Development of hypertension in rats during chronic exposure to cold

1989 ◽  
Vol 66 (2) ◽  
pp. 741-749 ◽  
Author(s):  
M. J. Fregly ◽  
D. C. Kikta ◽  
R. M. Threatte ◽  
J. L. Torres ◽  
C. C. Barney
Keyword(s):  
Heart Rate ◽  
Gradual Increase ◽  
Heart Weight ◽  
Acute Administration ◽  
Adrenergic Agonist ◽  
Pretreatment Level ◽  
Exposure To Cold ◽  
Blood Pressures ◽  
Beta Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

Resting systolic, diastolic, and mean blood pressures (MBP), as well as heart rates, of unanesthetized, unrestrained, cold-acclimated (CA, 4 wk, 6 degrees C) rats were measured by direct arterial cannula and compared with those of controls maintained at 25 degrees C. Exposure to cold increased all these measurements significantly. Mean heart weight of CA rats was also increased significantly above that of controls. The responsiveness of MBP and heart rate to administration of the beta-adrenergic agonist, isoproterenol (3, 5, and 8 micrograms/kg ip), to unanesthetized, unrestrained, CA rats during exposure to air at 6 degrees C was similar to, and possibly less than, that of warm-acclimated (WA) rats measured at 25 degrees C. Acute administration of the alpha-adrenergic agonist, phenylephrine (100 micrograms/kg ip), to CA rats while in air at 6 degrees C induced less of a change in MBP from pretreatment level than was observed in WA rats. However, no differences were observed between groups when changes in heart rate from pretreatment level were compared. A similar statement may be made for a higher dose of phenylephrine (150 micrograms/kg ip), although MBP were elevated to higher levels in both groups with the higher dose. Abrupt exposure of WA rats to cold (6 degrees C) resulted in a sharp increase in heart rate and a more gradual increase in MBP over a period of 1 h. Removal of CA rats from 6 to 25 degrees C resulted in a gradual decrease in heart rate with no significant change in MBP during the ensuing hour.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of adrenergic agonists on big and small renin

1980 ◽  
Vol 238 (5) ◽  
pp. E416-E420
Author(s):  
H. Iwao ◽  
C. S. Lin ◽  
A. M. Michelakis
Keyword(s):  
Submaxillary Gland ◽  
Plasma Renin ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Molecular Weights ◽  
Submaxillary Glands ◽  
Beta Adrenergic Agonists ◽  
Beta Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

The effect of alpha- and beta-adrenergic agonists on renal and submaxillary renin of different molecular weights was studied using male albino mice as experimental animals. Phenylephrine or isoproterenol was administered intravenously after removal of the submaxillary glands and/or kidneys. Renin was isolated from plasma by column chromatography and then measured by a direct radioimmunoassay. Phenylephrine increased both 68,500-dalton renin (big renin) and 38,000-dalton renin (small renin) in the plasma of nephrectomized mice. Isoproterenol increased big and small renin in the plasma of mice whose submaxillary glands were removed. In both cases, the increase of small renin was significantly greater than that of big renin. The results suggest that the alpha-adrenergic agonist phenylephrine affects the submaxillary gland, leading to the increase of both big and small plasma renin. In contrast, the beta-adrenergic agonist isoproterenol affects the kidney, leading to the increase of both big and small plasma renin.

scholarly journals Activities of enzymes of glycerolipid synthesis in brown adipose tissue after treatment of rats with the adrenergic agonists BRL 26830A and phenylephrine, after exposure to cold and in streptozotocin-diabetes

1991 ◽  
Vol 277 (3) ◽  
pp. 665-669 ◽  
Author(s):  
J R D Mitchell ◽  
E D Saggerson
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Streptozotocin Diabetes ◽  
Fatty Acyl ◽  
Adrenergic Agonist ◽  
Interscapular Brown Adipose Tissue ◽  
Exposure To Cold ◽  
Brown Adipose ◽  
Glycerolipid Synthesis ◽  
Beta Adrenergic Agonist

1. Measurements were made, relative to tissue DNA, of the activities of enzymes of glycerolipid synthesis in homogenates of interscapular brown adipose tissue. These were: mitochondrial and microsomal forms of glycerolphosphate acyltransferase (GPAT), Mg(2+)-dependent phosphatidate phosphohydrolase (PPH) and fatty acyl-CoA synthetase (FAS). 2. In normal animals, 3 days of cold-exposure (4 degrees C) increased all activities. The increase in mitochondrial GPAT activity was particularly pronounced (5-fold). Administration of the beta-adrenergic agonist BRL 26830A mimicked the effect of cold on microsomal GPAT activity. Mitochondrial GPAT, PPH and FAS activities were unresponsive to BRL 26830A. The alpha-adrenergic agonist phenylephrine significantly decreased activities of GPAT and PPH. 3. Streptozotocin-diabetes decreased mitochondrial GPAT activity, but did not abolish the effect of cold to increase this activity or the activity of microsomal GPAT. Diabetes abolished the effect of cold on PPH and FAS activities. 4. The findings are relevant to signals that drive early events in mitochondriogenesis and cell proliferation in brown adipose tissue on exposure to cold.

