scholarly journals THE INFLUENCE OF ETHER ANESTHESIA, OF HEMORRHAGE, AND OF PLETHORA FROM TRANSFUSION ON THE PRESSOR EFFECT OF MINUTE QUANTITIES OF EPINEPHRINE

1919 ◽  
Vol 29 (2) ◽  
pp. 173-186 ◽  
Author(s):  
Peyton Rous ◽  
George W. Wilson
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Pressure Rise ◽  
Pressor Effect ◽  
Normal Height ◽  
Ether Anesthesia ◽  
Marked Influence ◽  
Low Blood Pressure ◽  
Small Doses ◽  
Considerable Period

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.

Selective Depletion of Rat Aorta Potassium by Small Pressor Doses of Norepinephrine

1957 ◽  
Vol 190 (1) ◽  
pp. 67-70 ◽  
Author(s):  
Edwin E. Daniel ◽  
Oswald Dawkins ◽  
J. Hunt
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Pressure Rise ◽  
Psoas Muscle ◽  
Sodium Concentration ◽  
Rat Aorta ◽  
Stomach Muscle ◽  
Pressor Effect ◽  
Average Blood Pressure ◽  
Time Required

Intravenous norepinephrine (1.0 µg/kg body weight) produced a strikingly uniform pressor effect in rats. The average blood pressure rise was 54 mm Hg, the peak rise occurred in less than 20 seconds, and the blood pressure returned to baseline in about 2 minutes. The aorta was rapidly depleted of potassium (15–18%) by the norepinephrine injection, depletion occurring within 20 seconds (time required for exsanguination) after the peak of the pressor effect and persisting throughout the period of the pressor response. Aorta sodium concentration did not increase concomitantly either in time or in quantity. No other tissue studied (stomach muscle, left ventricle, psoas muscle) showed a parallel alteration in electrolytes. Therefore, injections of norepinephrine appear to selectively affect permeability of vascular smooth muscle to potassium.

Comparison of fast and slow pressor effects of angiotensin II in the conscious rat

1981 ◽  
Vol 241 (3) ◽  
pp. H381-H388 ◽  
Author(s):  
A. J. Brown ◽  
J. Casals-Stenzel ◽  
S. Gofford ◽  
A. F. Lever ◽  
J. J. Morton
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Control Period ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Pressor Effect ◽  
Ang Ii ◽  
Conscious Rat ◽  
Female Wistar Rats

Female Wistar rats were infused intravenously with 5% dextrose for 3 days, then with angiotensin II (ANG II) in 5% dextrose at 20 ng . kg-1 . min-1 for 7 days, and finally with dextrose for 2.5 days. ANG II raised mean arterial pressure (MAP) gradually; by the 7th day it was 49.7 mmHg higher than during the dextrose control period in the same rats. Control rats were infused with dextrose for 12.5 days; MAP did not change. Plasma ANG II concentration was measured during infusion. In hypertensive rats on the 7th day of ANG II infusion, it was six times higher than in control rats infused with dextrose. Changes of blood pressure and plasma ANG II concentration were compared in further rats infused with much larger doses of ANG II. Rats receiving 270 ng . kg-1 . min-1 for 1 h had an almost maximal direct pressor response, MAP rising 45.3 mmHg and plasma ANG II rising 32-fold compared with controls. Thus, infusion of ANG II at low dose without direct pressor effect gradually raises blood pressure to a level similar to the maximum direct pressor effect produced by larger doses of ANG II. Sodium balance and food and water intakes were also measured and did not change during prolonged infusion of ANG II at 20 ng . kg-1 . min-1. Thus, the slow pressure effect of ANG II develops at a lower and more nearly physiological plasma concentration of the peptide than do the direct pressor effect and the effects on drinking, eating, and urinary sodium excretion.

