Increased Presynaptic α-Adrenoceptor-Mediated Regulation of Noradrenaline Release in the Isolated Perfused Kidney of Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 309s-311s ◽  
Author(s):  
R. D. Ekas ◽  
M. L. Steenberg ◽  
M. F. Lokhandwala
Keyword(s):  
Nerve Stimulation ◽  
Noradrenaline Release ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Isolated Perfused Kidney ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Hypertensive Rat ◽  
Wistar Kyoto

1. Release of [3H]noradrenaline during peri-arterial nerve stimulation and its inhibition by the presynaptic α-adrenoceptor mechanism were studied in the isolated perfused kidney from spontaneously hypertensive and Wistar-Kyoto rats. 2. A frequency related vasoconstriction as well as [3H]noradrenaline release were observed over the stimulating range of 0.25-32 Hz in both the Wistar-Kyoto and spontaneously hypertensive rats. The spontaneously hypertensive rat kidneys exhibited both an increased vasoconstrictor response and a greater [3H]noradrenaline release when compared with the Wistar-Kyoto rat kidneys. 3. Presynaptic inhibition of [3H]noradrenaline release was evaluated at 2 Hz by using the α-adrenoceptor agonist, tramazoline. Increasing concentrations of tramazoline from 2 × 10−9 mol/l to 2 × 10−7 mol/l caused a dose-dependent decrease in the stimulus-induced release of [3H]noradrenaline in spontaneously hypertensive rats but not in Wistar-Kyoto rats. Only 2 × 10−7 mol/l tramazoline had an inhibitory effect in the Wistar-Kyoto rats. 4. These data indicate that noradrenaline release during sympathetic nerve stimulation is greater in the spontaneously hypertensive rat. The supersensitivity of presynaptic α-adrenoceptors observed in spontaneously hypertensive rats may be a consequence of the greater noradrenaline release present in these animals.

Renal and Vascular Wall Prostaglandins in Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 253s-255s ◽  
Author(s):  
Yukio Ozawa ◽  
Keika Kan ◽  
Konosuke Konishi ◽  
Waichi Kitajima ◽  
Yasuo Matsumura
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Aortic Wall ◽  
Spontaneously Hypertensive Rat ◽  
Prostaglandin E ◽  
Prostaglandin I2 ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Medullary Tissue ◽  
Hypertensive Rat ◽  
Wistar Kyoto

1. Renal cortical and medullary tissue and aortic wall were removed from spontaneously hypertensive rats and from age-matched Wistar-Kyoto control animals at ages 30, 60, 90 and 120 days. The tissues were incubated and the release of prostaglandins into the incubation medium was measured. 2. Compared with Wistar-Kyoto control animals, the release of prostaglandin E from renal medullary tissue in spontaneously hypertensive rats was raised at 30 days (pre-hypertensive stage) and 90 days (early hypertensive stage), but decreased later with further establishment of hypertension. No such trend was seen with renal cortical tissue. Tissue release of prostaglandin F tended to be generally high in the spontaneously hypertensive rats compared with that in the control animals, but the difference was not significant. 3. The release of prostaglandin I2, as indicated by measurements of 6-keto prostaglandin F1α, from aortic wall tissue in the spontaneously hypertensive rat during its pre-hypertensive and early hypertensive stages was similar to values obtained in the age-matched control animal. However, aortic wall prostaglandin I2 release in spontaneously hypertensive rats increased thereafter, and was significantly raised at 90 and 120 days. No similar trend was observed with thromboxan A2 release. Release of prostaglandin I2 and thromboxan A2 from renal tissues in spontaneously hypertensive rats did not differ significantly from that in control animals. 4. It is suggested that indomethacin-induced aggravation of hypertension in the spontaneously hypertensive rat may result from suppression of aortic wall prostaglandin I2 formation rather than from the suppression of renal prostaglandin E2 production.

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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