scholarly journals The α-adrenergic-mediated activation of Ca2+ influx into cardiac mitochondria. A possible mechanism for the regulation of intramitochondrial free CA2+

1981 ◽  
Vol 200 (2) ◽  
pp. 379-388 ◽  
Author(s):  
P Kessar ◽  
M Crompton
Keyword(s):  
Steady State ◽  
Isolated Heart ◽  
Cardiac Mitochondria ◽  
Adrenergic Agonist ◽  
Adrenergic Regulation ◽  
Simultaneous Measurements ◽  
Rat Hearts ◽  
Oxoglutarate Dehydrogenase ◽  
Beta Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

Mitochondria isolated from rat hearts perfused with adrenaline, and from hearts excised from adrenaline-treated rats, showed an enhanced rate of respiration-dependent Ca2+ uptake. Adrenaline pretreatment did not change the activity of the Na+/Ca2+-antiporter of isolated heart mitochondria. Simultaneous measurements of the membrane potential revealed that perfusion with adrenaline has no significant effect on this parameter during Ca2+ accumulation. The activation of Ca2+ uptake was induced also by the alpha-adrenergic agonist, methoxamine, but not by the beta-adrenergic agonist, isoprenaline. Methoxamine pretreatment also increased the sensitivity of alpha-oxoglutarate dehydrogenase in intact mitochondria to 10 nM--300 nM extramitochondrial Ca2+ during steady-state Ca2+ recycling across the inner membrane. Possible implications of these data for the adrenergic regulation of oxidative metabolism are discussed.

β-Adrenergic responsiveness of rats treated chronically with isoproterenol

1980 ◽  
Vol 58 (10) ◽  
pp. 1170-1173 ◽  
Author(s):  
C. C. Barney ◽  
M. J. Katovich ◽  
M. J. Fregly ◽  
P. E. Tyler
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Water Intake ◽  
Chronic Administration ◽  
Male Rats ◽  
Heart Weight ◽  
Adrenergic Agonist ◽  
Significant Attenuation ◽  
Challenging Dose ◽  
Induced Changes

The effect of chronic administration of isoproterenol on isoproterenol-induced thirst and isoproterenol-induced changes in heart rate and selected organ weights of male rats was studied. Administration of 25 μg isoproterenol/kg, s.c., in saline daily for 10 days was accompanied by a significant attenuation of the characteristic increase in water intake following a challenging dose of isoproterenol (25 μg/kg, s.c.) on the 11th day. Administration of 25 μg isoproterenol/kg, s.c., every 2nd, 3rd, or 4th day for 10 days was without significant effect on water intake following isoproterenol (25 μg/kg, s.c.) on the 11th day. Administration of 25 μg isoproterenol/kg, s.c., every day for 10 days led to a slight increase in cardiac responsiveness to a challenging dose of isoproterenol (25 μg/kg) on the 11th day. Chronic treatment with this low dose of isoproterenol for 10 days was also accompanied by a significant increase in the ratio of heart weight to body weight but no significant changes in the ratio of kidney, adrenal, thyroid, spleen, or interscapular brown fat to body weight. Thus, daily administration of the β-adrenergic agonist isoproterenol for 10 days can alter β-adrenergic responsiveness in the rat with β1 (heart rate) and β2 (thirst) mediated responses showing opposite effects. In addition, the results suggest that tests of β-adrenergic responsiveness must be assessed in terms of the frequency of administration of the agonist.

Effect of hypothyroidism on responsiveness to β-adrenergic stimulation

1976 ◽  
Vol 54 (3) ◽  
pp. 200-208 ◽  
Author(s):  
M. J. Fregly ◽  
G. E. Resch ◽  
E. L. Nelson Jr. ◽  
F. P. Field ◽  
P. E. Tyler
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Glucose Concentration ◽  
Chronic Administration ◽  
Acute Administration ◽  
Adrenergic Agonists ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Thyroid Activity ◽  
Change In Mean

Chronic administration of aminotriazole (0.5 g/kg food) to rats was accompanied by a reduced responsiveness to acute administration of the β-adrenergic agonist, l-isoproterenol (50–100 μg/kg, sc). The responses tested included water intake, change in heart rate in the anesthetized and unanesthetized rat, change in mean blood pressure, and change in blood glucose concentration. In addition, the increase in tail skin temperature accompanying administration of epinephrine (1 mg/kg, sc) was significantly reduced in the hypothyroid group. Administration of l-thyroxine (25 μg/kg per day, ip) to aminotriazole-treated rats prevented the reduction in responsiveness to β-adrenergic stimulation. Thus, an interaction appears to exist between the level of thyroid activity and responsiveness to β-adrenergic agonists in rats.