Evidence that centrally released arginine vasopressin is involved in central pressor action of angiotensin II

1996 ◽  
Vol 270 (1) ◽  
pp. H167-H173 ◽  
Author(s):  
S. Lon ◽  
E. Szczepanska-Sadowska ◽  
M. Szczypaczewska
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Pressor Effect ◽  
Ang Ii ◽  
Central Administration ◽  
Hypotensive Action ◽  
Series Of Experiments

Five series of experiments were performed on conscious trained dogs to find out whether intracranially released arginine vasopressin (AVP) is involved in mediation of central cardiovascular effects of angiotensin II (ANG II). The dogs were implanted with guide tubes leading to the third cerebral ventricle (ICV) and implanted with the intra-arterial catheters. Blood pressure and heart rate were continuously monitored during intracerebroventricular administration of 1) ANG II alone (250 ng), 2) AVP alone (0.01 ng/min during 10 min), 3) ANG II together with AVP, 4) AVP together with AVP V1-receptor antagonist 1(1-mercapto-4-methylcyclohexaneacetic acid)-8-AVP [MeCAAVP, V1ANT,100 ng/min], and 5) ANG II together with V1ANT. The results revealed that 1) ANG II and AVP applied separately elicited significant, long-lasting increases of blood pressure; 2) the maximum pressor effect after ANG II and AVP applied together did not differ from that after separate application of either of these peptides, but the duration of the pressor response was significantly shorter; 3) pretreatment with V1ANT effectively prevented blood pressure increases elicited by central administration of AVP and ANG II; and 4) after blockade of V1 receptors administration of AVP resulted in a significantly delayed decrease of blood pressure below baseline. The results strongly suggest that 1) centrally released AVP mediates the pressor effect of intracerebroventricularly applied ANG II by means of V1 receptors; 2) intracerebroventricularly applied ANG II and AVP interact to activate the mechanism involved in extinction of their pressor effect; and 3) blockade of central V1 receptors uncovers the hypotensive action of centrally applied AVP.

ON THE HYPERTENSIVE ACTION OF TOLAZOLINE AND HYDERGINE

1963 ◽  
Vol 41 (1) ◽  
pp. 941-946 ◽  
Author(s):  
B. G. Benfey ◽  
D. R. Varma
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Contractility ◽  
Pressure Rise ◽  
Pressor Effect ◽  
Blood Pressure Rise ◽  
Chronotropic Effects

The effects of tolazoline and Hydergine on blood pressure, cardiac contractility, and heart rate have been studied in dogs under pentobarbitone anesthesia. Whereas in the absence of reserpine, tolazoline had a pressor effect in two of four dogs, following reserpine it had a marked pressor action in each of eight dogs. The blood pressure rise was associated with positive inotropic and negative chronotropic effects. Phenoxybenzamine abolished these effects of tolazoline. Hydergine had pressor and negative chronotropic effects in the absence of reserpine. Following reserpine these effects were associated with positive inotropic actions. Phenoxybenzamine reduced these effects of Hydergine. It is concluded that the pressor action of tolazoline is wholly due to adrenergic vasoconstriction, whereas that of Hydergine is only partly an adrenergic effect.

Pressor effect of arginine vasopressin in progressive autonomic failure

1986 ◽  
Vol 71 (2) ◽  
pp. 173-178 ◽  
Author(s):  
T. D. M. Williams ◽  
D. DaCosta ◽  
C. J. Mathias ◽  
R. Bannister ◽  
S. L. Lightman
Keyword(s):  
Blood Pressure ◽  
Arginine Vasopressin ◽  
Autonomic Failure ◽  
Pressor Response ◽  
Normal Subjects ◽  
Pressor Effect ◽  
Normal Volunteers ◽  
Pressor Responses ◽  
Transient Bradycardia ◽  
Related Increase

1. The blood pressure (BP) and heart rate (HR) responses to 5 min incremental intravenous infusions of noradrenaline (NA) and arginine vasopressin (AVP) were investigated both in patients with progressive autonomic failure (PAF) and in normal volunteers. 2. Stepwise infusion of NA at rates of 300–3000 pmol min−1 kg−1 produced a bradycardia and a dose related increase in BP in normal subjects. In subjects with PAF there was no significant HR response but the dose-BP response was shifted to the left with significant pressor responses at infusion rates of 60–300 pmol min−1 kg−1. 3. Stepwise infusion of AVP at 0.2–5.0 pmol min−1 kg−1 caused transient bradycardia but no pressor response in seven normal volunteers. Further increases in AVP infusion in three other subjects achieved plasma AVP levels as high as 3000–4000 pmol/l, and still no significant pressor response was observed. 4. Stepwise infusion of AVP at 0.05–2.0 pmol min−1 kg−1 in the eight subjects with PAF resulted in a pressor response without any change in HR. During this infusion plasma AVP increased from 0.8 ± 0.2 (mean ± se) to 30 ± 2 pmol/l. A significant pressor response was already apparent at a plasma AVP level of 5.5 ± 1.8 pmol/l.

