Role of dopamine in the angiotensin II-induced vasopressin release in the conscious dehydrated dog

1982 ◽  
Vol 94 (2) ◽  
pp. 243-249 ◽  
Author(s):  
D. P. Brooks ◽  
J. R. Claybaugh
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Mean Arterial Blood Pressure ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Dopamine Antagonist ◽  
Vasopressin Release ◽  
Arterial Blood

The effect of the dopamine antagonist, haloperidol, on arginine-vasopressin (AVP) release induced by angiotensin II was studied in six dehydrated conscious dogs. Angiotensin II (10 ng/kg per min) alone caused a twofold increase (P<0·05) in plasma AVP concentration, a 25 mmHg increase (P<0·01) in mean arterial blood pressure (ABP) and a 70% decrease (P<0·01) in plasma renin activity (PRA). In the presence of haloperidol (3 μg/kg per min), angiotensin II caused similar changes in mean ABP (+25 mmHg; P<0·01) and PRA (−65%, P<0·01), but a small insignificant decrease in plasma AVP (−22%). The AVP response to angiotensin II in the presence of haloperidol was significantly (P<0·05) different from its response to angiotensin II alone. Neither haloperidol alone nor the two vehicles had any effect on plasma AVP or mean ABP but PRA dropped slightly. The results suggest that a dopaminergic mechanism may be involved in angiotensin II-induced AVP release.

Pharmacological and genetic evidence that cathepsin B is not the physiological activator of rodent prorenin

2010 ◽  
Vol 391 (12) ◽  
Author(s):  
M. David Percival ◽  
Sylvie Toulmond ◽  
Nathalie Coulombe ◽  
Wanda Cromlish ◽  
Sylvie Desmarais ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Cathepsin B ◽  
Plasma Renin ◽  
Renin Activity ◽  
Spontaneously Hypertensive ◽  
Protein Levels ◽  
Arterial Blood ◽  
Gene Compensation

Abstract Renin is the first enzyme in the renin-angiotensin-aldosterone system which is the principal regulator of blood pressure and hydroelectrolyte balance. Previous studies suggest that cathepsin B is the activator of the prorenin zymogen. Here, we show no difference in plasma renin activity, or mean arterial blood pressure between wild-type and cathepsin B knockout mice. To account for potential gene compensation, a potent, selective, reversible cathepsin B inhibitor was developed to determine the role of cathepsin B on prorenin processing in rats. Pharmacological inhibition of cathepsin B in spontaneously hypertensive and double transgenic rats did not result in a reduction in renal mature renin protein levels or plasma renin activity. We conclude that cathepsin B does not play a significant role in this process in rodents.

Hormonal responses to synthetic atrial natriuretic peptide in patients on regular hemodialysis

1988 ◽  
Vol 119 (2) ◽  
pp. 257-262 ◽  
Author(s):  
Sadao Nakajima ◽  
Hiromichi Suzuki ◽  
Yo Kageyama ◽  
Takashi Takita ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Regular Hemodialysis

Abstract. The effects of atrial natriuretic peptide (ANP) on mean arterial blood pressure, heart rate, plasma renin activity, aldosterone, cortisol, norepinephrine, epinephrine and arginine vasopressin were studied in 6 anuric subjects receiving regular hemodialysis. An iv bolus injection of 8 nmol of ANP followed by infusion at 32 pmol·kg−1·min−1 for 1 h in the pre- and posthemodialysis period was performed. Basal plasma ANP was higher before than after hemodialysis. ANP administration produced a reduction in mean arterial blood pressure accompanied by an elevation of norepinephrine and of plasma renin activity (from 2.49 ± 0.52 to 3.39 ± 0.85 nmol·l−1·h−1 predialysis and from 2.78 ± 0.71 to 3.15 ± 0.86 nmol·l−1·h−1 postdialysis, respectively, mean ± sem; P < 0.05). Plasma aldosterone and cortisol were significantly decreased. Plasma epinephrine and AVP remained unchanged. These hemodynamic and hormonal changes were similar in the pre- and the postdialysis period. These results suggest that 1) ANP causes a fall in mean arterial blood pressure, which in turn induces reflex tachycardia and activation of the sympathetic nervous system without diuresis; 2) the activated sympathetic nervous system as reflected in elevation of plasma norepinephrine may increase plasma renin activity; 3) reduced plasma aldosterone is not influenced by enhancement of the reninangiotensin system; therefore, 4) reduction of plasma aldosterone as well as cortisol is probably due to direct action of ANP, and finally 5) AVP had no direct relation with ANP administration.

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.

