Pressor Effect of Beta Blocking Agents in Rats

1972 ◽  
Vol 50 (3) ◽  
pp. 207-214 ◽  
Author(s):  
D. Regoli ◽  
U. Regoli ◽  
E. Gysling

In rats anesthetized with urethane, intravenous injection of oxprenolol, propranolol, and d-propranolol increases arterial pressure, while practolol is ineffective. These changes of arterial pressure occur in rats previously treated with phentolamine or phenoxybenzamine, indicating that the pharmacological block of alpha receptors does not prevent vasoconstriction by oxprenolol and propranolol. On the contrary, beta receptor blocking agents have little effect on the arterial pressure of rats treated with a ganglion blocker (pentolinium).The pressor action of adrenaline and angiotensin is significantly depressed by alpha blockers, but small doses of oxprenolol restore completely the action of angiotensin and, in part, that of adrenaline. Adrenaline produces a biphasic effect on the blood pressure of anesthetized rats. Both phases of the effect are eliminated by alpha blockers while ganglion blocker abolishes the hypotensive phase only. Administration of small doses of oxprenolol and propranolol (1–10 μg/kg) in untreated rats or in animals treated with alpha blockers increases significantly the blood pressure, but does not modify the biphasic effect of adrenaline.The results indicate that the pressor effect of small doses of beta blocker may not be entirely related to the elimination of the beta inhibitory effect of exogenous adrenaline on the vascular system. No changes of blood pressure occur when beta blockers are administered to animals treated with ganglion blockers, suggesting that the vasoconstriction produced by propranolol and oxprenolol is not due to a direct effect on the vascular smooth muscles.

1970 ◽  
Vol 48 (7) ◽  
pp. 481-489 ◽  
Author(s):  
D. Regoli

Propranolol (10 to 30 μg/kg), oxprenolol (trasicor) (5 to 10 μg/kg), and sotalol (10 to 50 μg/kg) evoke an acute and prolonged increase of arterial pressure in normal and nephrectomized rats, while after adrenalectomy the arterial pressure remains unchanged or is reduced. The pressor effect is accompanied by a reduction of heart rate. The dose of the three beta blockers evoking an arterial pressure increase does not antagonize the effect of isopropylnoradrenaline. To block the beta receptors, doses 10 to 100 times higher than those effective on arterial pressure have to be used. The block of the beta receptors is accompanied by an initial fall of the blood pressure and by a significant decrease of the heart rate. The pressor effect of beta blockers is not antagonized but rather is potentiated by phenoxybenzamine and phentolamine. Moreover, in the presence of an alpha receptor blockade, the administration of beta blockers partially restores the response to catecholamines. These results support the hypothesis that the pressor effect evoked by beta receptor blocking agents may be due: (a) to the release of endogenous catecholamines and (b) to the interference by beta blockers with phenoxybenzamine and phentolamine on the alpha receptors.


1996 ◽  
Vol 271 (2) ◽  
pp. H812-H822 ◽  
Author(s):  
W. C. Rose ◽  
J. S. Schwaber

Vagal control of the heart is the most rapidly responding limb of the arterial baroreflex. We created a mathematical model of the left heart and vascular system to evaluate the ability of heart rate to influence blood pressure. The results show that arterial pressure depends nonlinearly on rate and that changes in rate are of limited effectiveness, particularly when rate is increased above the basal level. A 10% change in heart rate from rest causes a change of only 2.4% in arterial pressure due to the reciprocal relation between heart rate and stroke volume; at higher rates, insufficient filling time causes stroke volume to fall. These findings agree well with published experimental data and challenge the idea that changes in heart rate alone can strongly and rapidly affect arterial pressure. Possible implications are that vagally mediated alterations in inotropic and dromotropic state, which are not included in this model, play important roles in the fast reflex control of blood pressure or that the vagal limb of the baroreflex is of rather limited effectiveness.


