Interaction between CRF and angiotensin II in control of ACTH and adrenal steroids

1986 ◽  
Vol 250 (3) ◽  
pp. R396-R402 ◽  
Author(s):  
M. Keller-Wood ◽  
B. Kimura ◽  
J. Shinsako ◽  
M. I. Phillips
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Arteries ◽  
Corticotropin Releasing Factor ◽  
Adrenal Steroids ◽  
Ang Ii ◽  
Plasma Angiotensin ◽  
Acth Release

These experiments were designed to test for interactions between plasma angiotensin II (ANG II) and corticotropin-releasing factor (CRF) in the control of plasma adrenocorticotropin (ACTH), aldosterone, and corticosteroids, mean arterial pressure (MAP), and heart rate (HR) in conscious dogs. Five trained dogs with exteriorized carotid arteries were studied. Each dog was infused with saline and with CRF at three rates (2.5, 5, and 10 ng X kg-1 X min-1) and ANG II at three rates (5, 10, and 20 ng X kg-1 X min-1) for 60 min. The same animals were also coinfused with 10 ng X kg-1 X min-1 ANG II at each rate of CRF infusion and with 10 ng CRF X kg-1 X min-1 at each rate of ANG II infusion. Infusion of ANG II alone caused dose-related increases in aldosterone, corticosteroids, and MAP but did not alter ACTH or HR. Infusion of CRF alone increased ACTH, aldosterone, and corticosteroids but not MAP or HR. Coinfusion of CRF and ANG II caused ANG II dose-related ACTH responses but did not alter the sensitivity of the ACTH responses to CRF. Thus it appears that ANG II alone does not stimulate ACTH release but requires increased CRF concentrations to effect ACTH release.

Angiotensin II induces insulin resistance independent of changes in interstitial insulin

1999 ◽  
Vol 277 (5) ◽  
pp. E920-E926 ◽  
Author(s):  
Joyce M. Richey ◽  
Marilyn Ader ◽  
Donna Moore ◽  
Richard N. Bergman
Keyword(s):  
Insulin Resistance ◽  
Heart Rate ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glucose Uptake ◽  
Peripheral Resistance ◽  
Glucose Turnover ◽  
Ang Ii

We set out to examine whether angiotensin-driven hypertension can alter insulin action and whether these changes are reflected as changes in interstitial insulin (the signal to which insulin-sensitive cells respond to increase glucose uptake). To this end, we measured hemodynamic parameters, glucose turnover, and insulin dynamics in both plasma and interstitial fluid (lymph) during hyperinsulinemic euglycemic clamps in anesthetized dogs, with or without simultaneous infusions of angiotensin II (ANG II). Hyperinsulinemia per se failed to alter mean arterial pressure, heart rate, or femoral blood flow. ANG II infusion resulted in increased mean arterial pressure (68 ± 16 to 94 ± 14 mmHg, P < 0.001) with a compensatory decrease in heart rate (110 ± 7 vs. 86 ± 4 mmHg, P < 0.05). Peripheral resistance was significantly increased by ANG II from 0.434 to 0.507 mmHg ⋅ ml−1⋅ min ( P < 0.05). ANG II infusion increased femoral artery blood flow (176 ± 4 to 187 ± 5 ml/min, P < 0.05) and resulted in additional increases in both plasma and lymph insulin (93 ± 20 to 122 ± 13 μU/ml and 30 ± 4 to 45 ± 8 μU/ml, P < 0.05). However, glucose uptake was not significantly altered and actually had a tendency to be lower (5.9 ± 1.2 vs. 5.4 ± 0.7 mg ⋅ kg−1⋅ min−1, P > 0.10). Mimicking of the ANG II-induced hyperinsulinemia resulted in an additional increase in glucose uptake. These data imply that ANG II induces insulin resistance by an effect independent of a reduction in interstitial insulin.

Control of blood pressure and hindlimb conductance during hemorrhage in conscious renal hypertensive rabbits

1995 ◽  
Vol 268 (6) ◽  
pp. H2302-H2310 ◽  
Author(s):  
G. Weichert ◽  
C. A. Courneya
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Similar Pattern ◽  
Ang Ii ◽  
Autonomic Nervous

We examined the response to hemorrhage in conscious normotensive and hypertensive rabbits under control conditions and during efferent blockade of 1) the hormones vasopressin (AVP) and angiotensin II (ANG II), 2) the autonomic nervous system, and 3) autonomic and hormonal inputs. We recorded mean arterial pressure, heart rate, and hindlimb conductance. The response to hemorrhage was unchanged with hormonal blockade alone. Blockade of the autonomic nervous system caused a faster rate of blood pressure decline, but the rate of decrease in hindlimb conductance was maintained at control levels. Blocking the autonomic nervous system and the hormones resulted in rapid blood pressure decline and an increase in hindlimb conductance. Although the three types of efferent blockade had a similar pattern of effects in normotensive and hypertensive rabbits, hypertensive rabbits exhibited less cardiovascular support during hemorrhage than normotensive rabbits. During hemorrhage, hypertensive rabbits had an attenuation of hindlimb vasoconstriction, a reduction in the heart rate-mean arterial pressure relationship, and reduced ability to maintain blood pressure compared with normotensive rabbits.

