Does intracarotid PGE2 increase plasma ACTH concentration in conscious adult ewes?

1991 ◽  
Vol 261 (3) ◽  
pp. E395-E401
Author(s):  
T. A. Cudd ◽  
C. E. Wood
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Carotid Artery ◽  
Arterial Pressure ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Human Contact ◽  
Acth Concentration

The hypothesis that prostaglandin E2 (PGE2) is a circulating mediator of adrenocorticotropic hormone (ACTH) secretion in sheep was tested in conscious adult ewes using 30-min carotid artery infusions of 0, 5, 10, 100, and 500 ng.kg-1. min-1 PGE2 in saline. ACTH, cortisol, and aldosterone were significantly increased during the 500 ng.kg-1.min-1 infusion (166 +/- 61 to 233 +/- 38 pg/ml, 27 +/- 5 to 45 +/- 2 ng/ml, and 52 +/- 11 to 85 +/- 25 pg/ml, respectively). PGE2 infusions of 100 ng.kg-1.min-1 increased ACTH from 104 +/- 31 to 168 +/- 31 pg/ml and cortisol from 18 +/- 5 to 42 +/- 2 ng/ml. PGE2 infusions did not increase arginine vasopressin, plasma renin activity, or hematocrit. Heart rate and mean arterial pressure were minimally but significantly increased during the 500 ng.kg-1.min-1 infusion, from 84.9 +/- 2.8 to 99.3 +/- 5.4 beats/min and 95.5 +/- 1.8 to 101.0 +/- 3.4 mmHg, respectively. In a second study to test whether lower infusion rates of PGE2 increase plasma ACTH in sheep with lower resting hormone concentrations, sheep were infused and sampled through a tether system, preventing any disturbances due to human contact the day of an experiment. For all infusion rates ACTH baselines were less than or equal to 55 +/- 17 pg/ml, and cortisol baselines were less than or equal to 6 +/- 3 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal Denervation Prevents Sodium Retention and Hypertension in Salt-Sensitive Rabbits with Genetic Baroreflex Impairment

1996 ◽  
Vol 90 (4) ◽  
pp. 287-293 ◽  
Author(s):  
Marta Weinstock ◽  
Elena Gorodetsky ◽  
Ronald Kalman
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Renal Denervation ◽  
Plasma Renin ◽  
High Salt ◽  
Renin Activity ◽  
Group I ◽  
Group Ii

1. Rabbits with a genetic impairment in baroreflex control of heart rate become hypertensive on a high salt diet. The present study determined the effect of bilateral renal denervation on blood pressure and sodium balance after salt loading (four times normal intake; 28–36 mEq NaCl/day) in normotensive rabbits with high (Group I) and low (Group II) baroreflex sensitivity, respectively. 2. Eight rabbits in each group were denervated or sham-denervated 1 week before commencement of the high salt diet. Before operation, the two groups differed only in the gain of their cardiac baroreflex (Group I, −6.4 ± 0.4 beats min−1 mmHg−1; Group II, −3.2 ± 0.15 beats min−1 mmHg−1). 3. In Group I sham-denervated rabbits, mean arterial pressure remained unchanged, and plasma renin activity and heart rate fell significantly in response to the high salt. In Group II sham-denervated rabbits, mean arterial pressure increased by 10.6 ± 1.2 mmHg, and heart rate and plasma renin activity remained unchanged. Their cumulative Na+ retention and weight gain was more than twice that of Group I sham-denervated rabbits. 4. Renal denervation decreased plasma renin activity in both groups to <1 pmol Ang I h−1 ml−1, lowered cumulative Na+ retention from 102 ± 4 to 35 ± 5 mEq (P<0.01) and completely prevented the increase in mean arterial pressure in response to high salt in Group II. 5. The results suggest that Group II rabbits retain salt and fluid in response to their diet because of an abnormality in their control of renal nerve activity, possibly via vagal afferents. This results in blood pressure elevation because of an inability to lower peripheral resistance and heart rate in response to the increase in cardiac output. 6. Since they display several of the characteristics of salt-sensitive hypertensive humans, i.e. salt retention, normal plasma renin activity, but abnormal regulation of plasma renin activity and blood flow in response to salt loading, Group II are an appropriate model of human salt-induced hypertension.