1958 ◽  
Vol 195 (2) ◽  
pp. 407-411 ◽  
Author(s):  
G. M. C. Masson ◽  
A. C. Corcoran ◽  
S. Franco-Browder

Experiments with pharmacologic blocking agents indicate that, in the barbiturate anesthetized rat, the depressor response to injected histamine-liberators is attributable to the release into the circulation of a mixture of serotonin and histamine. The data do not suggest participation of any other depressor agent. The effect of such release on blood pressure can be simulated by infusion of a mixture of serotonin and histamine, indicating that the depressor response to endogenous release or exogenous administration is undistinguishable, although tissue responses are very different. The depressor responses to histamine liberators or to infusions of histamine-serotonin mixtures can be suppressed by pretreatment with an antihistamine such as promethazine and an antiserotonin agent such as BOL. Inhibition is also obtained with drugs possessing both properties such as phenoxybenzamine.


1919 ◽  
Vol 29 (2) ◽  
pp. 173-186 ◽  
Author(s):  
Peyton Rous ◽  
George W. Wilson

Ether anesthesia has a marked influence in diminishing the pressor response to minute amounts of epinephrine injected directly into the circulation. Hemorrhage also acts to lessen or abolish the response, and to a degree directly proportional to the lowering of the blood pressure it causes. In the exsanguinated animal an amount of epinephrine three or four times that sufficient to produce a pressure rise of 10 to 15 mm. of mercury under normal conditions, may be entirely without effect. The response to large doses, on the other hand, is uninfluenced by ether or hemorrhage. The facts stated have a practical bearing not only on the employment of epinephrine to tide over collapse but on its possible utilization in the future to raise a low blood pressure to the normal height and maintain it during a considerable period. For the amount of epinephrine which under normal conditions will suffice to bring up the blood pressure may have little or no effect on an etherized individual or on one who has lost blood. The same difficulty will doubtless be encountered under other conditions. In animals rendered plethoric by transfusion the response to small doses of epinephrine lessens in proportion as the blood pressure is increased by the plethora.


Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 711-712
Author(s):  
William M Manger ◽  
Shlomoh Simchon ◽  
Kung-Ming Jan ◽  
Francis Haddy ◽  
Charles T Stier ◽  
...  

P103 Dietary K supplementation was reported to lower blood pressure and prevent strokes in humans and to prevent strokes in hypertensive DS rats. We report a biphasic effect as a function of KCl dose in DS rats that were fed 1% NaCl with increasing dietary KCl, namely, 0.7, 2.6, 4, and 8%. After 8 months on 1% NaCl supplemented with 0.7% KCl, mean arterial pressure (MAP), plasma volume (PV), cardiac output (CO), total peripheral, renal and cerebral vascular resistances (TPR, RVR, CVR) increased compared to salt-resistant DR rats; on 2.6% KCl all these parameters decreased compared with DS on 0.7% KCl diet. When KCl was increased to 4 and 8%, MAP, PV, CO and RVR progressively increased in DS and DR rats, without changing TPR; these changes were accompanied by parallel increases in plasma aldosterone. Only DS rats on the ”optimal“ 2.6% KCl supplement maintained hemodynamics most similar to control DR rats and thus prevented Na retention, hypertension, increases in RVR and CVR. These beneficial hemodynamic effects may explain stroke prevention.


1958 ◽  
Vol 194 (3) ◽  
pp. 597-600 ◽  
Author(s):  
Irvine H. Page ◽  
J. W. McCubbin

Pentobarbital anesthesia produces an important change in the dog's arterial pressure response to TEAC. Without anesthesia, the response, instead of being sharply depressor, is characteristically pressor, or biphasic and mainly pressor. Only occasionally is it depressor. Small doses of TEAC more often elicited depressor responses than did large ones. Mecamylamine, hexamethonium and chlorisondamine usually also failed to cause appreciable lowering of arterial pressure in unanesthetized dogs, but did not show as much pressor activity as did TEAC. Responses to TEAC in hypertensive conscious man showed considerable variability, but the overall pattern of response tended more to resemble that of anesthetized than that of unanesthetized dogs. Atropine caused narrowing of pulse pressure, tachycardia, little change in mean pressure, and the response to TEAC to become mainly depressor—though not to the same degree as did pentobarbital. The greatly augmented depressor activity of ganglion blocking agents after pentobarbital anesthesia probably depends in large part upon nearly complete inhibition of parasympathetic cardioinhibitory activity by the anesthetic agent, and upon partial suppression of sympathetic compensatory reflexes by the ganglion blocking action of pentobarbital. Cardiovascular reactivity measurements are closely dependent on the conditions of the experiment and anesthesia is one of the most important of these conditions.


