Inhibition by cinnarizine of the responses of smooth muscle from spontaneously hypertensive and normotensive rats

1983 ◽  
Vol 61 (12) ◽  
pp. 1523-1525 ◽  
Author(s):  
C. Nghiem ◽  
V. C. Swamy ◽  
D. J. Triggle
Keyword(s):  
Smooth Muscle ◽  
Calcium Antagonist ◽  
Spontaneously Hypertensive Rats ◽  
Carotid Arteries ◽  
Induced Responses ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Tissue Responses ◽  
Wistar Kyoto ◽  
Carotid Arterial

A comparison was made of the inhibition by cinnarizine, a calcium antagonist, of the contractile responses of aortic, carotid, and iliac arterial strips and vasa deferentia from 15- to 17-week-old spontaneously hypertensive rats (SHR) and their normotensive counterparts, Wistar Kyoto (WKY) rats. KCl-induced responses of the aorta from both strains of rats and carotid arteries from WKY only were more sensitive to inhibition than were responses to norepinephrine. No significant differences were observed in the inhibition of tissue responses from the two strains of rats with the exception of the K+-induced responses of carotid arterial strips from SHR which were significantly less sensitive to inhibition when compared with carotid strips from WKY.

The responses of carotid vascular strips from spontaneously hypertensive and normotensive rats

1980 ◽  
Vol 58 (1) ◽  
pp. 53-59 ◽  
Author(s):  
V. C. Swamy ◽  
D. J. Triggle
Keyword(s):  
Smooth Muscle ◽  
Spontaneously Hypertensive Rats ◽  
Carotid Arteries ◽  
Age Groups ◽  
Extracellular Calcium ◽  
Induced Responses ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Vascular Responses ◽  
Carotid Arterial

The responses to noradrenaline (NA) and KCl of carotid arterial strips from spontaneously hypertensive rats (SHR) and three strains of normotensive rats (NR) were compared using tissues obtained from young (5–7 weeks) or older (15–17 weeks) rats. The maximum responses and sensitivity of strips from SHR were less than those of NR in both age groups. Relaxation of maximum NA-induced responses was consistently faster, and relaxation of KCl-induced responses generally slower with strips from SHR. Carotid strips from young SHR showed a greater dependence on extracellular calcium in their responses to NA and a lesser dependence in their KCl-induced responses than tissues from NR. We conclude that the smooth muscle of carotid arteries from SHR differs intrinsically from that of NR and that the differences in vascular responses may be related to altered excitation-contraction processes in the SHR.

scholarly journals Spontaneously hypertensive rats and platelet Ca2+-ATPases: specific up-regulation of the 97 kDa isoform

1993 ◽  
Vol 295 (3) ◽  
pp. 685-690 ◽  
Author(s):  
B Papp ◽  
E Corvazier ◽  
C Magnier ◽  
T Kovàcs ◽  
N Bourdeau ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Spontaneously Hypertensive Rats ◽  
Human Platelets ◽  
Hypertensive Rats ◽  
Extreme Caution ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Peptide Antibody ◽  
Sds Page ◽  
Wistar Kyoto

The use of platelets instead of smooth muscle cells (SMC) to study the abnormal Ca2+ handling found in hypertension was investigated using spontaneously hypertensive rats (SHR). We studied the regulation of platelet Ca(2+)-ATPases, as we have recently demonstrated that human platelets, like SMC, contain the Ca(2+)-ATPase isoform termed SERCA2-b (sarco-endoplasmic reticulum Ca(2+)-ATPase). In mixed membranes isolated from platelets of normotensive Wistar-Kyoto (WKY) rats and SHR, total Ca(2+)-ATPase activity was found to be 43% higher in SHR than in WKY rats. By the use of autophosphorylation of rat platelet Ca(2+)-ATPases with [gamma-32P]ATP, followed by SDS/PAGE and Western blotting, we found that rat platelets express two distinct Ca(2+)-ATPases: a 100 kDa isoform, recognized by a SERCA2-b-specific anti-peptide antibody, and a 97 kDa isoform, specifically recognized by a polyclonal anti-SERCA antibody. Comparative analysis of platelet membrane Ca(2+)-ATPases from WKY rats and SHR demonstrated that the expression of the SERCA2-b isoform did not change significantly (128 +/- 22%), whereas that of the 97 kDa isoform reached 300 +/- 35% in SHR when compared with WKY rats. We concluded that the upregulation of total platelet Ca(2+)-ATPases in SHR is not due to the 100 kDa SERCA2-b isoform found in SMC, but is specific to the 97 kDa Ca(2+)-ATPase isoform which is not present in SMC. Therefore platelets should be used with extreme caution as a surrogate model of vascular smooth muscle Ca2+ homeostasis.

Calcium reactivity and antagonism in portal veins from spontaneously hypertensive and normotensive rats

1984 ◽  
Vol 62 (1) ◽  
pp. 146-150 ◽  
Author(s):  
A. L. Harris ◽  
V. C. Swamy ◽  
D. J. Triggle
Keyword(s):  
Inhibitory Activity ◽  
Spontaneously Hypertensive Rats ◽  
Age Groups ◽  
Induced Responses ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Activity Frequency ◽  
Blood Pressures ◽  
Portal Veins ◽  
Wistar Kyoto

Reactivities of portal veins from spontaneously hypertensive rats (SHR) and normotensive controls (Wistar Kyoto, WKY) at 5–7 and 15–17 weeks of age were compared. Systolic blood pressures were not different at 5–7 weeks but those of SHR were significantly elevated (177 ± 4 mmHg) (1 mmHg = 133.322 Pa) at 15–17 weeks. Spontaneous activity, frequency, and tension were greater in SHR for both age groups. Young SHR were more sensitive to K+ at 5–7 weeks but less sensitive at 15–17 weeks than age-matched WKY rats. Sensitivity to Ca2+ in a K+-depolarizing medium was higher in SHR than in WKY for both age groups. Maximum tension responses to K+ or Ca2+ were greater in SHR. The Ca2+ channel antagonists nifedipine, nitrendipine, and nisoldipine were potent inhibitors of both noradrenaline- and K+-induced responses but did not show differences in inhibitory activity between WKY and SHR.

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