Role of vasopressin in blood pressure regulation in conscious water-deprived dogs

1983 ◽  
Vol 244 (1) ◽  
pp. R74-R77 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pressure Regulation

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.

Responses of the Systemic Circulation and of the Renin—Angiotensin—Aldosterone System to Ketanserin at Rest and Exercise in Normal Man

1984 ◽  
Vol 66 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Robert Fagard ◽  
Anne Cattaert ◽  
Paul Lijnen ◽  
Jan Staessen ◽  
Luc Vanhees ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Systemic Circulation ◽  
Work Rate ◽  
Plasma Aldosterone ◽  
Sitting Position ◽  
The Mean

1. The systemic circulation at rest and during exercise was studied in ten normal male volunteers, after placebo on one occasion and after acute intravenous administration of the serotonergic antagonist ketanserin on another occasion. The effects of ketanserin on the components of the renin—angiotensin—aldosterone system, on plasma catecholamines and on exercise capacity for graded uninterrupted exercise were also investigated. 2. At rest in recumbency rapid intravenous injection of 10 mg of ketanserin, followed by a continuous infusion of 2 mg/h, produced an acute but transient fall in mean intra-arterial pressure of 6 mmHg compared with placebo. After 15 min the mean arterial pressure with ketanserin was within 2 mmHg of the mean pressure with placebo. In the sitting position both at rest and up to 30% of maximal work rate, the mean arterial pressure during ketanserin did not differ from the pressure on placebo. However, at higher levels of physical activity the rise in mean arterial pressure was lower with ketanserin; the pressure achieved with placebo was 7.5 mmHg higher at maximal work rate. Heart rate and cardiac output were significantly higher during ketanserin. 3. When the subjects were lying down and resting, plasma noradrenaline and adrenaline levels, plasma renin activity and angiotensin II concentration were not affected by ketanserin; however, these values were higher in the sitting position both at rest and during exercise. Plasma aldosterone was reduced by ketanserin during exercise and also when the subject was resting in the recumbent position. 4. Exercise capacity as measured by peak oxygen uptake was similar during ketanserin (3.09 ± se 0.12 litres/min) and during placebo (3.11 ± 0.13). 5. The data suggest that 5-hydroxytryptamine can have only a small role, if any, in pressure homoeostasis in sodium replete man at rest in recumbency. At moderate and heavy levels of exercise, the results are compatible with a role for 5-hydroxytryptamine in pressure regulation. Activation of the sympathetic nervous system by ketanserin is suggested by increases of plasma catecholamines, heart rate, cardiac output and plasma renin. The suppression of plasma aldosterone suggests that 5-hydroxytryptamine may have a role in the regulation of aldosterone secretion which is independent of angiotensin II.

scholarly journals Transient hypertension and sustained tachycardia in mice housed individually in metabolism cages

2009 ◽  
pp. 69-75 ◽  
Author(s):  
CC Hoppe ◽  
KM Moritz ◽  
SM Fitzgerald ◽  
JF Bertram ◽  
RG Evans
Keyword(s):  
Heart Rate ◽  
Renal Function ◽  
Sex Differences ◽  
Mean Arterial Pressure ◽  
Carotid Artery ◽  
Arterial Pressure ◽  
Cardiovascular Function ◽  
The Novel ◽  
Males And Females ◽  
Surgical Implantation

The novel environment of a metabolic cage can be stressful for rodents, but few studies have attempted to quantify this stressresponse. Therefore, we determined the effects on mean arterial pressure (MAP) and heart rate (HR), of placing mice of both sexes in metabolism cages for 2 days. After surgical implantation of a carotid artery catheter mice recovered individually in standard cages for 5 days. Mice then spent 2 days in metabolism cages. MAP and HR were monitored in the standard cage on Day 5 and in metabolism cages on Days 6-7. MAP increased by 18±3 and 22±4 %, while HR increased by 27±4 and 27±6 %, in males and females, respectively, during the first hours after cage switch. MAP decreased to baseline in the fourth and eighth h following metabolism cage switch in males and females, respectively. However, HR remained significantly elevated in both sexes during the entire two-day period in metabolism cages. Females had lower MAP than males both pre- and postmetabolism cage switch, but there were no sex differences in HR. These results demonstrate sustained changes in cardiovascular function when mice are housed in metabolism cages, which could potentially affect renal function.