Treatment of Hypotension after Hyperbaric Tetracaine Spinal Anesthesia 

1997 ◽  
Vol 86 (4) ◽  
pp. 797-805 ◽  
Author(s):  
Robert F. Brooker ◽  
John F. IV Butterworth ◽  
Dalane W. Kitzman ◽  
Jeffrey M. Berman ◽  
Hillel I. Kashtan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Systolic Blood Pressure ◽  
Spinal Anesthesia ◽  
Adrenergic Agonist ◽  
Induced Hypotension ◽  
Alpha Adrenergic Agonist ◽  
Hyperbaric Tetracaine

Background Despite many advantages, spinal anesthesia often is followed by undesirable decreases in blood pressure, for which the ideal treatment remains controversial. Because spinal anesthesia-induced sympathectomy and management with a pure alpha-adrenergic agonist can separately lead to bradycardia, the authors hypothesized that epinephrine, a mixed alpha- and beta-adrenergic agonist, would more effectively restore arterial blood pressure and cardiac output after spinal anesthesia than phenylephrine, a pure alpha-adrenergic agonist. Methods Using a prospective, double-blind, randomized, cross-over study design, 13 patients received sequential infusions of epinephrine and phenylephrine to manage hypotension after hyperbaric tetracaine (10 mg) spinal anesthesia. Blood pressure, heart rate, and stroke volume (measured by Doppler echocardiography using the transmitral time-velocity integral) were recorded at baseline, 5 min after injection of tetracaine, and before and after management of hypotension with epinephrine and phenylephrine. Cardiac output was calculated by multiplying stroke volume x heart rate. Results Five min after placement of a hyperbaric tetracaine spinal anesthesia, significant decrease in systolic (from 143 +/- 6 mmHg to 125 +/- 5 mmHg; P < 0.001), diastolic (from 81 +/- 3 to 71 +/- 3; P < 0.001), and mean (from 102 +/- 4 to 89 +/- 3; P < 0.001) arterial pressures occurred. Heart rate (75 +/- 4 beats/min to 76 +/- 4 beat/min; P = 0.9), stroke volume (115 +/- 17 to 113 +/- 13; P = 0.9), and cardiac output (8.0 +/- 1 l/m to 8.0 +/- 1l/m; P = 0.8) did not change significantly after spinal anesthesia. Phenylephrine was effective at restoring systolic blood pressure after spinal anesthesia (120 +/- 6 mmHg to 144 +/- 5 mmHg; P < 0.001) but was associated with a decrease in heart rate from 80 +/- 5 beats/min to 60 +/- 4 beats/min (P < 0.001) and in cardiac output from 8.6 +/- 0.7 l/m to 6.2 +/- 0.7 l/m (P < 0.003). Epinephrine was effective at restoring systolic blood pressure after spinal anesthesia (119 +/- 5 mmHg to 139 +/- 6 mmHg; P < 0.001) and was associated with an increase in stroke volume from 114 +/- 12 ml to 142 +/- 17 (P < 0.001) and cardiac output from 7.8 +/- 0.6 l/m to 10.8 +/- 1.1 l/m (P < 0.001). Conclusions Epinephrine management of tetracaine spinal-induced hypotension increases heart rate and cardiac output and restores systolic arterial pressure but does not restore mean and diastolic blood pressure. Phenylephrine management of tetracaine spinal-induced hypotension decreases heart rate and cardiac output while restoring systolic, mean, and diastolic blood pressure.

Changes in beta-adrenergic responsiveness of rats during chronic cold exposure

1980 ◽  
Vol 49 (6) ◽  
pp. 923-929 ◽  
Author(s):  
C. C. Barney ◽  
M. J. Katovich ◽  
M. J. Fregly ◽  
P. E. Tyler
Keyword(s):  
Heart Rate ◽  
Cold Exposure ◽  
Chronic Exposure ◽  
Cardiovascular Responses ◽  
Time Dependent ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Heart Rates ◽  
Beta Adrenergic Agonist

