Effects of Tonin on Vascular Smooth Muscle of the Hypertensive Rat and Normal Rabbit

1980 ◽  
Vol 59 (s6) ◽  
pp. 339s-342s ◽  
Author(s):  
R. Garcia ◽  
E. L. Schiffrin ◽  
G. Thibault ◽  
R. Boucher ◽  
J. Genest
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Calcium Ion ◽  
Contractile Response ◽  
Control Group ◽  
Hypertensive Rats ◽  
Contralateral Kidney ◽  
Aortic Smooth Muscle ◽  
The One ◽  
Normotensive Control

1. The response of arterial smooth muscle to noradrenaline was studied in one-clip hypertensive rats with or without the contralateral/kidney and in normotensive rabbits. 2. Strips of aorta from one-kidney, one-clip hypertensive animals were less responsive to noradrenaline than normotensive control rats. The contractile response of strips from two-kidney, one-clip hypertensive animals was not different from the control group. These results suggest that the mechanisms responsible for the lesser reactivity in the one-kidney hypertensive group are not a consequence of elevated blood pressure itself, but may be related to the intrinsic contractility of aortic smooth muscle. 3. Tonin potentiated the contraction induced by noradrenaline in aortic strips from hypertensive and normotensive rats. However, this effect was more important in the one-kidney, one-clip hypertensive animals. In the aortic and mesenteric strips from normal rabbits, tonin produced not only potentiation to noradrenaline but direct contraction. 4. The potentiation to noradrenaline and the direct effect of tonin were not affected by a variety of antagonists but were blocked by a calcium ion antagonist, verapamil, suggesting that tonin may act directly on vascular smooth muscle through mechanisms which might be mediated by calcium ions.

Effects of tonin on the response to norepinephrine by the aortic strip of the hypertensive rat

1981 ◽  
Vol 59 (8) ◽  
pp. 790-793 ◽  
Author(s):  
R. Garcia ◽  
E. L. Schiffrin ◽  
G. Thibault ◽  
R. Boucher ◽  
J. Genest
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Hypertensive Rats ◽  
Aortic Smooth Muscle ◽  
Hypertensive Group ◽  
Aortic Strip ◽  
The One

The response to norepinephrine (NE) of arterial smooth muscle from two types of experimental hypertensive rats was investigated. Aortic strips from one-kidney, one-clip hypertensive animals were less responsive to NE than those from their normotensive controls but strips from two-kidney, one-clip hypertensive animals showed no difference from their corresponding controls. The contractility in response to NE was the same in all groups. These results suggest that the mechanisms responsible for the lesser reactivity in the one-kidney hypertensive group are not a consequence of elevated blood pressure itself but may be related to changes in the intrinsic sensitivity of aortic smooth muscle.Tonin potentiated the contraction induced by NE in aortic strips from hypertensive and normotensive rats. This effect was more pronounced in the one-kidney, one-clip hypertensive animals, so that although the aortic smooth muscle from these animals is less reactive to NE, the decreased reactivity can be more than compensated by the presence of tonin. The mechanism of potentiation is not yet clear but the fact that Saralasin did not inhibit it suggests that angiotensin Il is not generated in situ.

Increased Na+ and decreased Mg2+ intracellular concentrations in vascular smooth muscle cells from spontaneously hypertensive rats

1998 ◽  
Vol 95 (5) ◽  
pp. 583-587 ◽  
Author(s):  
Klaus KISTERS ◽  
Ernst-Rudolf KREFTING ◽  
Claus SPIEKER ◽  
Walter ZIDEK ◽  
Karl Heinz DIETL ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Cells ◽  
Dry Weight ◽  
Muscle Cells ◽  
Sodium Content ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Aortic Smooth Muscle

1.Although in blood cells decreased magnesium concentrations and increased sodium concentrations in essential hypertension have often been described, only sparse data exist on cellular magnesium or sodium content and exchange in vascular smooth muscle cells. 2.Therefore in aortic smooth muscle cells from 10 spontaneously hypertensive rats (SHR) of the Münster strain and 10 normotensive Wistar–Kyoto rats (WKY) aged 3 and 8–10 months, the intracellular magnesium and sodium content was measured. 3.Electron-probe X-ray microanalysis was used to determine intracellular Mg2+ and Na+ concentrations in aortic cryosections 3 ;μm thick. The Mg2+ content was 47±13 ;mmol/kg dry weight in SHR versus 48±19 ;mmol/kg dry weight in WKY aged 3 months, and 37±6 ;mmol/kg dry weight in SHR versus 47±4 ;mmol/kg dry weight in WKY aged 8–10 months (P< 0.05). Vascular smooth muscle Na+ content was 283±59 ;mmol/kg dry weight in WKY and 402±123 ;mmol/kg dry weight in SHR aged 3 months (P< 0.05), and 289±17 ;mmol/kg dry weight in WKY versus 548±39 ;mmol/kg dry weight in SHR aged 8–10 months (P< 0.05). 4.Aortic smooth muscle cells from SHR are characterized by a markedly lower intracellular Mg2+ content in 8–10-month-old animals and increased Na+ concentrations compared with normotensive cells in 3- and 8–10-month-old rats. The results may be due to genetically determined disturbances in transmembrane Mg2+ and Na+ transport. Cellular magnesium and sodium handling may be disturbed in SHR aortic smooth muscle as it is in hypertensive blood cells. In addition, it is concluded that vascular smooth muscle cell Mg2+–Na+ exchanger can be altered in a subgroup of SHR.

Angiotensin II modulates frizzled-2 receptor expression in rat vascular smooth muscle cells

2005 ◽  
Vol 108 (6) ◽  
pp. 523-530 ◽  
Author(s):  
Giovanna CASTOLDI ◽  
Serena REDAELLI ◽  
Willy M. M. van de GREEF ◽  
Cira R. T. di GIOIA ◽  
Giuseppe BUSCA ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Ang Ii ◽  
Aortic Smooth Muscle

Ang II (angiotensin II) has multiple effects on vascular smooth muscle cells through the modulation of different classes of genes. Using the mRNA differential-display method to investigate gene expression in rat aortic smooth muscle cells in culture in response to 3 h of Ang II stimulation, we observed that Ang II down-regulated the expression of a member of the family of transmembrane receptors for Wnt proteins that was identified as Fzd2 [Fzd (frizzled)-2 receptor]. Fzds are a class of highly conserved genes playing a fundamental role in the developmental processes. In vitro, time course experiments demonstrated that Ang II induced a significant increase (P<0.05) in Fzd2 expression after 30 min, whereas it caused a significant decrease (P<0.05) in Fzd2 expression at 3 h. A similar rapid up-regulation after Ang II stimulation for 30 min was evident for TGFβ1 (transforming growth factor β1; P<0.05). To investigate whether Ang II also modulated Fzd2 expression in vivo, exogenous Ang II was administered to Sprague–Dawley rats (200 ng·kg−1 of body weight·min−1; subcutaneously) for 1 and 4 weeks. Control rats received normal saline. After treatment, systolic blood pressure was significantly higher (P<0.01), whereas plasma renin activity was suppressed (P<0.01) in Ang II- compared with the saline-treated rats. Ang II administration for 1 week did not modify Fzd2 expression in aorta of Ang II-treated rats, whereas Ang II administration for 4 weeks increased Fzd2 mRNA expression (P<0.05) in the tunica media of the aorta, resulting in a positive immunostaining for fibronectin at this time point. In conclusion, our data demonstrate that Ang II modulates Fzd2 expression in aortic smooth muscle cells both in vitro and in vivo.

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