Cytoplasmic Free [Ca2+] is Increased in the Platelets of Spontaneously Hypertensive Rats and Essential Hypertensive Patients

1985 ◽  
Vol 68 (2) ◽  
pp. 179-184 ◽  
Author(s):  
Giacomo Bruschi ◽  
Maria E. Bruschi ◽  
Maurizio Caroppo ◽  
Guido Orlandini ◽  
Marco Spaggiari ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Calcium Concentration ◽  
Free Calcium ◽  
Cytoplasmic Calcium ◽  
Hypertensive Rats ◽  
Hypertensive Patients ◽  
Spontaneously Hypertensive ◽  
Human Control ◽  
Free Calcium Concentration ◽  
Wistar Kyoto

1. The cytoplasmic free calcium concentration ([Ca2+]i) was assessed with the fluorescent dye Quin 2 in platelets and lymphocytes of spontaneously hypertensive rats (SHR), normotensive Wistar—Kyoto rats (WKY), essential hypertensive patients (EHP) and normotensive human control subjects (NCS). 2. [Ca2+]i was significantly higher in the platelets of 8- and 20-week-old SHR in comparison with WKY. However, no difference was evident after weaning. Changes of cellular calcium in hypertensive rats apparently evolved simultaneously with the development of high arterial pressure. 3. [Ca2+]i was significantly higher in platelets of EHP than in NCS. 4. In lymphocytes of SHR, [Ca2+]i was not different from WKY at 4 and 8 weeks, but was increased at 14 weeks and at older ages. In EHP, intralymphocytic [Ca2+] was only modestly higher than in controls. On the whole, the results suggest that control of cytoplasmic calcium in these blood cells is similarly affected in human and animal models of primary hypertension.

Free calcium concentration in brain nerve endings of spontaneously hypertensive rats

1987 ◽  
Vol 103 (5) ◽  
pp. 609-612 ◽  
Author(s):  
S. N. Orlov ◽  
N. I. Pokudin ◽  
G. M. Kravtsov ◽  
Yu. V. Postnov ◽  
I. M. Okun' ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Calcium Concentration ◽  
Nerve Endings ◽  
Free Calcium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Free Calcium Concentration

Cytoplasmic free [Ca2+] is not increased in the platelets of deoxycorticosterone–salt and spontaneously hypertensive rats

1986 ◽  
Vol 71 (1) ◽  
pp. 121-123 ◽  
Author(s):  
Koh-Ichi Murakawa ◽  
Yoshiharu Kanayama ◽  
Masakazu Kohno ◽  
Takahiko Kawarabayashi ◽  
Kenichi Yasunari ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Free Calcium ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Acetoxymethyl Ester ◽  
Spontaneously Hypertensive ◽  
Sprague Dawley Rats ◽  
Significant Difference ◽  
Free Calcium Concentration ◽  
Wistar Kyoto

1. The cytoplasmic free calcium concentration ([Ca2+]i) in the platelets of spontaneously hypertensive rats (SHR), Wistar–Kyoto rats (WKY), deoxycorticosterone–salt hypertensive rats (DOC) and normotensive Sprague–Dawley rats (SD) was measured with the fluorescent dye, quin-2-tetra-acetoxymethyl ester. 2. No significant difference in platelet [Ca2+]i was found between SHR and WKY or between DOC and SD rats. 3. No correlations were found between systolic blood pressure and [Ca2+]i. 4. These results suggest that the elevation of platelet [Ca2+]i does not necessarily accompany hypertension in rats.

Cytosolic free calcium regulation in renal tubules from spontaneously hypertensive rats

1990 ◽  
Vol 258 (1) ◽  
pp. F175-F182 ◽  
Author(s):  
W. R. Jacobs ◽  
C. M. Ferrari ◽  
P. C. Brazy ◽  
L. J. Mandel
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Metabolic Inhibitors ◽  
Free Calcium ◽  
Renal Tubules ◽  
Hypertensive Rats ◽  
Cytosolic Free Calcium ◽  
Spontaneously Hypertensive ◽  
Circulating Cells ◽  
The Difference ◽  
Wistar Kyoto

Cytosolic free calcium (Caf) was measured in isolated renal cortical tubules from spontaneously hypertensive rats (SHR) and age-matched control Wistar-Kyoto (WKY) rats to evaluate whether the onset of hypertension is associated with a change in Caf. At the same time, the cellular mechanism by which differences in Caf occur between these two strains of rats was examined. Caf was significantly lower in renal tubules from 4- to 5-wk (142 +/- 6 vs. 187 +/- 15 nM), 6- to 7-wk (138 +/- 15 vs. 187 +/- 8 nM), and 8- to 9-wk-old (161 +/- 5 vs. 216 +/- 9 nM) SHR compared with age-matched WKY. The lower Caf in SHR tubules was considered to be the result of either an increase in Ca efflux or a reduction in Ca permeability. To the extent that metabolic inhibitors increased Caf but did not alter the difference between SHR and WKY, a primary difference in Caf efflux was excluded. Conversely, when Ca permeability was altered, either with Ca ionophores or incubation in Ca-free medium, Caf changed in the appropriate direction and the difference between SHR and WKY was no longer apparent. These results demonstrate that 1) the previously reported increase in Caf in circulating cells is not a universal feature of hypertension and 2) the lower Caf in renal tubules from SHR appears to be related to a lower Ca permeability. Whether the differences in Caf between SHR and WKY is a permissive factor for the renal contribution to hypertension remains to be elucidated.

Norepinephrine-induced calcium signaling pathways in afferent arterioles of genetically hypertensive rats

2001 ◽  
Vol 281 (2) ◽  
pp. F264-F272 ◽  
Author(s):  
Max Salomonsson ◽  
William J. Arendshorst
Keyword(s):  
Strain Difference ◽  
Strain Differences ◽  
External Solution ◽  
Free Calcium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Free Calcium Concentration ◽  
Afferent Arterioles ◽  
Wistar Kyoto ◽  
A Site

This study provides new information about the relative importance of calcium mobilization and entry in the renal vascular response to adrenoceptor activation in afferent arterioles isolated from 7- to 8-wk-old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Intracellular free calcium concentration ([Ca2+]i) was measured in microdissected arterioles utilizing ratiometric photometry of fura 2 fluorescence. There was no significant strain difference in baseline [Ca2+]i. Norepinephrine (NE; 10−6 and 10−7 M) elicited immediate, sustained increases in [Ca2+]i. The general temporal pattern of response to 10−6 M NE consisted of an initial peak and a maintained plateau phase. The response to NE was partially blocked by nifedipine (10−6 M) or 8-( N,N-diethylamino) octyl-3,4,5-trimetoxybenzoate (TMB-8; 10−5 M). A calcium-free external solution abolished the sustained [Ca2+]i plateau response to NE, with less influence on the peak response. In the absence of calcium entry, TMB-8 (10−5 M) completely blocked the calcium response to NE in WKY but not SHR, suggesting strain differences in mobilization. A higher concentration of TMB-8 (10−4 M), however, blocked all discernible mobilization in both strains. We conclude that there are differences in Ca2+ handling in renal resistance vessels between young WKY and SHR with respect to mobilization stimulated by α-adrenoceptors. Afferent arterioles of young SHR appear to have a larger inositol-1,4,5-trisphosphate-sensitive pool or release from a site less accessible to TMB-8.

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