Effect of Propranolol on Blood Pressure in Normal and Hypertensive Rats

1. Propranolol has been given orally in a dose sufficient to achieve beta-blockade throughout the day in normal rats, renal hypertensive animals with and without contralateral nephrectomy, spontaneously hypertensive and deoxycorticosterone (DOCA) hypertensive rats. The drug was given either after hypertension had become fully established or during the phase of rising blood pressure. 2. With this treatment, heart rate was reduced by approximately 100 beats/min in all experimental groups. 3. In established hypertension, treatment with propranolol for 7–9 days was ineffective in lowering blood pressure in any of the models of experimental hypertension. It also had no effect on blood pressure in normal animals. 4. Chronic treatment with propranolol during the phase of rising blood pressure had no effect in renal hypertensive animals. In spontaneous hypertension, the rise in blood pressure was limited to 28 mmHg with propranolol treatment as compared with 58 mmHg in control animals. Likewise, in DOCA hypertension, the rise in pressure was limited to 18 mmHg as compared with 46 mmHg in control animals.

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Cardiac hypertrophy and brain natriuretic peptide in experimental hypertension

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1994.266.2.r451 ◽

1994 ◽

Vol 266 (2) ◽

pp. R451-R457 ◽

Cited By ~ 1

Author(s):

M. Kohno ◽

T. Fukui ◽

T. Horio ◽

K. Yokokawa ◽

K. Yasunari ◽

...

Keyword(s):

Blood Pressure ◽

Brain Natriuretic Peptide ◽

Natriuretic Peptide ◽

Spontaneously Hypertensive Rats ◽

Chronic Treatment ◽

Experimental Hypertension ◽

Acute Administration ◽

Hypertensive Rats ◽

Secretory Rate ◽

Spontaneously Hypertensive

The blood pressure was decreased after chronic treatment with enalapril, MK-954, and hydralazine in deoxycorticosterone acetate (DOCA)-salt-induced malignant hypertension of spontaneously hypertensive rats (SHR); however, ventricular weight and plasma brain natriuretic peptide (BNP) concentration were decreased after enalapril and MK-954 but not after hydralazine. The BNP secretory rates from the ventricle in enalapril- and MK-954-treated DOCA-salt SHR were decreased to approximately 50% of those in untreated DOCA-salt SHR. The BNP secretory rate from the ventricle was positively correlated with ventricular weight in untreated and treated DOCA-salt SHR. In contrast, acute administration of captopril or MK-954 did not decrease the BNP secretory rate from the heart. Results suggest that the decrease in plasma BNP after enalapril and MK-954 is attributed to a decline in the secretion from the ventricle but not from the atrium. The reduction in ventricular mass appeared to be related to this decline.

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

Clinical Science ◽

10.1042/cs059235s ◽

1980 ◽

Vol 59 (s6) ◽

pp. 235s-237s ◽

Cited By ~ 17

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.

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Regression of myocardial hypertrophy and influence of adrenergic system

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1983.244.1.h97 ◽

1983 ◽

Vol 244 (1) ◽

pp. H97-H101 ◽

Cited By ~ 4

Author(s):

S. Sen ◽

R. C. Tarazi

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Regression Analysis ◽

Arterial Pressure ◽

Spontaneously Hypertensive Rats ◽

Myocardial Hypertrophy ◽

Cardiac Response ◽

Adrenergic System ◽

Hypertensive Rats ◽

Spontaneously Hypertensive

Studies of regression of myocardial hypertrophy in spontaneously hypertensive rats (SHR) suggest that the adrenergic system may play an important role in the reversal of hypertrophy. The effect of propranolol on reversal of hypertrophy, however, is still controversial. This study describes the effect of propranolol, given alone or in combination with hydralazine in different ratios for 4 wk, on blood pressure (BP), ventricular weight, and myocardial catecholamine (MC) concentrations. The data show that a certain ratio of propranolol to hydralazine (750:30) leads to moderate BP control (196-156 mmHg) without increased MC (634 vs. 552 ng/g) and moderately reduced hypertrophy. Reduction of BP alone with increased MC (hydralazine alone) or reduction of MC without BP control (propranolol alone) failed to reduce hypertrophy. A significant correlation between both ventricular weight and heart rate with MC (r = 0.6) was obtained by multiple regression analysis. This study suggests that adrenergic factors seem to play an important role in modulating structural cardiac response to variations in arterial pressure.

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