Hemodynamic effects of neurohypophyseal peptides with antidiuretic activity in dogs

1985 ◽  
Vol 249 (5) ◽  
pp. H1001-H1008 ◽  
Author(s):  
J. Schwartz ◽  
J. F. Liard ◽  
C. Ott ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Hemodynamic Effects ◽  
Antidiuretic Activity

Arginine vasopressin (AVP) is known to produce increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) and decreases in heart rate (HR), cardiac output (CO), and plasma renin activity (PRA). Some recent observations with AVP and synthetic analogues have suggested that under certain conditions, AVP can induce cardiovascular and reninsecretory responses in the opposite directions. To characterize the receptors mediating these responses, the effects of AVP, oxytocin, and synthetic neurohypophyseal analogues with specific antidiuretic, vasoconstrictor, or oxytocic activities were studied in conscious dogs. AVP and 2-phenylalanine-8-ornithine-oxytocin (Phe2Orn8OT, a selective vasoconstrictor agonist) produced similar responses when infused at 10 ng X kg-1 X min-1. That is, TPR and MAP increased, and CO, HR, and PRA decreased. Pretreatment with a selective vasoconstrictor antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]AVP, abbreviated d(CH2)5Tyr(Me)-AVP (10 micrograms/kg), blocked the actions of Phe2Orn8OT. However, in the presence of d(CH2)5Tyr(Me)AVP, AVP actually decreased TPR and increased CO, HR, and PRA. An analogue with selective antidiuretic activity, 4-valine-8-D-AVP (VDAVP, 10 ng X kg-1 X min-1), produced the same effects as the combination of vasopressin plus d(CH2)5Tyr(Me)AVP. Neither the effects of VDAVP nor of AVP plus antagonist were blocked by propranolol (1 mg/kg). These data indicate that vasopressin, by its antidiuretic activity, produces cardiovascular effects that are opposite to many of those produced by its vasoconstrictor action and that these effects are not dependent on mediation by beta-adrenoceptors.

Role of the vasoconstrictor and antidiuretic activities of vasopressin in inhibition of renin secretion in conscious dogs

1986 ◽  
Vol 250 (1) ◽  
pp. F92-F96 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Conscious Dogs ◽  
Specific Antagonist

The nature of the activity of vasopressin that is responsible for the inhibition of renin secretion was studied in normally hydrated conscious dogs using intravenous infusions of vasopressin and analogues of vasopressin with selective antidiuretic and vasoconstrictor activity. Vasopressin (1.0 ng . kg-1 . min-1) increased mean arterial pressure (MAP) from 106 +/- 2 to 115 +/- 3 mmHg (P less than 0.05) and decreased heart rate (HR) from 81 +/- 6 to 56 +/- 5 beats/min (P less than 0.001). Plasma renin activity (PRA) decreased from 4.4 +/- 1.1 to 2.4 +/- 0.8 ng . ml-1 . 3 h-1 (P less than 0.05). A specific antagonist of the vasoconstrictor activity of vasopressin, d(CH2)5MeTyrAVP (10 micrograms/kg), completely blocked the cardiovascular and renin responses to vasopressin. A selective vasoconstrictor agonist, 2-phenylalanine-8-ornithine oxytocin (1.0 ng . kg-1 . min-1), increased MAP from 112 +/- 4 to 128 +/- 6 mmHg (P less than 0.001) and decreased HR from 69 +/- 3 to 47 +/- 4 beats/min (P less than 0.001). PRA decreased from 5.5 +/- 1.1 to 2.7 +/- 0.2 ng . ml-1 X 3 h-1 (P less than 0.001). In contrast, a selective antidiuretic agonist, 1-deamino-8-D-arginine vasopressin (1.0 ng . kg-1 . min-1) did not alter PRA, MAP, or HR. These results demonstrate that the acute inhibition of renin secretion by vasopressin in normally hydrated conscious dogs is due to vasoconstrictor rather than antidiuretic activity.