2008 ◽  
Vol 99 (6) ◽  
pp. 1284-1292 ◽  
Author(s):  
Alessandro Braschi ◽  
Donald J. Naismith

Blood pressure (BP) shows a continuous relationship with the risk of CVD. There is substantial evidence that dietary potassium exerts an anti-pressor effect. Most clinical trials have used KCl. However, the chloride ion may have a pressor effect and in foods potassium is associated with organic anions. In a double-blind randomized placebo-controlled trial we explored the effect on BP of two salts of potassium, KCl and potassium citrate (K-cit), in predominantly young healthy normotensive volunteers. The primary outcome was the change in mean arterial pressure as measured in a clinic setting. After 6 weeks of supplementation, compared with the placebo group (n31), 30 mmol K-cit/d (n28) changed mean arterial pressure by − 5·22 mmHg (95 % CI − 8·85, − 4·53) which did not differ significantly from that induced by KCl (n26), − 4·70 mmHg ( − 6·56, − 2·84). The changes in systolic and diastolic BP were − 6·69 (95 % CI − 8·85, − 4·43) and − 4·26 (95 % CI − 6·31, − 2·21) mmHg with K-cit and − 5·24 (95 % CI − 7·43, − 3·06) and − 4·30 (95 % CI − 6·39, − 2·20) mmHg with KCl, and did not differ significantly between the two treatments. Changes in BP were not related to baseline urinary electrolytes. A greater treatment-related effect was observed in those with higher systolic BP. Increasing dietary potassium could therefore have a significant impact on the progressive rise in BP in the entire population.


1918 ◽  
Vol 27 (5) ◽  
pp. 539-561 ◽  
Author(s):  
J. P. Simonds

1. In peptone shock there is a marked, precipitate fall in arterial pressure. At the same time there is a fall in venous pressure. 2. In experimental fat embolism, (a) the fall in blood pressure is always gradual; (b) approximately 1 cc. of oil for each pound of body weight must be injected before a lasting fall in arterial pressure is produced; (c) it makes only a slight difference whether this amount is injected in small doses at a time or in relatively large quantities; and (d) when the arterial pressure falls, but not till then, the venous pressure rises. 3. In peptone shock, dyspnea, by its suction and force-pump action upon the reservoir of stagnating blood in the liver, brings more blood to the heart and causes a rise in arterial pressure. By repeatedly inducing short periods of dyspnea at frequent intervals, permanently beneficial results are obtained and the life of the animal can be saved. 4. In experimental fat embolism, dyspnea will cause a rise in blood pressure. But permanently beneficial results have not been obtained by this method. If dyspnea is found to bring permanent improvement in surgical shock, it is indirect evidence that this condition is not due to fat embolism. Respiratory suction is probably not responsible for the rise in blood pressure in experimental fat embolism. It seems more likely that the dyspnea in some way facilitates the passage of blood through the embarrassed pulmonary circulation. Artificial respiration with a bellows will also frequently cause a rise in blood pressure in experimental fat embolism. 5. In peptone shock the respiration is usually not affected, although there is some evidence that the respiratory center may be in a state of increased irritability. In experimental fat embolism, in some animals a violent dyspnea develops spontaneously. This is usually accompanied by edema of the lungs. In other instances, an apnea occurs, even before the blood pressure has begun to decline.


2009 ◽  
Vol 11 (10) ◽  
pp. 783-792 ◽  
Author(s):  
Eduardo R. Monteiro ◽  
Daniela Campagnol ◽  
Letícia R. Parrilha ◽  
Luísa Z. Furlan

The cardiovascular effects of dexmedetomidine alone or in combination with atropine were studied in six cats. Cats underwent four treatments in a randomized crossover design as follows: DEX15, saline+dexmedetomidine 15 μg/kg; DEX30, saline+dexmedetomidine 30 μg/kg; ADEX15, atropine+dexmedetomidine 15 μg/kg; ADEX30, atropine+dexmedetomidine 30 μg/kg. Pulse rate (PR) and systolic arterial pressure (SAP) decreased in DEX15 and DEX30. Premedication with atropine was effective in preventing bradycardia (PR<100 beats/min) and resulted in a biphasic effect in blood pressure. Hypertension was followed by a gradual decrease in SAP. Rate pressure product decreased in DEX15 and DEX30 whereas in ADEX15 and ADEX30 it remained within baseline values for at least 60 min. Although premedication with atropine in cats sedated with dexmedetomidine prevents bradycardia, it induces hypertension and increases myocardial oxygen consumption. The magnitude of cardiovascular effects produced by dexmedetomidine in cats does not seem to be dose-related.