Plasma renin activity, angiotensin II, and aldosterone during intense heat stress

1976 ◽  
Vol 41 (3) ◽  
pp. 323-327 ◽  
Author(s):  
K. J. Kosunen ◽  
A. J. Pakarinen ◽  
K. Kuoppasalmi ◽  
H. Adlercreutz
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Arterial Blood ◽  
Main Components ◽  
Intense Heat

Plasma renin activity (PRA), angiotensin II, and aldosterone levels, arterial blood pressure, and heart rate of six male students were investigated during and after heat stress in a sauna bath. Increased PRA, angiotensin II, and aldosterone levels were found both during and after sauna. The greatest mean increases in PRA (94.9 +/- 10.4% SE, P less than 0.005) and angiotensin II (196 +/- 54.7% SE, P less than 0.02) were observed at the end of the heat stress (at 20 min), and that in plasma aldosterone (505 +/- 209% SE, P less than 0.02) 30 min after the sauna. The heart rate roughly doubled during the heat stress and there was a transient increase followed by a decrease in systolic blood pressure and a decrease in diastolic blood pressure. This study demonstrates that intense heat stress can cause remarkable changes in the three main components of the renin-angiotensin-aldosterone system.

Antagonism of Hydrochlorothiazide-Induced Elevations in Plasma-Renin Activity by Methyldopa in Conscious Renal-Hypertensive Dogs

1974 ◽  
Vol 52 (5) ◽  
pp. 1036-1040 ◽  
Author(s):  
Charles S. Sweet ◽  
Herbert C. Wenger ◽  
Theresa A. O'Malley
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Treatment Period ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Day Treatment ◽  
Plasma Renin ◽  
Significant Decline ◽  
Renin Activity ◽  
Arterial Blood

Hydrochlorothiazide, 2.5 and 10 mg/kg per day, was administered alone and in combination with methyldopa, 200 mg/kg per day, and changes in plasma-renin activity and mean arterial blood pressure were measured in conscious hypertensive dogs during a 7-day treatment period. Hydrochlorothiazide did not lower mean arterial blood pressure although there was a substantial increase in plasma-renin activity. When methyldopa was administered in combination with hydrochlorothiazide, a significant decline in both blood pressure and plasma-renin activity was observed. Since methyldopa was hypotensive only when coadministered with hydrochlorothiazide, the results suggest that antihypertensive effects of methyldopa in the diuretic-treated dog may depend in part on suppression of renin release.

Increased circulating plasma catecholamines and plasma renin activity in dogs after chemical sympathectomy with 6-hydroxydopamine

1977 ◽  
Vol 55 (3) ◽  
pp. 724-733 ◽  
Author(s):  
Gérald A. Porlier ◽  
Réginald A. Nadeau ◽  
Jacques de Champlain ◽  
Daniel G. Bichet
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Renin Activity ◽  
Mean Arterial Blood Pressure ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Renin Activity ◽  
Chemical Sympathectomy ◽  
Arterial Blood ◽  
6 Hydroxydopamine

Circulating plasma catecholamines, plasma renin activity, and other variables were measured in unanesthetized dogs before and after chemical sympathectomy with 6-hydroxydopamine (6-OHDA, 50 mg/kg). Chemical sympathectomy resulted in an immediate fall in mean arterial blood pressure and a delayed reduction in heart rate. Significant increases in plasma glucose and lactate concentrations, circulating plasma catecholamines, and plasma renin activity were found 24 h after 6-OHDA treatment. Circulating catecholamine levels decreased rapidly as time elapsed after sympathectomy and were half the initial values after 2 weeks. Plasma renin activity remained elevated during the 1st week after 6-OHDA treatment and returned to control levels during the 2nd week. Significant correlations were found between circulating catecholamines and heart rate mean arterial pressure, and plasma glucose and lactate concentrations. A significant correlation was also found between plasma renin activity and the mean arterial blood pressure. These results confirm that the adrenal medulla increases its catecholamine secretion rate into the circulation to compensate for the loss of adrenergic innervation after 6-OHDA treatment. They also indicate that the rennin–angiotensin system represents another important compensatory mechanism for circulatory homeostasis in sympathec-tomized animals.

Angiotensin causes vasoconstriction during hemorrhage in baroreceptor-denervated dogs

1983 ◽  
Vol 245 (4) ◽  
pp. H667-H673
Author(s):  
D. B. Averill ◽  
A. M. Scher ◽  
E. O. Feigl
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Aortic Pressure ◽  
Ang Ii ◽  
Arterial Blood ◽  
Aortic Blood ◽  
Aortic Blood Pressure ◽  
Mean Aortic Pressure