Effects of althesin and urethan-chloralose on neurohumoral cardiovascular regulation

1989 ◽  
Vol 256 (3) ◽  
pp. R757-R765 ◽  
Author(s):  
J. E. Faber
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Reactivity ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Cardiovascular Regulation ◽  
Pulse Interval ◽  
Base Line

The cardiovascular effects of althesin (ALT) and urethan-chloralose (UC) anesthesia were compared in conscious, chronically instrumented rats. Althesin had no effect on arterial pressure or base-line resistance in the renal, superior mesenteric, and hindquarters vasculatures but increased heart rate. In contrast, UC decreased arterial pressure, heart rate, and mesenteric resistance. Although UC attenuated depressor responses to nitroglycerin, neither anesthetic significantly altered regional vascular reactivity to intravenous phenylephrine and nitroglycerin. The cardiac chronotropic baroreflex was examined by comparing the slope of the curves relating maximal changes (delta) in heart rate (pulse interval) that occurred at the point coinciding in time with the maximal changes in mean arterial pressure produced by phenylephrine and nitroglycerin. Neither anesthetic significantly altered the baroreflex slope (delta pulse interval/delta mean arterial pressure) for pressor and depressor stimuli. Both anesthetics attenuated the sympathoexcitatory response to cerebroventricular angiotensin II, although ALT had less of a depressive effect (pressor response during ALT and UC = 65 and 30%, respectively, of conscious). Plasma renin activity (PRA) and the hemodynamic response to peripheral angiotensin-receptor antagonism were significantly increased (PRA by almost 6-fold) during UC, whereas ALT was without effect. Similarly, UC but not ALT induced vasopressin-dependent vascular tone. Ganglionic blockade indicated that peripheral neurogenic tone was not altered by ALT anesthesia. These data suggest that althesin produces fewer hemodynamic disturbances than urethan-chloralose and largely maintains cardiovascular regulation intact.

Hemorrhage decreases arterial pressure sooner in pregnant compared with nonpregnant dogs: role of baroreflex

1994 ◽  
Vol 266 (4) ◽  
pp. H1610-H1619 ◽  
Author(s):  
V. L. Brooks ◽  
L. C. Keil
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Cortisol Concentration ◽  
Right Atrial ◽  
Ang Ii ◽  
The Relationship ◽  
Initial Blood

This study was performed to test the hypothesis that smaller reflex increases in vasopressin, cortisol, adrenocorticotropic hormone (ACTH), and angiotensin II (ANG II) concentrations are produced by hemorrhage in pregnant compared with nonpregnant conscious dogs. Equivalent hemorrhages (1% of the initial blood volume per minute) produced larger decreases in arterial pressure [P < 0.01; 107 +/- 6 to 73 +/- 10 mmHg (pregnant); 109 +/- 6 to 90 +/- 5 mmHg (nonpregnant)] but produced similar increases in plasma vasopressin concentration in the pregnant animals. As a result, the slope of the arterial pressure-to-vasopressin relationship was reduced (P < 0.05). During pregnancy, smaller increases in plasma cortisol concentration and heart rate were also produced for a given decrease in arterial pressure, but the relationship between pressure and ACTH was not significantly affected. In contrast, higher levels of plasma renin activity and plasma ANG II concentration were achieved in the pregnant dogs. In general, the relationships between plasma hormone levels and either left or right atrial pressure were not significantly altered. These results indicate that reflex increases in heart rate, vasopressin, and cortisol concentration are attenuated in pregnant dogs and that this attenuation may contribute to the inability of pregnant animals to achieve normal cardiovascular homeostasis during hemorrhage.