Angiotensin II does not alter ACTH responses to hypoglycemia in conscious dogs

1987 ◽  
Vol 252 (3) ◽  
pp. R526-R530
Author(s):  
M. Keller-Wood ◽  
B. Kimura ◽  
M. I. Phillips
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Carotid Artery ◽  
Arterial Pressure ◽  
Negative Feedback ◽  
Intravenous Infusion ◽  
Carotid Arteries ◽  
Plasma Aldosterone ◽  
Conscious Dogs ◽  
Ang Ii

These experiments were designed to test for an interaction between angiotensin II (ANG II) and stress in the control of plasma adrenocorticotropin hormone (ACTH), corticosteroids, and aldosterone. The stimulus to ACTH used in this study was insulin-induced hypoglycemia, a stimulus that does not increase plasma ANG II concentrations. Five trained dogs with exteriorized carotid arteries were studied. Each dog was infused with ANG II intravenously (10 ng X kg-1 X min-1) or into the carotid artery (1 ng X kg-1 X min-1) or with saline (iv) for 80 min. Twenty minutes after the start of the infusion, insulin (0.10 U/kg iv) was injected. Intravenous infusion of ANG II increased mean arterial pressure (MAP) and plasma aldosterone concentrations but did not increase ACTH or corticosteroid responses to hypoglycemia. Intracarotid infusion of ANG II did not increase MAP and also failed to increase ACTH and corticosteroid responses to hypoglycemia. Since ANG II infusions did not increase basal corticosteroids, the failure of ANG II to stimulate ACTH is not a result of steroid negative feedback. Thus it appears that increased plasma ANG II concentrations do not increase ACTH responses to hypoglycemic stress.

scholarly journals Brain Prostaglandin D2 Increases Neurogenic Pressor Activity and Mean Arterial Pressure in Angiotensin II-Salt Hypertensive Rats

Hypertension ◽  
2019 ◽  
Vol 74 (6) ◽  
pp. 1499-1506 ◽  
Author(s):  
Ninitha Asirvatham-Jeyaraj ◽  
A. Daniel Jones ◽  
Robert Burnett ◽  
Gregory D. Fink
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Developmental Stage ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Salt Hypertension ◽  
Pressor Activity

This study tested whether brain L-PGDS (lipocalin-type prostaglandin [PG] D synthase), through prostanoid signaling, might increase neurogenic pressor activity and thereby cause hypertension. Sprague Dawley rats on high-salt diet received either vehicle or Ang II (angiotensin II) infusion. On day 4, the developmental stage of hypertension, brains from different sets of control and Ang II–treated rats were collected for measuring L-PGDS expression, PGD2 levels, and DP1R (type 1 PGD2 receptor) expression. In a different set of 14-day Ang II-salt–treated rats, mini-osmotic pumps were used to infuse either a nonselective COX (cyclooxygenase) inhibitor ketorolac, L-PGDS inhibitor AT56, or DP1R inhibitor BWA868C to test the role of brain COX-PGD2-DP1R signaling in Ang II-salt hypertension. The acute depressor response to ganglion blockade with hexamethonium was used to quantify neurogenic pressor activity. During the developmental stage of Ang II-salt hypertension, L-PGDS expression was higher in cerebrospinal fluid, and PGD2 levels were increased in the choroid plexus, cerebrospinal fluid, and the cardioregulatory brain region rostral ventrolateral medulla. DP1R expression was decreased in rostral ventrolateral medulla. Both brain COX inhibition with ketorolac and L-PGDS inhibition with AT56 lowered mean arterial pressure by altering neurogenic pressor activity compared with vehicle controls. Blockade of DP1R with BWA868C, however, increased the magnitude of Ang II-salt hypertension and significantly increased neurogenic pressor activity. In summary, we establish that the development of Ang II-salt hypertension requires increased COX- and L-PGDS–derived PGD2 production in the brain, making L-PGDS a possible target for treating neurogenic hypertension.

