The Reflex Control of Arginine-Vasopressin Release in Essential Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 145s-147s ◽  
Author(s):  
B. Ricciardelli ◽  
M. Volpe ◽  
B. Trimarco ◽  
M. Chiariello ◽  
F. Rengo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arginine Vasopressin ◽  
Carotid Sinus ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Vasopressin Release ◽  
Head Up Tilt ◽  
Reflex Control ◽  
Plasma Arginine ◽  
Neck Chamber

1. The reflex control of arginine-vasopressin release was studied in 12 essential established hypertensive patients and in 12 age-matched normal subjects by comparing the effects of head-up tilt and a variable-pressure neck-chamber. 2. After 45 min 85° head-up tilt, normal subjects showed an increase in plasma arginine-vasopressin and in plasma renin activity, while plasma volume decreased. In hypertensive patients, plasma arginine-vasopressin showed changes after tilt opposite to those of controls, while the changes in plasma renin activity and plasma volume were similar to those observed in the normal group. In both groups the changes in systolic and diastolic blood pressure were not statistically significant. A reduction in carotid sinus transmural pressure obtained by increasing neck-tissue pressure (+ 50 mmHg) by means of a neck-chamber, evoked different responses in mean blood pressure in the two groups, but failed to induce any significant change in plasma arginine-vasopressin concentration both in the normal and in the hypertensive subjects. 3. These results seem to suggest that carotid sinus baroreceptors, though active in blood pressure control, do not play a direct role in arginine-vasopressin release and, therefore, the opposite response of arginine-vasopressin observed after tilt in the two groups of subjects should be ascribed to more complex mechanisms.

Carotid baroreflexes and plasma vasopressin in humans during head-up tilt

1992 ◽  
Vol 263 (2) ◽  
pp. R318-R323 ◽  
Author(s):  
M. Kamegai ◽  
M. S. Kristensen ◽  
J. Warberg ◽  
P. Norsk
Keyword(s):  
Heart Rate ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Plasma Renin ◽  
Time Increase ◽  
Central Venous ◽  
Plasma Vasopressin ◽  
Head Up Tilt ◽  
Plasma Arginine ◽  
Healthy Males

To investigate the influence of carotid baroreflexes on plasma arginine vasopressin (AVP) in humans, eight healthy males underwent two sessions of passive head-up tilt to 60 degrees for 15 min each. During one of the sessions (sequence randomized), carotid baroreflexes were simultaneously stimulated by static neck suction of 23 +/- 1 mmHg during the whole period of head-up tilt. Only subjects who did not develop presyncopal symptoms during head-up tilt were included. Head-up tilt increased AVP significantly from 1.0 +/- 0.3 to 4.2 +/- 1.3 pg/ml (P less than 0.05). In contrast to this, AVP did not at any point in time increase significantly during head-up tilt when neck suction was applied. Plasma renin activity and heart rate were unaffected by neck suction, whereas mean arterial pressure and central venous pressure decreased. We conclude that the moderate but significant increase in plasma AVP during nonhypotensive head-up tilt is in part mediated by deloading of carotid baroreceptors induced by the acute fall in hydrostatic pressure at the level of the carotid sinus.

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.

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.

The Effect of the Methionine Enkephalin Analogue DAMME on the Vasopressin Response to Tilt in Man

1980 ◽  
Vol 59 (6) ◽  
pp. 501-503 ◽  
Author(s):  
S. L. Lightman ◽  
Mary L. Forsling
Keyword(s):  
Blood Pressure ◽  
Pulse Rate ◽  
Plasma Volume ◽  
Arginine Vasopressin ◽  
Pressure Pulse ◽  
Volume Changes ◽  
Methionine Enkephalin ◽  
Head Up Tilt ◽  
Plasma Arginine

1. Infusion of the methionine enkephalin analogue DAMME (Sandoz) inhibits the rise in plasma arginine vasopressin after a 65° head-up tilt. 2. DAMME does not significantly affect the blood pressure, pulse rate or plasma volume changes produced by tilt.

Renin Release during Head-up Tilt Occurs Independently of Sympathetic Nervous Activity in Tetraplegic Man

1980 ◽  
Vol 59 (4) ◽  
pp. 251-256 ◽  
Author(s):  
C. J. Mathias ◽  
N. J. Christensen ◽  
H. L. Frankel ◽  
W. S. Peart
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Nervous Activity ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous Activity ◽  
Head Up Tilt ◽  
Sympathetic Nervous

1. The role of the sympathetic nervous system in the release of renin during head-up tilt has been studied in five normal subjects and in four tetraplegic patients with cervical spinal-cord transection above the sympathetic outflow. Blood pressure, heart rate and concentrations of plasma noradrenaline, plasma adrenaline and plasma renin activity were measured during head-up tilt to 45° before and after acute β-adrenoreceptor blockade with intravenous propranolol. 2. In the normal subjects there were minimal changes in blood pressure during head-up tilt and there was a rise in both plasma noradrenaline concentration and plasma renin activity. After propranolol values of plasma renin activity at rest fell with little change occurring during head-up tilt. 3. In the tetraplegic patients there was a substantial fall in blood pressure during head-up tilt. Concentrations of plasma noradrenaline and adrenaline did not change but there was a marked increase in plasma renin activity. Values of plasma renin activity both at rest and during head-up tilt were unaffected by propranolol. 4. We conclude that in tetraplegic patients renin release during head-up tilt may occur independently of sympathetic nervous activity and is probably largely dependent on activation of renal vascular receptors.