Dual adrenergic control of renin during nonhypotensive hemorrhage in conscious dogs

1991 ◽  
Vol 260 (6) ◽  
pp. E910-E919 ◽  
Author(s):  
M. L. Blair ◽  
H. Hisa ◽  
C. D. Sladek ◽  
K. J. Radke ◽  
F. M. Gengo
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Beta Adrenoceptors ◽  
Alpha Adrenoceptors ◽  
Adrenergic Control ◽  
Arterial Plasma

These experiments evaluated the contribution of renal alpha-adrenoceptors, renal beta-adrenoceptors, and extrarenal beta-adrenoceptors to increased plasma renin activity (PRA) during nonhypotensive hemorrhage in conscious dogs. Blood withdrawal at a rate of 16 g/kg body wt over 20 min increased PRA to nearly threefold control levels without decreasing mean arterial pressure. The PRA response to hemorrhage was reduced to a greater extent by simultaneous direct renal arterial (ira) infusion of phenoxybenzamine and propranolol than by propranolol alone. Phenoxybenzamine infusion ira did not block alpha-adrenoceptors located outside of the kidney. The PRA and heart rate responses to hemorrhage were both significantly reduced when propranolol was infused either ira or intravenously (iv) at a rate of 2 micrograms.kg-1.min-1 for 20 min followed by 0.5 microgram.kg-1.min-1 continuous infusion. Propranolol infusion at a lower rate (0.5 microgram.kg-1.min-1 for 20 min followed by 0.12 microgram.kg-1.min-1) had little effect on the magnitude of increase in PRA when infused either iv or ira. The calculated renal arterial plasma propranolol concentration was at least fivefold higher or more during ira than during iv propranolol infusion at each rate and was approximately the same during ira infusion at the lower rate (17.5 +/- 0.7 ng/ml) as during iv infusion at the higher rate (16.7 +/- 2.4 ng/ml). These data indicate that the hemorrhage-induced increase in PRA is mediated by renal alpha-adrenoceptors and extrarenal beta-adrenoceptors, whereas renal beta-adrenoceptors appear to play little or no role.

Vasopressin and ANG II in the control of ACTH secretion and arterial and atrial pressures

1989 ◽  
Vol 256 (2) ◽  
pp. R339-R347 ◽  
Author(s):  
V. L. Brooks
Keyword(s):  
Arterial Pressure ◽  
Right Atrial ◽  
Ang Ii ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Arterial Blood ◽  
Acth Concentration ◽  
Left And Right ◽  
Dose Dependent

Hypotension stimulates the secretion of adrenocorticotropin (ACTH) and vasopressin (AVP) and increases plasma levels of angiotensin II (ANG II). Because AVP and ANG II increase ACTH secretion, the present experiments were performed to evaluate the role of these peptides in the increases in plasma ACTH and glucocorticoid concentrations produced by hypotension in conscious dogs. This was accomplished by determining whether administration of receptor antagonists to vasopressin, [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine]Arg8-vasopressin, and ANG II (saralasin), reduced the ACTH and glucocorticoid responses to infusion of four doses of the vasodilator nitroprusside. Nitroprusside (NP) infusion produced dose-dependent decreases in mean arterial pressure. Larger decreases in arterial pressure were produced in dogs pretreated with the AVP antagonist or with both saralasin and the vasopressin antagonist. Left and right atrial pressures also fell with NP infusion, and larger decreases in atrial pressures were found in dogs pretreated with the AVP antagonist. Finally, NP infusion increased plasma glucocorticoid concentration and plasma ACTH concentration. Both the glucocorticoid and the ACTH responses to hypotension were reduced in dogs given the AVP antagonist and in dogs given both saralasin and the AVP antagonist, but there was no difference in the effect of AVP blockade alone vs. the effect of combined AVP and ANG II blockade. These data suggest that AVP, but not ANG II, is required for normal glucocorticoid and ACTH responses to hypotension. They also suggest that AVP is necessary for normal maintenance of arterial blood pressure and atrial pressures during NP infusion.

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