Disparate Effects of Methyldopa and Clonidine on Cardiac Mass and Haemodynamics in Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 449s-452s ◽  
Author(s):  
Shozo Ishise ◽  
Barbara L. Pegram ◽  
E. D. Frohlich
Keyword(s):  
Heart Rate ◽  
Total Peripheral Resistance ◽  
Spontaneously Hypertensive Rats ◽  
Peripheral Resistance ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. Wistar-Kyoto and spontaneously hypertensive rats were given either methyldopa (400 mg day−1 kg−1) or clonidine (0.1 or 0.3 mg day−1 kg−1) for 3 weeks commencing at 20 weeks of age. 2. Both drugs significantly decreased mean arterial pressure in spontaneously hypertensive but not Wistar-Kyoto rats. Heart rate was significantly increased in spontaneously hypertensive rats by methyldopa, whereas clonidine significantly decreased heart rate. The higher dose of clonidine also decreased heart rate in Wistar-Kyoto rats. Both cardiac output and total peripheral resistance decreased slightly, but not significantly, with both agents. 3. Methyldopa, but not the lower equipotent depressor dose of clonidine, reduced left ventricular hypertrophy in spontaneously hypertensive rats. However, the higher dose of clonidine also significantly decreased the heart to body weight ratio despite an increased total peripheral resistance presumably due to the α-adrenergic agonist effect. 4. Minimal changes in organ blood flows were noted with both drugs. 5. These results suggest that neither systemic haemodynamics nor central inhibition of adrenergic drive are primary factors responsible for the regression of hypertrophy.

Blood Pressure and Heart Rate Responses to Centrally Administered Substance P Are Increased in Spontaneously Hypertensive Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 299s-302s ◽  
Author(s):  
T. Unger ◽  
R. W. Rockhold ◽  
T. Yukimura ◽  
R. Rettig ◽  
D. Ganten
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Substance P ◽  
Spontaneously Hypertensive Rats ◽  
Similar Degree ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Intracerebroventricular Injections ◽  
Wistar Kyoto

1. The cardiovascular effects after intracerebroventricular injections of substance P were investigated in normotensive Wistar-Kyoto and in spontaneously hypertensive rats. 2. Substance P increased blood pressure in both rat strains. Wistar-Kyoto rats responded with moderate, dose-dependent blood pressure increases, and heart rate decreased; spontaneously hypertensive rats showed two- to three-fold increased pressor effects and, concomitantly, marked heart rate increases to intracerebroventricular injections of substance P. 3. Sino-aortic baroreceptor denervation rendered Wistar-Kyoto rats supersensitive to intracerebroventricular substance P to a similar degree as unoperated spontaneously hypertensive rats. Sino-aortic denervation had no effect on the blood pressure responses to the peptide in spontaneously hypertensive rats. 4. The central pressor actions of substance P could be markedly attenuated. by intracerebroventricular pretreatment with the derivative of γ-aminobutyric acid, baclofen. 5. We conclude that the baroreceptor reflex is disturbed in spontaneously hypertensive rats. Substance P may contribute to the pathogenesis of hypertension. The effector pathways appear to be different from angiotensin.

Natural biventricular hypertrophy in normotensive rats. I. Physical and hemodynamic characteristics

1979 ◽  
Vol 236 (4) ◽  
pp. H640-H643 ◽  
Author(s):  
M. A. Pfeffer ◽  
J. M. Pfeffer ◽  
F. G. Dunn ◽  
K. Nishiyama ◽  
M. Tsuchiya ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Spontaneously Hypertensive Rats ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Volume Load ◽  
Hemodynamic Characteristics ◽  
Wistar Kyoto ◽  
Cardiac Enlargement

The Wistar-Kyoto strain of normotensive rats (WKY) is being used as a control animal for studies involving the spontaneously hypertensive rats (SHR). A subset of the WKY demonstrating an inheritable transmission of biventricular cardiac hypertrophy (BVH) has been identified. The cardiac enlargement is pronounced, with right and left ventricular weights greater than twice normal in some animals. This natural development of BVH appears to be in response to an increased cardiac output. Blood pressure is normal and, therefore, peripheral resistance is reduced. Left ventricular injection of 15-micrometer radioactively labeled microspheres demonstrated that WKY with BVH had a substantial shunt fraction of their cardiac output (45 +/- 7% radioactivity recovered in the lungs vs. 3 +/- 2% in normal WKY). This subset of WKY with BVH provides a natural model of volume-load hypertrophy. In addition, investigators using the WKY for comparison with SHR should exclude animals with BVH.

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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