Administration of isoproterenol (50 micrograms/kg sc) to rats that had been exposed to cold (6 degrees C) for 10, 15, and 25 days was accompanied by a greater increase in tail skin and colonic temperatures than in controls kept at 25 degrees C. Administration of isoproterenol (8 micrograms/kg sc) to cold-treated rats (1, 3, 5, 7, 14, and 28 days) increased heart rates above that of controls. However, resting unstimulated heart rates of cold-treated rats were also increased above that of controls after 1, 3, 5, and 7 days of cold exposure but were not different from controls after 14 and 28 days. Cold exposure also led to time-dependent increases in the weights of heart, adrenals, and interscapular brown fat. Thus, chronic exposure of rats to cold is accompanied by an increase in responsiveness of both heart rate and tail skin and colonic temperatures to beta-adrenergic stimulation. The results also suggest that increases in responsiveness to a beta-adrenergic agonist may not occur at the same time for the different beta-adrenergic-mediated metabolic and cardiovascular responses in cold-treated rats.

Mechanism of inhibition by methacholine of norepinephrine-stimulated ANP secretion

1988 ◽  
Vol 255 (6) ◽  
pp. H1429-H1433 ◽  
Author(s):  
R. J. Schiebinger
Keyword(s):  
Adenylate Cyclase ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Base Line ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Mechanism Of Inhibition ◽  
Beta Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

We have previously reported that methacholine inhibits norepinephrine-stimulated immunoreactive atrial natriuretic peptide (ANP-IR) secretion by 65% in vitro. In the present study, we examined the mechanism by which methacholine inhibits norepinephrine-stimulated secretion using isolated, paced rat left atria superfused in vitro. Norepinephrine has beta- and alpha-adrenergic properties, both of which stimulate ANP secretion. Thus we separately examined the effect of 10 microM methacholine on ANP-IR secretion stimulated by the beta-adrenergic agonist isoproterenol (0.1 microM) and by the alpha-adrenergic agonist phenylephrine (10 microM). Methacholine lowered isoproterenol-stimulated ANP-IR secretion to base line but did not inhibit phenylephrine-stimulated ANP-IR secretion. Atria were superfused with 0.5 mM dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP) to determine whether inhibition of isoproterenol-stimulated secretion by methacholine occurred by a reduction in adenylate cyclase activity or at a point distal to cAMP. Methacholine inhibited dibutyryl cAMP-stimulated ANP-IR secretion by 50%. This inhibition could not be reversed by 20 microM isobutylmethylxanthine. We conclude that 1) methacholine completely blocks isoproterenol-stimulated ANP-IR secretion; 2) inhibition appears to be primarily due to a decrease in adenylate cyclase activity; however, inhibition occurs at a point(s) distal to cAMP production; 3) methacholine does not inhibit phenylephrine-stimulated ANP-IR secretion; and 4) inhibition by methacholine of norepinephrine-stimulated ANP-IR secretion reflects a block in beta-adrenergic activity.

Central effects of catecholamine antagonists on angiotensin-induced vasopressin secretion in conscious rats

1988 ◽  
Vol 118 (1) ◽  
pp. 82-88 ◽  
Author(s):  
Ken'ichi Yamaguchi ◽  
Takeo Karakida ◽  
Mamoru Koike ◽  
Hitoshi Hama
Keyword(s):  
Angiotensin Ii ◽  
Ang Ii ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Central Effects ◽  
Conscious Rats ◽  
Vasopressin Secretion ◽  
Beta Adrenergic Agonist ◽  
Alpha Antagonist ◽  
Alpha Adrenergic Agonist

Abstract. To evaluate the roles for catecholamines in angiotensin II (ANG II)-induced vasopressin (AVP) release, we examined in conscious rats the effects of intraventricular (ivt) administrations of catecholamine antagonists on plasma AVP responses to ivt applications of its agonists and ANG II. Plasma AVP was determined by RIA using trunk blood collected after decapitation. Dopamine (0.15 μmol), phenylephrine (an alpha-adrenergic agonist, 0.15 μmol) or ANG II (48.2 pmol) augmented plasma AVP 90 sec after the injection, whereas after isoproterenol (a beta-adrenergic agonist, 0.15 μmol) plasma AVP was unaffected. The plasma AVP responses to both dopamine and ANG II were significantly (P < 0.01) inhibited by haloperidol (a dopamine blocker, 0.15 μmol) given 10 min before administration of these agents. Pre-administration of phenoxybenzamine (an alpha antagonist, 0.15 μmol) which was confirmed to abolish the effect of phenylephrine, or propranolol (a beta antagonist, 0.15 μmol) did not block the effect of ANG II. Administration of haloperidol, phenoxybenzamine or propranolol alone was without effect on plasma AVP level. On the basis of these results, we concluded that ANG II-induced AVP secretion may be mediated and/or modulated by dopamine.

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