scholarly journals Methylphenidate and fluphenazine, but not amphetamine, differentially affect impulsive choice in Spontaneously Hypertensive, Wistar–Kyoto and Sprague–Dawley rats

2011 ◽  
Vol 1396 ◽  
pp. 45-53 ◽  
Author(s):  
Thomas E. Wooters ◽  
Michael T. Bardo
1991 ◽  
Vol 260 (6) ◽  
pp. F890-F897 ◽  
Author(s):  
M. S. Mozaffari ◽  
S. Jirakulsomchok ◽  
Z. H. Shao ◽  
J. M. Wyss

This study tested the hypothesis that NaCl-sensitive spontaneously hypertensive rats (SHR-S) display a defect in natriuretic and diuretic responses to acute volume loading that contributes to the rise in arterial pressure observed when the rats are fed a high-NaCl diet. Seven-week-old SHR-S and NaCl-resistant SHR rats (SHR-R) and normotensive (Wistar-Kyoto and Sprague-Dawley rats) were fed high- or basal NaCl diets. After 2.5 wk on the diets, preinstrumented conscious rats received an intravenous infusion (5% body wt; 0.5 ml/min) of isotonic saline, and urine was collected through a bladder catheter for 90 min. Control rats on the high-NaCl diet (compared with basal) excreted a significantly greater percentage of Na+ and volume load. In contrast, SHR-S on high-NaCl diet (compared with basal) had a very small increase in natriuretic response and no increase in diuretic response to volume expansion. The effect of renal denervation on natriuretic and diuretic responses to volume load was tested. In SHR-R on 1 and 8% NaCl diets, renal denervation had little or no effect on these responses, suggesting that renal nerves do not play a prominent role in the dietary NaCl-induced increases in the natriuretic and diuretic responses to volume load. These results demonstrate that NaCl-resistant rats rapidly adapt to diets high in NaCl content with increased natriuretic and diuretic responses to acute volume loading. The failure of SHR-S to adapt to the dietary challenge may result in volume loading and a secondary increase in arterial pressure after feeding.


1995 ◽  
Vol 6 (4) ◽  
pp. 1209-1215
Author(s):  
Q C Meng ◽  
J Durand ◽  
Y F Chen ◽  
S Oparil

This study used a novel simple method for the extraction, separation, identification, and quantitation of angiotensin-like immunoactivity from tissue to examine the effects of altering dietary NaCl intake on intrarenal angiotensin I, II, and III levels in salt-sensitive, spontaneously hypertensive rats, salt-resistant Wistar-Kyoto rats, and Sprague-Dawley rats. Seven-week-old male spontaneously hypertensive rats, Wistar-Kyoto rats, and Sprague-Dawley rats were assigned randomly to a diet containing either 8% (high) or 1% (basal) salt and were maintained on these diets for 3 wk. Rats were then decapitated without prior anesthesia, and kidneys were rapidly (< 30 s) removed, snap frozen in liquid nitrogen, and stored at -80 degrees C. Frozen tissue was extracted in 2 M acetic acid and then subjected to solid-phase extraction with the cation exchange resin AG 50W X4. Angiotensin peptides were separated by reversed-phase high-performance liquid chromatography on a phenyl silica gel column with an eluent consisting of 20% acetonitrile in 0.1 M ammonium phosphate buffer, pH 4.9, and quantitated by radioimmunoassay. The elution of standard peptides under isocratic conditions revealed clear resolution of angiotensin I, II, and III and the (1-7) and (3-8) peptides. Recoveries of both labeled and unlabeled angiotensin peptide standards from the extraction step were > 90%. Renal angiotensin II stores were significantly higher in spontaneously hypertensive rats than in Wistar-Kyoto or Sprague-Dawley rats, independent of diet. Renal angiotensin II and III were further suppressed during dietary salt supplementation in both salt-resistant strains but not in the spontaneously hypertensive rat. These findings are consistent with an enhanced (compared with Wistar-Kyoto and Sprague-Dawley rats) role for angiotensin II in the kidney of the salt-sensitive, spontaneously hypertensive rat, particularly under conditions of dietary salt supplementation.


1981 ◽  
Vol 61 (s7) ◽  
pp. 315s-318s ◽  
Author(s):  
G. J. Dusting ◽  
R. Di Nicolantonio ◽  
T. Drysdale ◽  
A. E. Doyle

1. Vasodepressor responses to prostacyclin and nitroprusside were compared in anaesthetized, spontaneously hypertensive rats of the Okamoto strain and Wistar—Kyoto controls, and also in one-kidney, one-clip hypertensive rats and unilaterally nephrectomized controls of the Sprague—Dawley strain. The responses, measured as a percentage of resting blood pressure, did not differ significantly between the hypertensive rats and the normotensive controls within each strain. 2. The effects of intravenous injections of arachidonic acid were also studied in each strain. 3. The vasodepressor effects of high doses of arachidonic acid (1 or 3 mg/kg) were much greater and more prolonged in both groups of hypertensive rats. These differences were abolished by indomethacin (2 mg/kg). 4. Comparisons between the strains showed that whereas Okamoto rats have significantly greater depressor responsiveness to nitroprusside and prostacyclin than Sprague—Dawley rats, the depressor effects of high doses of arachidonic acid (1 and 3 mg/kg) were smaller in the normotensive Wistar-Kyoto than in the Sprague—Dawley rats. 5. It is concluded that hypertensive rats have enhanced ability to transform exogenous arachidonic acid into vasodilator prostanoids. This occurs both in spontaneous hypertension and in experimental renal hypertension. However, rats of the Okamoto strain appear to have reduced ability to form prostacyclin when compared with Sprague—Dawley rats.


1986 ◽  
Vol 71 (1) ◽  
pp. 121-123 ◽  
Author(s):  
Koh-Ichi Murakawa ◽  
Yoshiharu Kanayama ◽  
Masakazu Kohno ◽  
Takahiko Kawarabayashi ◽  
Kenichi Yasunari ◽  
...  

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.


1985 ◽  
Vol 249 (3) ◽  
pp. R341-R347 ◽  
Author(s):  
R. Casto ◽  
M. I. Phillips

We have reported that microinjection of angiotensin II (ANG II) into the nucleus tractus solitarius of urethan-anesthetized normotensive rats produces an increase in mean arterial pressure (MAP) over the dose range 50-500 pmol. The effect in spontaneously hypertensive rats (SHR) is now reported. Over the range 100-500 pmol SHR exhibit increases in MAP and heart rate greater than Wistar-Kyoto or Sprague-Dawley rats. SHR did not exhibit exaggerated responses to intravenous phenylephrine, suggesting a central site of increased responsiveness to ANG II. We also found depressor effects in Sprague-Dawley at lower doses (0.1 and 1 pmol). The decreases in MAP were extremely variable and not dose related. A selected dose of additional neuropeptides identified in the NTS was tested. Somatostatin, bradykinin, and vasoactive intestinal peptide (0.5 nmol) were without cardiovascular effects. Oxytocin and vasopressin, however, produced significant increases in MAP. Substance P produced a very small but significant increase in heart rate and MAP. Interaction between the vasopressin and ANG II pressor effects was studied, and each proved to be independent.


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