Effect of baroreceptor denervation on stimulation of drinking by angiotensin II in conscious dogs

1991 ◽  
Vol 260 (3) ◽  
pp. E333-E337 ◽  
Author(s):  
C. K. Klingbeil ◽  
V. L. Brooks ◽  
E. W. Quillen ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Plasma Osmolality ◽  
Plasma Angiotensin ◽  
High Doses ◽  
Stimulation Of

Angiotensin II causes marked stimulation of drinking when it is injected centrally but is a relatively weak dipsogen when administered intravenously. However, it has been proposed that the dipsogenic action of systemically administered angiotensin II may be counteracted by the pressor action of the peptide. To test this hypothesis, the dipsogenic action of angiotensin II was investigated in dogs, in which low and high baroreceptor influences had been eliminated by denervation of the carotid sinus, aortic arch, and heart. In five sham-operated dogs, infusion of angiotensin II at 10 and 20 ng.kg-1.min-1 increased plasma angiotensin II concentration to 109.2 +/- 6.9 and 219.2 +/- 38.5 pg/ml and mean arterial pressure by 20 and 29 mmHg, respectively, but did not induce drinking. In four baroreceptor-denervated dogs, the angiotensin II infusions produced similar increases in plasma angiotensin II concentration and mean arterial pressure but, in contrast to the results in the sham-operated dogs, produced a dose-related stimulation of drinking. Water intake with the low and high doses of angiotensin II was 111 +/- 44 and 255 +/- 36 ml, respectively. The drinking responses to an increase in plasma osmolality produced by infusion of hypertonic sodium chloride were not different in the sham-operated and baroreceptor-denervated dogs. These results demonstrate that baroreceptor denervation increases the dipsogenic potency of intravenous angiotensin II and provides further support for the hypothesis that the dipsogenic action of intravenous angiotensin II is counteracted by the rise in blood pressure.

scholarly journals Acute sympathoexcitatory action of angiotensin II in conscious baroreceptor-denervated rats

2002 ◽  
Vol 283 (2) ◽  
pp. R451-R459 ◽  
Author(s):  
Ling Xu ◽  
Alan F. Sved
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Baroreceptor Reflex ◽  
Ang Ii ◽  
Nerve Activity ◽  
Induced Hypotension ◽  
Baroreceptor Reflexes

Angiotensin II (ANG II) has complex actions on the cardiovascular system. ANG II may act to increase sympathetic vasomotor outflow, but acutely the sympathoexcitatory actions of exogenous ANG II may be opposed by ANG II-induced increases in arterial pressure (AP), evoking baroreceptor-mediated decreases in sympathetic nerve activity (SNA). To examine this hypothesis, the effect of ANG II infusion on lumbar SNA was measured in unanesthetized chronic sinoaortic-denervated rats. Chronic sinoaortic-denervated rats had no reflex heart rate (HR) responses to pharmacologically evoked increases or decreases in AP. Similarly, in these denervated rats, nitroprusside-induced hypotension had no effect on lumbar SNA; however, phenylephrine-induced increases in AP were still associated with transient decreases in SNA. In control rats, infusion of ANG II (100 ng · kg−1 · min−1 iv) increased AP and decreased HR and SNA. In contrast, ANG II infusion increased lumbar SNA and HR in sinoaortic-denervated rats. In rats that underwent sinoaortic denervation surgery but still had residual baroreceptor reflex-evoked changes in HR, the effect of ANG II on HR and SNA was variable and correlated to the extent of baroreceptor reflex impairment. The present data suggest that pressor concentrations of ANG II in rats act rapidly to increase lumbar SNA and HR, although baroreceptor reflexes normally mask these effects of ANG II. Furthermore, these studies highlight the importance of fully characterizing sinoaortic-denervated rats used in experiments examining the role of baroreceptor reflexes.

Median preoptic nucleus ablation does not affect angiotensin II-induced hypertension

1986 ◽  
Vol 251 (1) ◽  
pp. H148-H152
Author(s):  
G. D. Fink ◽  
C. A. Bruner ◽  
M. L. Mangiapane
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Base Line ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Water Excretion ◽  
Median Preoptic Nucleus ◽  
Induced Hypertension