Cardiovascular and neuroendocrine responses to baroreceptor denervation in baboons

1990 ◽  
Vol 258 (4) ◽  
pp. R930-R938 ◽  
Author(s):  
R. E. Shade ◽  
V. S. Bishop ◽  
J. R. Haywood ◽  
C. K. Hamm
Keyword(s):  
Blood Pressure ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Vasopressin Secretion ◽  
Blood Pressure Responses

The purpose of this study was to describe the hormonal and blood pressure responses to partial (carotid sinus) and complete (carotid sinus + aortic arch) baroreceptor denervation in baboons. Experiments were performed in eight adult male baboons maintained on a tether system for the continuous measurement of mean arterial blood pressure (MAP) and heart rate (HR). Bilateral carotid sinus denervation (CSD) immediately increased MAP from 83 +/- 2.2 to 124 +/- 7.3 mmHg. MAP gradually decreased over the next 14 days to intact levels. There were also transient decreases in HR variability and increases in blood pressure variability after CSD. Subsequent denervation of the aortic arch to produce sinoaortic denervation (SAD) resulted in another abrupt large increase in MAP followed by a small but significant increase in MAP of 11 mmHg that was maintained for up to 4 wk after SAD. The short-term variability of HR and blood pressure was chronically decreased and increased, respectively, after SAD. Plasma renin activity, vasopressin, and epinephrine were not changed from intact levels either after CSD or SAD. Plasma norepinephrine was only transiently increased by CSD and chronically elevated by 72% over intact levels after SAD. Thus CSD in the baboon does not produce a sustained increase in MAP. SAD chronically increases MAP and is associated with evidence for an increased sympathetic tone. There is no indication that either increased renin secretion or vasopressin secretion contributes to the chronic cardiovascular effects of SAD in baboons.

γ-l-Glutamyl-l-Dopa is a Dopamine Pro-Drug, Relatively Specific for the Kidney in Normal Subjects

1985 ◽  
Vol 69 (2) ◽  
pp. 207-214 ◽  
Author(s):  
D. P. Worth ◽  
J. N. Harvey ◽  
J. Brown ◽  
M. R. Lee
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Glomerular Filtration Rate ◽  
Plasma Renin Activity ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Urinary Sodium Excretion ◽  
Systemic Effects

1. γ-l-Glutamyl-l-dopa was given by intravenous infusion to eight normal subjects at doses of 12.5 and 100 μg min−1 kg−1. 2. Both doses of the dipeptide resulted in an increase in mean urinary sodium excretion. 3. Mean effective renal plasma flow rose at both doses, but mean glomerular filtration rate increased only at the lower dose. 4. There was a fall in mean plasma renin activity after the infusion of both 12.5 and 100 μg min−1kg−1. 5. Mean urine free dopamine excretion increased by 280- and 2500-fold at infusion rates of 12.5 and 100 μg min−1 kg−1 respectively. 6. Mean plasma free dopamine rose at both doses but the increase at 12.5 μg min−1 kg−1 was not to a level previously associated with systemic effects of the catecholamine. 7. On administration of the dipeptide at 12.5 μg min−1 kg−1 there were no changes in blood pressure or heart rate, but at the higher dose there was a fall in diastolic blood pressure. 8. At a dose of 12.5 μg min−1 kg−1 in man, there is kidney specific conversion of gludopa to dopamine.

Vascular effects of arginine vasopressin, angiotensin II, and norepinephrine in adrenal insufficiency

1984 ◽  
Vol 246 (1) ◽  
pp. H104-H113
Author(s):  
S. Ishikawa ◽  
R. W. Schrier
Keyword(s):  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Vascular Effects ◽  
Vascular Effect ◽  
A Value ◽  
Angiotensin Ii Antagonist ◽  
Adrenergic Blocker ◽  
Plasma Arginine

