Tertatolol: A beta-blocker with unique effects on human glomerular cell function

P. Shultz, Leopoldo Raij

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Tertatolol is a beta-blocker with unique renal vasodilatatory effects, mainly at the level of the microcirculation. Since many vasodilatory agents inhibit human mesangial cell (HMC) proliferation, the effects of tertatolol on the incorporation of 3H-thymidine in HMC were studied. Tertatolol plus mitogens (either fetal calf serum, platelet-derived growth factor (PDGF) or bovine thrombin) were incubated with HMC for 28 h, and 3H-thymidine was added during the last 4 h. Trichloroacetic acid-precipitable counts per well were divided by the mean number of cells in representative wells from the same experiment. The effect of tertatolol on angiotensin II (10-6 mmol/ l)-induced HMC contraction was also assessed by measuring the planar surface area of individual cells. In serum-free media, tertatolol did not significantly alter the incorporation of 3H-thymidine after 28 h of incubation in HMC. When tertatolol was added in the presence of 1% serum, 3H-thymidine incorporation was significantly reduced, compared to 1% serum alone. Tertatolol also inhibited 3H incorporation when PDGF and thrombin were used as the stimulus. The increase in cell number normally seen after 7 days in serum was also reduced by tertatolol. Tertatolol inhibited the reduction in planar surface area of HMC induced by angiotensin II. The inhibitory effect of tertatolol on HMC proliferation was also potentiated by ritanserin and MDL 72222, 5HT2 and 5HT3 antagonists, respectively. Conversely, the 5HT1A agonist 8-OH-DPAT did not modify the 3H-thymidine incorporation in HMC in the presence of tertatolol. In conclusion, tertatolol inhibits HMC proliferation. The mechanism cannot be explained by beta-blockade or stimulation of 5-HT1A receptors, and still remains unclear.

Original languageEnglish
Pages (from-to)51-56
Number of pages6
JournalCardiology
Volume83
Issue numberSUPPL. 1
StatePublished - Jan 1 1993
Externally publishedYes

Fingerprint

tertatolol
Mesangial Cells
Thymidine
Platelet-Derived Growth Factor
Cell Proliferation
Serum
Thrombin
Angiotensin II
Cell Count
Ritanserin
8-Hydroxy-2-(di-n-propylamino)tetralin

Keywords

  • Antihypertension
  • Beta-blocker
  • Human glomerular mesangial cells
  • Tertatolol

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Tertatolol : A beta-blocker with unique effects on human glomerular cell function. / Shultz, P.; Raij, Leopoldo.

In: Cardiology, Vol. 83, No. SUPPL. 1, 01.01.1993, p. 51-56.

Research output: Contribution to journalArticle

Shultz, P & Raij, L 1993, 'Tertatolol: A beta-blocker with unique effects on human glomerular cell function', Cardiology, vol. 83, no. SUPPL. 1, pp. 51-56.
Shultz, P. ; Raij, Leopoldo. / Tertatolol : A beta-blocker with unique effects on human glomerular cell function. In: Cardiology. 1993 ; Vol. 83, No. SUPPL. 1. pp. 51-56.
@article{7e6cb2c614fb4ce0be8c1a0c7a0a22d2,
title = "Tertatolol: A beta-blocker with unique effects on human glomerular cell function",
abstract = "Tertatolol is a beta-blocker with unique renal vasodilatatory effects, mainly at the level of the microcirculation. Since many vasodilatory agents inhibit human mesangial cell (HMC) proliferation, the effects of tertatolol on the incorporation of 3H-thymidine in HMC were studied. Tertatolol plus mitogens (either fetal calf serum, platelet-derived growth factor (PDGF) or bovine thrombin) were incubated with HMC for 28 h, and 3H-thymidine was added during the last 4 h. Trichloroacetic acid-precipitable counts per well were divided by the mean number of cells in representative wells from the same experiment. The effect of tertatolol on angiotensin II (10-6 mmol/ l)-induced HMC contraction was also assessed by measuring the planar surface area of individual cells. In serum-free media, tertatolol did not significantly alter the incorporation of 3H-thymidine after 28 h of incubation in HMC. When tertatolol was added in the presence of 1{\%} serum, 3H-thymidine incorporation was significantly reduced, compared to 1{\%} serum alone. Tertatolol also inhibited 3H incorporation when PDGF and thrombin were used as the stimulus. The increase in cell number normally seen after 7 days in serum was also reduced by tertatolol. Tertatolol inhibited the reduction in planar surface area of HMC induced by angiotensin II. The inhibitory effect of tertatolol on HMC proliferation was also potentiated by ritanserin and MDL 72222, 5HT2 and 5HT3 antagonists, respectively. Conversely, the 5HT1A agonist 8-OH-DPAT did not modify the 3H-thymidine incorporation in HMC in the presence of tertatolol. In conclusion, tertatolol inhibits HMC proliferation. The mechanism cannot be explained by beta-blockade or stimulation of 5-HT1A receptors, and still remains unclear.",
keywords = "Antihypertension, Beta-blocker, Human glomerular mesangial cells, Tertatolol",
author = "P. Shultz and Leopoldo Raij",
year = "1993",
month = "1",
day = "1",
language = "English",
volume = "83",
pages = "51--56",
journal = "Cardiology (Switzerland)",
issn = "0008-6312",
publisher = "S. Karger AG",
number = "SUPPL. 1",