Previous studies implicated the ventral median preoptic nucleus (MNPOv) in cardiovascular responses to circulating and intracerebroventricular angiotensin II (ANG II) and in normal cardiovascular and fluid homoeostasis. In the present experiments, chronically catheterized rats received continuous (24 h/day) intravenous infusions of ANG II (10 ng/min) for 5 days, and changes in mean arterial pressure, heart rate, water intake and urinary electrolyte and water excretion were determined daily. Three groups of rats were compared as follows: 1) sham-operated control rats (n = 12), 2) rats with 20-70% of the MNPOv ablated electrolytically (n = 6), and 3) rats with over 90% of the MNPOv ablated (n = 5). The organum vasculosum of the lamina terminalis was intact in all three groups. Base-line values of all measured variables were identical in the three groups on two control days preceding ANG II infusion and on two recovery days after infusion. During the administration of ANG II for 5 days, mean arterial pressure rose significantly (and similarly) in all three groups of rats; no other variable was significantly affected by ANG II infusion. These results suggest that neural pathways originating in, or passing through, the MNPOv region are not critical in the pathogenesis of ANG II-induced hypertension in the rat.

Differential baroreceptor reflex modulation by centrally infused angiotensin peptides

1992 ◽  
Vol 263 (1) ◽  
pp. R89-R94 ◽  
Author(s):  
M. J. Campagnole-Santos ◽  
S. B. Heringer ◽  
E. N. Batista ◽  
M. C. Khosla ◽  
R. A. Santos
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Baroreceptor Reflex ◽  
Reflex Modulation ◽  
Ang Ii ◽  
Average Ratio ◽  
Angiotensin Peptides ◽  
Reflex Bradycardia

The present study was designed to investigate the effect of intracerebroventricular (icv) and intravenous (iv) infusion of angiotensin (ANG)-(1-7), ANG III, and ANG II on the baroreceptor control of heart rate (BHR) in conscious rats. Reflex changes in HR were elicited by bolus iv injection of either phenylephrine or sodium nitroprusside before and within 1 and 3 h of icv infusion of ANG II (n = 10), ANG III (n = 9), ANG-(1-7) (n = 9), or saline (n = 9) at a rate of 3 nmol.7.5 microliter-1.h-1. In another group of animals (n = 23), iv infusion of the same amount of ANG peptides was carried out at a rate of 0.7 ml/h. The average ratio of changes in HR in beats per minute and changes in mean arterial pressure (MAP, mmHg) was used as an index of BHR sensitivity. ANG II and ANG III produced a significant increase in the basal levels of MAP, but only during the first hour of infusion (iv or icv). No significant changes in baseline HR were observed. ANG-(1-7) and saline infusion did not change basal levels of HR or MAP (iv or icv). ANG II (iv and icv) and ANG III (icv) caused a significant decrease in the BHR sensitivity for reflex bradycardia. In contrast, icv infusion of ANG-(1-7) induced a significant increase in BHR sensitivity for reflex bradycardia (-3.0 +/- 0.3, 1 h, and -2.8 +/- 0.1 beats.min-1.mmHg-1, 3 h vs. -2.1 +/- 0.2 beats.min-1.mmHg-1, before infusion).(ABSTRACT TRUNCATED AT 250 WORDS)

Renin–Angiotensin System in Mild Essential Hypertension. the Functional Significance of Angiotensin II in Untreated and Thiazide-Treated Hypertensive Patients

1978 ◽  
Vol 55 (s4) ◽  
pp. 319s-321s ◽  
Author(s):  
H. Ibsen ◽  
A. Leth ◽  
H. Hollnagel ◽  
A. M. Kappelgaard ◽  
M. Damkjaer Nielsen ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Functional Significance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

1. Twenty-five patients with mild essential hypertension, identified during a survey of a population born in 1936, were investigated. 2. Basal and post-frusemide values for plasma renin concentration and plasma angiotensin II concentration did not differ markedly from reference values in 25 40-year-old control subjects. In the untreated, sodium replete state saralasin infusion (5·4 nmol min−1 kg−1) produced an increase in mean arterial pressure in the patient group as a whole. 3. Twenty-one patients were treated with hydrochlorothiazide, mean dose 75 mg/day for 3 months. Pre-treatment, frusemide-stimulated plasma renin concentration and plasma angiotensin II, and values during thiazide treatment were higher in ‘non-responders’ (n = 10) to hydrochlorothiazide treatment than in ‘thiazide-responders’ (n = 11). During thiazide therapy, angiotensin II blockade induced a clear-cut decrease in mean arterial pressure in all ‘thiazide-nonresponders’ whereas only four out of 11 ‘thiazide-responders’ showed a borderline decline in mean arterial pressure. 4. The functional significance of the renin—angiotensin system in mild essential hypertension emerges only after thiazide treatment. Thiazide-induced stimulation of the renin—angiotensin system counter-balanced the hypotensive effect of thiazide in some 40% of the treated patients. Thus the responsiveness of the renin—angiotensin system determined the blood pressure response to thiazide treatment.

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