Plasma arginine vasopressin (AVP) levels were 9.6 pg/ml in the mineralocorticoid-deficient rats, a value significantly greater than 4.8 pg/ml in the glucocorticoid-deficient rats (P less than 0.05), and 1.6 pg/ml in controls (P less than 0.001). The AVP antagonist of the vascular effect of AVP, [1(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine] AVP, [d(CH2)5Tyr(Me)AVP] (5 micrograms/kg), decreased mean arterial pressure (MAP) from 76.5 to 71.6 mmHg (P less than 0.01) in mineralocorticoid-deficient rats on day 10 but not in glucocorticoid deficient rats on day 14 (113.2-111.6 mmHg, NS) or in control rats (109.7-110.2 mmHg, NS). Plasma renin activity was 40.7 ng X ml-1 X h-1 in mineralocorticoid-deficient rats and 7.2 in glucocorticoid-deficient rats (P less than 0.001). The angiotensin II antagonist, [Sar1-Gly8]angiotensin II (5 micrograms X kg-1 X min-1), decreased MAP from 69.3 to 53.2 mmHg in mineralocorticoid-deficient rats (P less than 0.001) but not in glucocorticoid-deficient rats. Plasma norepinephrine was 1,138 pg/ml in mineralocorticoid-deficient rats and 251 pg/ml in glucocorticoid-deficient rats (P less than 0.001). The alpha-adrenergic blocker, phenoxybenzamine (3 mg/kg), reduced MAP from 82 to 51 mmHg in mineralocorticoid deficient rats (P less than 0.005), a decrease in MAP greater (P less than 0.05) than that observed in glucocorticoid-deficient rats (107.7-84.8 mmHg, P less than 0.02). In addition, the AVP antagonist caused a greater and more prolonged reduction in MAP in mineralocorticoid-deficient rats after the administration of either the angiotensin II antagonist or alpha-blocker. These results indicate that AVP, norepinephrine, and angiotensin II are involved in maintaining blood pressure in the mineralocorticoid-deficient state.

Cardiovascular and renin responses to desmopressin in humans: role of prostacyclin and beta-adrenergic systems

1991 ◽  
Vol 260 (4) ◽  
pp. H1031-H1036 ◽  
Author(s):  
K. Hasunuma ◽  
K. Yamada ◽  
Y. Tamura ◽  
S. Yoshida
Keyword(s):  
Blood Pressure ◽  
Pulse Rate ◽  
Plasma Renin ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Receptor Activation ◽  
Renin Release ◽  
Beta Adrenoceptor ◽  
V2 Receptor

To investigate the involvement of prostacyclin and the sympathetic nervous system in cardiovascular responses to 1-desamino-8-D-arginine vasopressin (DDAVP), a selective V2-receptor agonist, in normal subjects, DDAVP (0.4 micrograms/kg) was infused with or without indomethacin, a cyclooxygenase inhibitor, or propranolol, a beta-adrenoceptor antagonist. A decrease in blood pressure and increases in pulse rate and plasma renin activity (PRA) were observed by DDAVP infusion. Indomethacin did not influence the DDAVP-induced changes in blood pressure and pulse rate but suppressed the increases in PRA and urinary 6-ketoprostaglandin F1 alpha excretion after DDAVP infusion. Even with propranolol administration, DDAVP produced a similar decrease in blood pressure with a reduction of the increased pulse rate. The DDAVP-induced increase in PRA was not affected either. Indomethacin or propranolol alone did not affect the basal levels of the parameters. DDAVP stimulated the in vitro renin release from rabbit renal cortical slices. The stimulation was inhibited by indomethacin or d(CH2)5[D-Ile2,Ile4]AVP, a selective V2-receptor antagonist. These findings suggest that DDAVP primarily elicits vasodilation, probably through the prostacyclin-independent endothelium-derived relaxation and DDAVP also causes an increase in renin release, which would be partly attributed to the increased synthesis of prostacyclin due to vasculoendothelial V2-like receptor activation but not mainly due to an increase in sympathetic nerve activity.

Plasma vasopressin and atrial natriuretic hormone levels in hypopituitarism with and without hydrocortisone treatments: responses to an acute water load

1992 ◽  
Vol 126 (3) ◽  
pp. 217-223 ◽  
Author(s):  
Tokihisa Kimura ◽  
Kozo Ota ◽  
Masaru Shoji ◽  
Minoru Inoue ◽  
Kazutoshi Sato ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Plasma Osmolality ◽  
Normal Subjects ◽  
Natriuretic Hormone ◽  
Water Load ◽  
Blood Volume Expansion ◽  
Atrial Natriuretic Hormone ◽  
Plasma Arginine ◽  
Glucocorticoid Deficiency ◽  
Atrial Natriuretic

To assess whether arginine vasopressin and atrial natriuretic hormone participate in impaired urinary dilution and excretion in glucocorticoid deficiency secondary to hypopituitarism. an acute oral water load of 20 ml·kg−1 BW was undertaken in the absence and presence of an oral hydrocortisone (60 mg) treatment in patients with ACTH deficiency (N= 7) and panhypopituitarism (N = 2). Plasma arginine vasopressin and atrial natriuretic hormone and renal water handling were simultaneously determined and compared with those in similarly water-loaded normal subjects. Plasma arginine vasopressin did not fall in response to decreased blood osmolality after an acute water load in the absence of hydrocortisone; plasma atrial natriuretic hormone did not change despite blood volume expansion; and impairment in urinary dilution and excretion remained. On the other hand, in the presence of hydrocortisone, plasma arginine vasopressin fell in response to a decrease in plasma osmolality and plasma atrial natriuretic hormone increased, thereby restoring urinary dilution and excretion. These results demonstrate that the impaired arginine vasopressin response to acute water loading play an essential role in deranged renal water and electrolyte handling in the state of glucocorticoid deficiency; the impaired release of atrial natriuretic hormone also may affect these disorders.

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