scholarly journals Estimated affinity of isoproterenol to cardiac chronotropic beta-receptor and of phenylephrine to vasoconstrictive alpha-receptor of the systemic resistance vessels in human borderline hypertension.

1983 ◽  
Vol 47 (2) ◽  
pp. 240-255 ◽  
Author(s):  
HIROYASU ITO ◽  
NAOKI TONAI ◽  
SENRI HIRAKAWA
Keyword(s):  
Systemic Resistance ◽  
Borderline Hypertension ◽  
Beta Receptor ◽  
Resistance Vessels

Cardiopulmonary reflexes and blood pressure in exercising sinoaortic-denervated dogs

1984 ◽  
Vol 57 (5) ◽  
pp. 1417-1421 ◽  
Author(s):  
D. A. Daskalopoulos ◽  
J. T. Shepherd ◽  
S. C. Walgenbach
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vagal Afferents ◽  
Systemic Resistance ◽  
Vigorous Exercise ◽  
Arterial Blood ◽  
Resistance Vessels ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Cardiopulmonary Receptors

To examine the role of cardiopulmonary receptors in arterial blood pressure regulation during and after exercise, conscious dogs with chronic sinoaortic denervation were subjected to 12 min of light exercise and 12 min of exercise that increased in severity every 3 min. Hemodynamic measurements were made before and after interruption of cardiopulmonary afferents by bilateral cervical vagotomy. During both exercise protocols, after an initial transient decrease, the arterial blood pressure remained close to resting values before and after vagotomy. On cessation of the graded exercise, the arterial blood pressure did not change before, but a rapid and sustained increase in pressure occurred after vagotomy. At the time of this increase the cardiac output and heart rate were returning rapidly to the resting level. The study demonstrates that in the chronic absence of arterial baroreflexes, vagal afferents prevent a rise in arterial blood pressure after vigorous exercise presumably by the action of cardiopulmonary receptors causing a rapid dilatation of systemic resistance vessels.

Nadolol prevents the exercise-induced rise in lymphocyte beta-receptor number in borderline hypertension

1989 ◽  
Vol 7 ◽  
pp. S46-47
Author(s):  
Laura Terzoli ◽  
Renato Bragato ◽  
Giovanni Battista Bella ◽  
Gastone Leonetti ◽  
Alberto Zanchetti
Keyword(s):  
Borderline Hypertension ◽  
Beta Receptor ◽  
Receptor Number ◽  
Exercise Induced

Vascular Reactivity in Post-Deoxycorticosterone Hypertension in Rats and its Relation to ‘Irreversible’ Hypertension in Man

1972 ◽  
Vol 42 (5) ◽  
pp. 579-590 ◽  
Author(s):  
L. J. Beilin ◽  
G. Ziakas
Keyword(s):  
Blood Pressure ◽  
High Pressure ◽  
Vascular Reactivity ◽  
Renal Hypertension ◽  
Peripheral Resistance ◽  
Systemic Resistance ◽  
Wall Thickening ◽  
Resistance Vessels ◽  
Arteriolar Wall ◽  
Rat Tail

1. The mechanism by which the blood pressure remains elevated after temporary administration of deoxycorticosterone (DOCA) and saline has been studied by comparing vascular reactivity in the resistance bed of the isolated perfused rat tail in animals with post-DOCA hypertension and normotensive controls. 2. Animals with post-DOCA hypertension showed increased arteriolar responses to noradrenaline and 5-hydroxytryptamine, increased maximum contractile responses to noradrenaline, and increased resistance to flow under conditions of maximum vasodilation. 3. These abnormalities may be explained largely on the basis of arteriolar wall thickening resulting from hypertension and they will lead to a high peripheral resistance. 4. Evidence from experiments on chronic renal hypertension indicates that hypertension only becomes irreversible when the ability of the kidneys to regulate blood pressure is impaired. When this has occurred the high resistance offered by abnormal systemic arterioles will be a significant factor in maintaining a high arterial pressure and the high pressure will in turn continue to exert deleterious effects on resistance vessels, including those of the kidney. 5. It is suggested that persistence of hypertension in patients in whom the initial cause of the hypertension has apparently been removed is due to changes in morphology and reactivity of renal and systemic resistance vessels similar to those described in arterioles of animals with post-DOCA hypertension.