The participation of angiotensin II (ANG II) in the maintenance of arterial blood pressure during hypotensive hemorrhage was examined in unanesthetized, baroreceptor-denervated dogs. When mean aortic blood pressure was reduced to 69.0 +/- 2.2 mmHg, plasma renin activity increased from 0.6 +/- 0.3 ng ANG I X ml-1 X h-1 during the prehemorrhage control period to 4.5 +/- 1.6. Twenty minutes after the hemorrhage, mean aortic blood pressure rose to 78.9 +/- 3.1 mmHg. Subsequent infusion of the angiotensin II antagonist saralasin (5.2-14.0 micrograms X kg-1 X min-1) decreased mean aortic pressure to 59.6 +/- 3.3 mmHg. When 5% dextrose was infused in place of saralasin, mean aortic pressure was 79.3 +/- 4.3 mmHg. The lower aortic blood pressure caused by saralasin infusion was the result of a significant decrease in total peripheral resistance. Resistance was 10.3 +/- 3.2 mmHg X l-1 X min lower during saralasin infusion than during dextrose infusion. We conclude that baroreceptor reflexes are not essential for the elevation of plasma renin activity during hemorrhage. In baroreceptor-denervated dogs subjected to hypotensive hemorrhage, the increased formation of ANG II has a vasoconstrictor action that contributes to the maintenance of arterial blood pressure.

ROLE OF ANGIOTENSIN III IN THE REGULATION OF BLOOD PRESSURE, PLASMA ALDOSTERONE AND PLASMA RENIN ACTIVITY IN RABBIT

1978 ◽  
Vol 89 (1) ◽  
pp. 132-141 ◽  
Author(s):  
Ikuo Saito ◽  
Takao Saruta ◽  
Toyohisa Eguchi ◽  
Kazuoki Kondo ◽  
Ryuichi Nakamura ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Pressure Plasma ◽  
Angiotensin Iii ◽  
Pre Treatment

ABSTRACT To evaluate the role of angiotensin III in the control of blood pressure, plasma aldosterone and plasma renin activity (PRA), the pressor, steroidogenic and PRA-suppressing effect of angiotensin III was studied in rabbits with or without simultaneous constant infusion of Ile7-angiotensin III, an analogue of angiotensin III, or Sar1Ala8-angiotensin II, an analogue of angiotensin II, and compared with the effect of angiotensin II. Infusion of 30 ng/kg/min of angiotensin III or angiotensin II produced a twofold increase in plasma aldosterone. Pressor response to angiotensin III was approximately one tenth of that of angiotensin II. Infusion of angiotensin II suppressed the PRA significantly, while infusion of angiotensin III did not suppress it. Angiotensin II or angiotensin III induced-increase in plasma aldosterone was attenuated by the pretreatment with either Ile7-angiotensin III or Sar1Ala8-angiotensin II. Pressor or PRA-suppressing action of angiotensin II was unaffected by the pre-treatment with Ile7-angiotensin III, while it was significantly inhibited by pre-treatment with Sar1Ala8-angiotensin II. This study indicates that angiotensin III or angiotensin III analogues affect the adrenal glands selectively and suggests that there are differences between the receptor sites for angiotensins in vascular smooth muscle, kidney and those in the adrenal cortex.

Effect of angiotensin II and of an Angiotensin II Analogue (Sar1-Ile8-Angiotensin II) on Blood Pressure, Plasma Aldosterone and Plasma Renin Activity in the Dog

1974 ◽  
Vol 48 (s2) ◽  
pp. 41s-44s
Author(s):  
R. Beckerhoff ◽  
G. Uhlschmid ◽  
W. Vetter ◽  
H. Armbruster ◽  
J. Nussberger ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Angiotensin Receptors ◽  
Pressure Plasma ◽  
Arterial Blood

1. The effect of infusions of equimolar doses of angiotensin II (AII) and of the angiotensin analogue Sar1-Ile8-angiotensin II on arterial blood pressure, plasma aldosterone and plasma renin activity were compared in normal anaesthetized dexamethasone suppressed dogs. 2. Angiotensin II induced a significant increase of blood pressure and of plasma aldosterone whereas plasma renin activity decreased. The blood pressure was only slightly affected by large doses of the analogue. Plasma aldosterone, however, increased and plasma renin activity decreased. These changes were significant but less pronounced than after the infusions of angiotensin II. Plasma aldosterone remained high and renin activity low for 40 min after the infusions of the analogue. 3. The results suggest a strong agonistic potency of Sar1-Ile8-angiotensin II at the adrenal and renal angiotensin receptors, and that it is almost ineffective at the vascular receptors. The inhibition of renin secretion by angiotensin seems not to be related to its vasoconstrictive activity.

Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension

1977 ◽  
Vol 232 (3) ◽  
pp. F260-F269 ◽  
Author(s):  
J. Mohring ◽  
B. Mohring ◽  
M. Petri ◽  
D. Haack
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Biologically Active ◽  
Hypertensive Rats ◽  
Marked Enhancement ◽  
Plasma Arginine ◽  
The Relationship

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.

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