Delayed and diminished pressor response to muscle sympathetic nerve activity in the elderly

1996 ◽  
Vol 80 (3) ◽  
pp. 869-875 ◽  
Author(s):  
Y. Sugiyama ◽  
T. Matsukawa ◽  
A. S. Shamsuzzaman ◽  
H. Okada ◽  
T. Watanabe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Pressure Rise ◽  
The Elderly ◽  
Young Group ◽  
Nerve Activity

We studied the effects of aging on alpha-receptor-mediated vasoconstrictive responses to sympathetic nerve activity in 16 healthy aged [75.8 +/- 2.7 (SE) yr] and young men (33.8 +/- 2.0 yr). Muscle sympathetic nerve activity (MSNA), heart rate, and blood pressure were analyzed during slow respiration (0.1 Hz). Peak amplitude and phase were calculated from a cosine function fitted with 0.1 Hz by using the least squares method. The latency of the pressor response to MSNA, defined as lag time from the peak of MSNA to diastolic blood pressure, was significantly longer in the aged than the young group (7.1 +/- 0.3 vs. 5.4 +/- 0.4 s; P < 0.01). The extent of pressor response to MSNA, defined as diastolic blood pressure rise in response to increase in total MSNA, was significantly lower in the aged than the young group (0.038 +/- 0.006 vs. 0.099 +/- 0.024 mmHg/unit, P < 0.001). These results suggest that alpha-receptor-mediated vasoconstrictive responses to MSNA may be attenuated in the elderly.

Role of AVP in malignant DOC-salt hypertension: studies using vascular and antidiuretic antagonists

1987 ◽  
Vol 253 (5) ◽  
pp. F952-F958 ◽  
Author(s):  
J. Filep ◽  
J. C. Frolich ◽  
E. Foldes-Filep
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Pressor Response ◽  
Plasma Renin ◽  
Pressor Effect ◽  
Salt Hypertension ◽  
Freely Moving

To investigate the role of arginine vasopressin (AVP) in the maintenance of blood pressure in deoxycorticosterone (DOC)-salt hypertension, the effects of specific pressor and antidiuretic antagonists of AVP were studied in conscious, freely moving rats with established malignant DOC-salt hypertension. Plasma AVP level was significantly higher in hypertensive than in normotensive animals (4.8 +/- 1.0 vs. 2.0 +/- 0.3 fmol/ml, n = 5, P less than 0.02). Administration of d(CH2)5-d-Leu-VAVP, 10 micrograms/kg, an AVP antagonist that blocked the antidiuretic, but not the pressor effect of exogenous AVP, induced diuresis, and caused a transient fall in blood pressure from 173 +/- 3 to 167 +/- 4 mmHg (n = 8, P less than 0.01) with a concomitant slight increase in heart rate. Similar changes were observed after administration of d(CH2)5Tyr(Et)VAVP, 10 micrograms/kg, an antidiuretic plus pressor antagonist of AVP. Intravenous injection of d(CH2)5Tyr(Me)AVP, 10 micrograms/kg, a specific AVP pressor antagonist had no effect on blood pressure or heart rate, although it completely abolished the pressor response to exogenous AVP. Plasma renin activity remained suppressed following administration of all AVP antagonists. These findings suggest that if AVP should contribute to maintaining high blood pressure in malignant DOC-salt hypertension it would have to be the results of its antidiuretic and not its vasoconstrictor property.