Effect of dopamine on systemic capacitance vessels and systemic resistance vessels

1994 ◽  
Vol 1 ◽  
pp. 373
Author(s):  
S. Minatoguchi ◽  
T. Segawa ◽  
H. Wada ◽  
K. Takai ◽  
K. Inoue ◽  
...  
Keyword(s):  
Systemic Resistance ◽  
Resistance Vessels ◽  
Capacitance Vessels

THE EFFECT OF BETA-RECEPTOR BLOCKADE ON EXERCISE AND ARGININE-INDUCED GROWTH HORMONE SECRETION IN MAN

1974 ◽  
Vol 77 (1_Suppl) ◽  
pp. S6 ◽  
Author(s):  
S. Raptis ◽  
H. Hirth-Schmidt ◽  
K. E. Schröder ◽  
E. F. Pfeiffer
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Receptor Blockade ◽  
Beta Receptor ◽  
Beta Receptor Blockade

CATECHOLAMINE ANTAGONISM TO OXYTOCIN-INDUCED MILK-EJECTION

1971 ◽  
Vol 68 (1_Suppla) ◽  
pp. S5-S38 ◽  
Author(s):  
Helmuth Vorherr
Keyword(s):  
Receptor Blockade ◽  
Milk Ejection ◽  
Beta Adrenergic ◽  
Beta Receptor ◽  
Beta Receptors ◽  
Alpha Receptors ◽  
Adrenergic Blockers ◽  
Beta Receptor Blockade ◽  
Second Pain ◽  
Stimulation Of

ABSTRACT In lactating rats and rabbits the mode of antagonism of sympathomimetics, angiotensin or pain toward oxytocin-induced milk-ejection was investigated. In rats intra-arterial (intrafemoral) doses of 0.01–0.02 μg or intravenous (iv) doses of 0.1–0.5 μg of either epinephrine, isoproterenol, norepinephrine, angiotensin or 10 μg of phenylephrine injected simultaneously with, or 30 seconds before an oxytocin dose (10 μU intrafemoral, 300 μU iv) greatly inhibited or suppressed the oxytocin response. A 15 second pain stimulus caused moderate inhibition. With alpha-receptor blockade pain, epinephrine, isoproterenol, norepinephrine, phenylephrine and angiotensin inhibition were, respectively, 70%, 75%, 100%, 40%, 0% and 100%. Under beta-receptor blockade the corresponding values were 14%, 40%, 0%, 70%, 100% and 100%; with simultaneous intrafemoral injections neither catecholamine was inhibitory toward oxytocin. In corresponding rabbit experiments approximately 10-fold higher iv drug dosages were applied and similar results were observed. In both species, combined alpha and beta-receptor blockade nearly eliminated the antagonistic actions of sympathomimetics toward oxytocin, whereas angiotensin inhibition persisted unchanged. The results indicate: 1) Mammary myoepithelial cells contain beta-adrenergic receptors but no alpha-receptors; 2) Inhibition of oxytocin-induced milk-ejection by isoproterenol and phenylephrine is meditated through stimulation of myoepithelial beta-receptors (myoepithelial relaxation) and vascular alpha-receptors (vasoconstriction), respectively; 3) Epinephrine and norepinephrine inhibition of milk-ejection is due to stimulation of vascular alpha-receptors and myoepithelial beta-receptors; 4) Angiotensin effects are unrelated to adrenergic receptor mechanisms; 5) Administration of both alpha and beta-adrenergic blockers is desirable for stabilizing the sensitivity of the oxytocin milk-ejection assay preparation against interference from endogenous or exogenous catecholamines; 6) Other than using adrenergic blockers, pharmacologic doses of oxytocin can correct nursing difficulties in animals and man with hyperfunction of the adrenal-sympathetic system.

Sign in / Sign up

Export Citation Format

Share Document