Studies on the Role of Sodium-Potassium-Activated ATPase as Determinant of Vascular Reactivity in Wistar-Kyoto and Spontaneously Hypertensive Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 187s-189s ◽  
Author(s):  
G. Gouthberg ◽  
B. Jandhyala ◽  
B. Folkow
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Vascular Reactivity ◽  
Sodium Pump ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto ◽  
Sodium Pump Inhibition

1. The role of Na+-K+-activated ATPase in the regulation of resistance vessel reactivity to barium chloride and noradrenaline was investigated with a pair-perfused hindquarter technique in spontaneously hypertensive rats and Wistar-Kyoto rats (6 and 12 week old). Ouabain (10−4 mol/l) was used to inhibit the sodium pump. 2. In all groups studied, dose-response curves to agonists were shifted to the left when ouabain was added to the perfusion medium. This potentiation in vascular reactivity produced by ouabain was expressed as ‘index for sodium-pump inhibition’ (ISPI = ED50 of an agonist/ED50 + ouabain). 3. In mature rats index for sodium-pump inhibition calculated for both agonists was significantly greater in spontaneously hypertensive rats in comparison with Wistar-Kyoto rats, but not so in young spontaneously hypertensive rats. There was, however, a trend towards increased noradrenaline sensitivity in spontaneously hypertensive rats although the difference from Wistar-Kyoto rats was not statistically significant. 4. The data may suggest that there is some increase in the activity of the sodium pump in the resistance vessels of mature spontaneously hypertensive rats, perhaps to compensate for an increased passive sodium permeability.

Effect of destruction of the vascular endothelium upon pressure/flow relations and endothelium-dependent vasodilatation in resistance beds of spontaneously hypertensive rats

1991 ◽  
Vol 80 (5) ◽  
pp. 463-469 ◽  
Author(s):  
Michael D. Randall ◽  
G. Roger Thomas ◽  
C. Robin Hiley
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Regression Line ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Pressure Flow ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Vascular Beds ◽  
Wistar Kyoto

1. Pressure/flow relationships were determined in the in situ blood-perfused superior mesenteric and hindquarters vascular beds of spontaneously hypertensive rats and Wistar-Kyoto normotensive rats before and after destruction of the endothelium with detergent. The effects of indomethacin on the regression of pressure on flow were also investigated in the spontaneously hypertensive rats, as were the endothelium-dependent relaxations in response to carbachol in the mesenteric bed. 2. In the spontaneously hypertensive rats the regression line of pressure on flow in the two vascular beds was both steeper and more elevated than in the Wistar-Kyoto rats, showing that there was greater resistance to flow in the hypertensive animals. Destruction of the endothelium significantly increased the slope of the regression in both Wistar-Kyoto and spontaneously hypertensive rats: the increases in the Wistar-Kyoto rats were 2.4 ± 0.3 fold (mesenteric) and 2.0 ± 0.5 fold (hindquarters) which were comparable with the respective increases of 1.6 ± 0.3 fold and 1.8 ± 0.3 fold in the spontaneously hypertensive rats. 3. Indomethacin (5 mg/kg, intravenously) had no effect on the pressure/flow relations in either of the vascular beds of the spontaneously hypertensive rats. 4. The dose-response curves for the endothelium-dependent vasodilatation in response to carbachol were not significantly different in spontaneously hypertensive and Wistar-Kyoto rats. 5. The results suggest that tonic release of endothelium-derived relaxing factor has similar effects in modulating resistance vessel tone in vivo in both hypertensive and normotensive rats. Further, endothelium-dependent vasodilatation does not appear to be impaired in the mesenteric vasculature in spontaneously hypertensive rats, and there appears to be no significant modulation of mesenteric vascular resistance by tonic release of cyclo-oxygenase products in spontaneously hypertensive rats.

Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

Contribution of Vascular Nitric Oxide to Basal Blood Pressure in Conscious Spontaneously Hypertensive Rats and Normotensive Wistar Kyoto Rats

1995 ◽  
Vol 89 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Naoyoshi Minami ◽  
Yutaka Imai ◽  
Jun-Ichiro Hashimoto ◽  
Keishi Abe
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Methyl Ester ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Basal Blood Pressure ◽  
Wistar Kyoto

1. The aim of this study was to clarify the extent to which vascular nitric oxide contributes to basal blood pressure in conscious spontaneously hypertensive rats and normotensive Wistar Kyoto rats. 2. The contribution of vascular nitric oxide to maintenance of blood pressure was estimated by measuring the pressor response to an intravenous injection of nitric oxide synthase inhibitor, Nω-l-arginine methyl ester, given after serial injections of captopril, vasopressin V1-receptor antagonist (V1-antagonist) and ganglion blocker (pentolinium) in conscious spontaneously hypertensive and Wistar Kyoto rats aged 20–28 weeks. To estimate the ‘amplifier property’ of hypertrophied vasculature in spontaneously hypertensive rats, which is known to modulate pressor responses, the lower blood pressure plateau after serial injections of captopril, V1-antagonist and pentolinium and the maximum blood pressure elicited by subsequent injection of increasing doses of phenylephrine were also measured. 3. The serial injections of captopril, V1-antagonist and pentolinium decreased mean arterial pressure from 164 ± 9 mmHg to 67 ± 2 mmHg and from 117 ± 2 mmHg to 49 ± 1 mmHg in spontaneously hypertensive and Wistar Kyoto rats respectively. The subsequent injection of Nω-l-arginine methyl ester restored mean arterial pressure almost to its control levels in both spontaneously hypertensive and Wistar Kyoto rats. The absolute changes in mean arterial pressure elicited by Nω-l-arginine methyl ester were significantly greater in spontaneously hypertensive than in Wistar Kyoto rats (P < 0.01), but there was no significant difference in the responses to Nω-l-arginine methyl ester when they were expressed as percentages of either the lower blood pressure plateau or maximum blood pressure. 4. These results indicate that basal blood pressure in both spontaneous hypertensive and Wistar Kyoto rats is maintained by a balance between vascular nitric oxide and major pressor systems. They also suggest that the vasodilatory effect of vascular nitric oxide does not differ between spontaneously hypertensive and Wistar Kyoto rats, and that the increased pressor effect of Nω-l-arginine methyl ester in spontaneously hypertensive rats is due to a vascular amplifier mechanism.

Calmodulin levels in hypertensive rats

1985 ◽  
Vol 68 (4) ◽  
pp. 407-410 ◽  
Author(s):  
J. Higaki ◽  
T. Ogihara ◽  
Y. Kumahara ◽  
E. L. Bravo
Keyword(s):  
Intracellular Calcium ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Deoxycorticosterone Acetate ◽  
Spontaneously Hypertensive ◽  
Calcium Dependent ◽  
Wistar Kyoto Rats ◽  
Regulatory Systems ◽  
Wistar Kyoto ◽  
The Brain

1. Intracellular calmodulin levels were measured by direct radioimmunoassay in spontaneously hypertensive rats (SHR) and Wistar—Kyoto rats (WKY). 2. Decreased calmodulin levels were demonstrated in the brain, heart, aorta and kidney of spontaneously hypertensive rats compared with those in Wistar—Kyoto rats. 3. Calmodulin levels in the brain were also decreased in deoxycorticosterone acetate (DOCA)-salt rats, but not changed significantly in the heart, aorta and kidney compared with those in Wistar—Kyoto rats. 4. These findings suggest that intracellular calcium-dependent regulatory systems are genetically disrupted in spontaneously hypertensive rats, but this is probably not an important factor in the development of hypertension.

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