Vasopressor and depressor actions of angiotensin in the anesthetized fowl

1982 ◽  
Vol 242 (3) ◽  
pp. H314-H324 ◽  
Author(s):  
H. Nishimura ◽  
Y. Nakamura ◽  
R. P. Sumner ◽  
M. C. Khosla
Keyword(s):  
Blood Pressure ◽  
Amino Acids ◽  
Smooth Muscle ◽  
Pressor Response ◽  
Pressor Effect ◽  
Ang Ii ◽  
6 Hydroxydopamine ◽  
Depressor Action ◽  
Biphasic Responses ◽  
Female Chicken

Vasopressor and depressor properties of angiotensins (ANG) were characterized in the anesthetized, adult female chicken Gallus gallus. [Asp1,Val5,Ser9]ANG I and [Asp1,Val5]ANG II (native fowl angiotensins) increased blood pressure, and removal or replacement of the amino acid in position 1 decreased pressor potency. The pressor effect of [Asp1,Val5]ANG II was inhibited nearly completely with [Sar1,Ile8]ANG II (5 micrograms.kg-1.min-1) and partially with [Sar1,Thr8]ANG II, [Ile8]ANG III, and [Ile8]ANG I. Phenoxybenzamine, reserpine, or 6-hydroxydopamine reduced the pressor action to one-third. After administration of these compounds [Asp1,Val5]ANG II caused biphasic responses, a depressor followed by a small pressor response. [Sar1,Ile8]ANG II completely, and meclofenamate partially, blocked the depressor response, whereas propranolol, methysergide, vasopressin antagonists, or atropine did not. These results suggest that in fowl 1) the first (Asp) and eighth (Phe) amino acids are important for receptor binding and action, 2) vasopressor action of angiotensin may be primarily caused by release of catecholamines, and 3) angiotensin may exert depressor action possibly by acting directly on the vascular smooth muscle.

Pressor Effect of Beta Blocking Agents in Rats

1972 ◽  
Vol 50 (3) ◽  
pp. 207-214 ◽  
Author(s):  
D. Regoli ◽  
U. Regoli ◽  
E. Gysling
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Vascular System ◽  
Beta Blockers ◽  
Smooth Muscles ◽  
Pressor Effect ◽  
Alpha Blockers ◽  
Blocking Agents ◽  
Biphasic Effect ◽  
Small Doses

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.

Nimodipine inhibits the pressor activity of diaspirin-crosslinked hemoglobin (DCLHb) in the rat

1998 ◽  
Vol 76 (10-11) ◽  
pp. 983-988 ◽  
Author(s):  
Francis Rioux ◽  
Mélanie St-Pierre ◽  
Nathalie Harvey ◽  
Steve Moisan ◽  
Kenneth E Burhop ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Calcium Channels ◽  
Calcium Antagonists ◽  
Pressor Response ◽  
Pressor Effect ◽  
Adrenoceptor Agonist ◽  
Pressor Activity ◽  
Tonic Phase ◽  
Diaspirin Crosslinked Hemoglobin

Impaired nitric oxide (NO) activity is associated with an increase in blood pressure in rats. Voltage-regulated calcium channels are believed to participate in this hemodynamic event. To further test this hypothesis, we examined the effect of nimodipine and verapamil (calcium antagonists) on the pressor activity of diaspirin-crosslinked hemoglobin (DCLHb), a well-known NO scavenger, in anesthetized rats. Nimodipine, the most potent of the two calcium antagonists used, was also tested against phenylephrine (alpha1-adrenoceptor agonist). The pressor effect of DCLHb was reduced markedly by nimodipine and verapamil, whereas that elicited by phenylephrine, particularly the tonic phase of its pressor response, was resistant to blockade by nimodipine. The bradycardia and tachycardia associated with the pressor effects of DCLHb and phenylephrine, respectively, were not affected by nimodipine. The pressor effect elicited by DCLHb and its alteration by nimodipine were also examined in rats pretreated with 100% O2. This treatment was found to potentiate the pressor effect of DCLHb. However, this synergism did not impair the inhibitory action of nimodipine towards the pressor activity of DCLHb. Altogether these results suggest that the pressor activity of DCLHb in our animal model might involve the participation of voltage-regulated calcium channels.Key words: hemoglobin, nitric oxide, calcium channels, blood pressure, diaspirin-crosslinked hemoglobin.

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