dihydropyridine-type Ca2+ channel blockers and with the
nondihydropyridine-type vasodilator hydralazine on the morphology of
kidney was investigated in 26-week-old spontaneously hypertensive rats
(SHR) and in age-matched Wistar-Kyoto rats. Fourteen-week-old
SHR were treated for 12 weeks with a nonhypotensive dose of
lercanidipine or with equihypotensive doses of lercanidipine, manidipine, nicardipine, and hydralazine. In control SHR, systolic pressure values were significantly higher in comparison with
Wistar-Kyoto rats. Treatment with the low dose of lercanidipine did not
reduce systolic blood pressure in SHR, whereas the higher dose of
lercanidipine or other compounds tested significantly decreased
systolic pressure values. Glomerular hypertrophy accompanied by signs
of glomerulosclerosis, increase of mesangial cells, and convoluted
tubules degeneration were observed in control SHR. Hypotensive doses of
Ca2+ antagonists countered glomerular injury, the increase
of mesangial cells, the reduction of capsular space, and tubular
degeneration. Hydralazine, in spite of its hypotensive activity,
displayed a slight nephroprotective action. The nonhypotensive dose of
lercanidipine countered in part glomerular injury, narrowing of
capsular space, and tubular degeneration, and decreased mesangial cell
augmentation in SHR. These results suggest that treatment with
dihydropyridine-type Ca+2 antagonists counters hypertensive
glomerular and tubular changes occurring in SHR. The demonstration of
nephroprotection by the nonhypotensive dose of lercanidipine suggests
that the renal effects of the compound may be in part unrelated to its
hemodynamic activity.
This article has been cited by other articles:
|
|
 |
|
  T. Rosenthal, E. Rosenmann, D. Tomassoni, and F. Amenta Effect of Lercanidipine on Kidney Microanatomy in Cohen-Rosenthal Diabetic Hypertensive Rats Journal of Cardiovascular Pharmacology and Therapeutics, June 1, 2007; 12(2): 145 - 152. [Abstract] [PDF]
|
|
|
|
 |
|
 J. Menne, J.-K. Park, R. Agrawal, C. Lindschau, J. T. Kielstein, T. Kirsch, A. Marx, D. Muller, F. H. Bahlmann, M. Meier, et al. Cellular and molecular mechanisms of tissue protection by lipophilic calcium channel blockers FASEB J, May 1, 2006; 20(7): 994 - 996. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Xue, Y.-L. Zhang, G.-S. Liu, and H. Wang A New ATP-Sensitive Potassium Channel Opener Protects the Kidney from Hypertensive Damage in Spontaneously Hypertensive Rats J. Pharmacol. Exp. Ther., November 1, 2005; 315(2): 501 - 509. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Wang, R. Mishra, and M. S. Simonson Ca2+/Calmodulin-Dependent Protein Kinase II Stimulates c-fos Transcription and DNA Synthesis by a Src-Based Mechanism in Glomerular Mesangial Cells J. Am. Soc. Nephrol., January 1, 2003; 14(1): 28 - 36. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-K. Park, A. Fiebeler, D. N. Muller, E. M.A. Mervaala, R. Dechend, F. Abou-Rebyeh, F. C. Luft, and H. Haller Lacidipine Inhibits Adhesion Molecule and Oxidase Expression Independent of Blood Pressure Reduction in Angiotensin-Induced Vascular Injury Hypertension, February 1, 2002; 39(2): 685 - 689. [Abstract] [Full Text] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