Author(s):  
M.A. Bubnova ◽  
O.N. Kryuchkova

Patients with hypertension (HT) and chronic obstructive pulmonary disease (COPD) have a high risk of cardiovascular complications. Up to now, there is no optimal strategy for combined antihypertensive therapy. Still, the data of 24-hour blood pressure monitoring (BPM) are important while choosing treatment tactics. The aim of the paper is to study the features of indicators in patients with arterial hypertension (AH) and COPD. Materials and methods. 130 patients with HT were included in the study. The main group (n=90) included comorbid patients with HT and COPD, their average age was 61.30±1.01; the comparison group (n=40) consisted of patients with HT, their average age was 59.10±1.53. All patients underwent 24-hour BPM. Results. Comorbid patients revealed an increase in the mean 24-hour and night systolic and mean arterial pressure values as well as a significant increase in the load index of systolic, diastolic and mean arterial pressure. Also, comorbid patients demonstrated higher blood pressure in contrast to the patients of the comparison group. They had increased systolic, diastolic and mean blood pressure variability and a quicker rate of morning blood pressure rise. According to 24-hour blood pressure dynamics, pathological types of the 24-hour blood pressure curve, a higher frequency of the night-peaker profile dominated in patients with COPD if compared to patients with HT. Conclusion. The obtained data indicated a high risk of cardiovascular complications in comorbid patients, early target organ damage and an unfavorable disease prognosis. It means that both further study of hypertension clinical course in such patients and personalization of antihypertensive therapy are relevant. Keywords: hypertension, chronic obstructive pulmonary disease, 24-hour monitoring, blood pressure. Пациенты с артериальной гипертензией (АГ) и хронической обструктивной болезнью легких (ХОБЛ) имеют высокий риск возникновения кардиоваскулярных осложнений. В настоящее время в лечении не определена наиболее оптимальная стратегия комбинированной антигипертензивной терапии. Для выбора тактики терапии важную роль играют показатели суточного мониторирования артериального давления (СМАД). Цель. Изучить особенности показателей СМАД у пациентов с АГ на фоне ХОБЛ. Материалы и методы. В исследование включено 130 пациентов с АГ. В основную группу (n=90) вошли пациенты с АГ и ХОБЛ (средний возраст – 61,30±1,01 года), в группу сравнения (n=40) – больные только АГ (средний возраст – 59,10±1,53 года). Всем пациентам проведено СМАД. Результаты. У пациентов с коморбидностью выявлены следующие особенности суточных показателей артериального давления: увеличение значений среднесуточных и средненочных показателей систолического и среднего артериального давления; существенное повышение индекса нагрузки систолическим, диастолическим и средним артериальным давлением. Также эти больные отличались от пациентов группы сравнения более высокими значениями пульсового давления, имели повышенную вариабельность систолического, диастолического и среднего артериального давления, у них наблюдалось увеличение скорости утреннего подъема артериального давления. Суточная динамика артериального давления у пациентов с ХОБЛ характеризовалась преобладанием патологических типов суточной кривой АД, более высокой частотой профиля night-peaker по сравнению с больными только АГ. Выводы. Выявленные особенности свидетельствуют о высоком риске сердечно-сосудистых осложнений у пациентов с коморбидностью, раннем поражении органов-мишеней и неблагоприятном прогнозе заболевания, что требует дальнейшего изучения особенностей клинического течения АГ у таких больных и индивидуализации антигипертензивной терапии. Ключевые слова: артериальная гипертензия, хроническая обструктивная болезнь легких, суточное мониторирование, артериальное давление.


Sign in / Sign up

Export Citation Format

Share Document