}

TY - JOUR

T1 - Tertatolol

T2 - A beta-blocker with unique effects on human glomerular cell function

AU - Shultz, P.

AU - Raij, Leopoldo

PY - 1993/1/1

Y1 - 1993/1/1

N2 - Tertatolol is a beta-blocker with unique renal vasodilatatory effects, mainly at the level of the microcirculation. Since many vasodilatory agents inhibit human mesangial cell (HMC) proliferation, the effects of tertatolol on the incorporation of 3H-thymidine in HMC were studied. Tertatolol plus mitogens (either fetal calf serum, platelet-derived growth factor (PDGF) or bovine thrombin) were incubated with HMC for 28 h, and 3H-thymidine was added during the last 4 h. Trichloroacetic acid-precipitable counts per well were divided by the mean number of cells in representative wells from the same experiment. The effect of tertatolol on angiotensin II (10-6 mmol/ l)-induced HMC contraction was also assessed by measuring the planar surface area of individual cells. In serum-free media, tertatolol did not significantly alter the incorporation of 3H-thymidine after 28 h of incubation in HMC. When tertatolol was added in the presence of 1% serum, 3H-thymidine incorporation was significantly reduced, compared to 1% serum alone. Tertatolol also inhibited 3H incorporation when PDGF and thrombin were used as the stimulus. The increase in cell number normally seen after 7 days in serum was also reduced by tertatolol. Tertatolol inhibited the reduction in planar surface area of HMC induced by angiotensin II. The inhibitory effect of tertatolol on HMC proliferation was also potentiated by ritanserin and MDL 72222, 5HT2 and 5HT3 antagonists, respectively. Conversely, the 5HT1A agonist 8-OH-DPAT did not modify the 3H-thymidine incorporation in HMC in the presence of tertatolol. In conclusion, tertatolol inhibits HMC proliferation. The mechanism cannot be explained by beta-blockade or stimulation of 5-HT1A receptors, and still remains unclear.

AB - Tertatolol is a beta-blocker with unique renal vasodilatatory effects, mainly at the level of the microcirculation. Since many vasodilatory agents inhibit human mesangial cell (HMC) proliferation, the effects of tertatolol on the incorporation of 3H-thymidine in HMC were studied. Tertatolol plus mitogens (either fetal calf serum, platelet-derived growth factor (PDGF) or bovine thrombin) were incubated with HMC for 28 h, and 3H-thymidine was added during the last 4 h. Trichloroacetic acid-precipitable counts per well were divided by the mean number of cells in representative wells from the same experiment. The effect of tertatolol on angiotensin II (10-6 mmol/ l)-induced HMC contraction was also assessed by measuring the planar surface area of individual cells. In serum-free media, tertatolol did not significantly alter the incorporation of 3H-thymidine after 28 h of incubation in HMC. When tertatolol was added in the presence of 1% serum, 3H-thymidine incorporation was significantly reduced, compared to 1% serum alone. Tertatolol also inhibited 3H incorporation when PDGF and thrombin were used as the stimulus. The increase in cell number normally seen after 7 days in serum was also reduced by tertatolol. Tertatolol inhibited the reduction in planar surface area of HMC induced by angiotensin II. The inhibitory effect of tertatolol on HMC proliferation was also potentiated by ritanserin and MDL 72222, 5HT2 and 5HT3 antagonists, respectively. Conversely, the 5HT1A agonist 8-OH-DPAT did not modify the 3H-thymidine incorporation in HMC in the presence of tertatolol. In conclusion, tertatolol inhibits HMC proliferation. The mechanism cannot be explained by beta-blockade or stimulation of 5-HT1A receptors, and still remains unclear.

KW - Antihypertension

KW - Beta-blocker

KW - Human glomerular mesangial cells

KW - Tertatolol

UR - http://www.scopus.com/inward/record.url?scp=0027449137&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027449137&partnerID=8YFLogxK

M3 - Article

C2 - 7903216

AN - SCOPUS:0027449137

VL - 83

SP - 51

EP - 56

JO - Cardiology (Switzerland)

JF - Cardiology (Switzerland)

SN - 0008-6312

IS - SUPPL. 1

ER -