Does vasopressin sustain blood pressure of normally hydrated healthy volunteers?

1984 ◽  
Vol 246 (1) ◽  
pp. H143-H147 ◽  
Author(s):  
J. P. Bussien ◽  
B. Waeber ◽  
J. Nussberger ◽  
M. D. Schaller ◽  
H. Gavras ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Healthy Volunteers ◽  
Renin Angiotensin System ◽  
Pressor Effect ◽  
Angiotensin System ◽  
Vasopressin Antagonist ◽  
Flow Response ◽  
Lysine Vasopressin ◽  
The Face

The inhibitor of the pressor effect of arginine vasopressin (AVP), d(CH2)5Tyr(Me)AVP, at a dose of 5 micrograms/kg iv was shown in four healthy volunteers to antagonize the blood pressure, heart rate, and skin blood flow response to a lysine vasopressin infusion of 1 mIU X kg-1 X min-1. The inhibition lasted for more than 2 h. When the same dose of the vasopressin antagonist was administered to 10 healthy normally hydrated volunteers with their renin system intact or acutely blocked by 25 mg of captopril po, none of the above parameters changed. It is concluded that circulating vasopressin, even in the face of a blocked renin-angiotensin system, does not actively contribute to maintenance of cardiovascular homeostasis.

Compensatory response to hemorrhage in conscious dogs on normal and low salt intake

1983 ◽  
Vol 244 (3) ◽  
pp. H351-H356 ◽  
Author(s):  
R. I. Kopelman ◽  
V. J. Dzau ◽  
S. Shimabukuro ◽  
A. C. Barger
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Salt Intake ◽  
Renin Angiotensin System ◽  
Conscious Dogs ◽  
Converting Enzyme ◽  
Compensatory Response ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Low Salt

The compensatory response to moderately severe hemorrhage (30 ml/kg) was studied in chronically catheterized conscious dogs maintained on normal and low salt intake. Although the fall in blood pressure and the increase in heart rate were similar in the two salt states, the salt-restricted animals had significantly greater rises in plasma renin activity and plasma catecholamines following hemorrhage than did the normal salt dogs. To compare further the relative roles of the alpha-adrenergic system and the renin-angiotensin system in the maintenance of blood pressure following hemorrhage, pharmacologic blockade with either phentolamine or converting enzyme inhibitor was performed 20 min after the completion of the hemorrhage. These latter experiments demonstrated that salt restriction resulted in a significantly greater role for the renin-angiotensin system. Moreover, interruption of the renin-angiotensin system blunted the anticipated rise in catecholamines and heart rate during the additional hypotension induced by converting enzyme blockade after hemorrhage.

Centrally induced cardiovascular and sympathetic responses to hydrocortisone in rats

1983 ◽  
Vol 245 (6) ◽  
pp. H1013-H1018 ◽  
Author(s):  
H. Takahashi ◽  
K. Takeda ◽  
H. Ashizawa ◽  
A. Inoue ◽  
S. Yoneda ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Sympathetic Nerve ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Angiotensin I Converting Enzyme ◽  
Angiotensin Ii Antagonist ◽  
Dose Dependent

Central effects of hydrocortisone were investigated by injecting it intracerebroventricularly (icv) while recording blood pressure and heart rate in awake rats. Dose-dependent increases in both blood pressure and heart rate occurred following injections of hydrocortisone. Pretreatment by icv injections of the angiotensin II antagonist, [Sar1-Ile8]angiotensin II, completely abolished vasopressor responses to subsequent injections of hydrocortisone. When rats were later anesthetized with urethan to allow recording of abdominal sympathetic nerve activity, hydrocortisone produced vasopressor responses accompanied by corresponding increases in sympathetic nerve firing, which were also abolished by central pretreatment with either [Sar1-Ile8]angiotensin II or angiotensin I converting-enzyme inhibitor, captopril. These results indicate that centrally administered hydrocortisone stimulates the brain renin-angiotensin system to produce vasopressor responses by increasing sympathetic nerve firing.

Investigation of hormonal effects during 10-h head-down tilt on heart rate and blood pressure variability

1995 ◽  
Vol 78 (2) ◽  
pp. 583-596 ◽  
Author(s):  
R. L. Hughson ◽  
A. Maillet ◽  
G. Gauquelin ◽  
P. Arbeille ◽  
Y. Yamamoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Diastolic Blood Pressure ◽  
Blood Pressure Variability ◽  
Diastolic Pressure ◽  
Plasma Concentrations ◽  
Animal Experiments ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

Head-down tilt (HDT) bed rest was used in this study to achieve physiological manipulation of the plasma concentrations of atrial natriuretic peptide (ANP) and the hormones of the renin-angiotensin system. The purpose of this was to achieve a parallel with previous animal experiments in which blockade of the renin-angiotensin system caused significant increases in low-frequency spectral power of heart rate variability, presumably as a consequence of increased blood pressure variability, although this was not measured in these animal experiments. Eight healthy young men completed 10 h of seated control and 6 degrees HDT. To gain a more complete understanding of the interactions between hormonal and neural factors involved in cardiovascular regulation, we measured heart rate, systolic and diastolic pressure variabilities, plasma hormone concentrations, and blood flow to selected vascular beds by pulsed Doppler. Resting R-R interval was not significantly different between seated and HDT tests. Stroke volume and cardiac output were elevated in the first 1–2 h of HDT (P < 0.05), whereas each of systolic (P < 0.01) and diastolic (P < 0.0001) pressures was lower during HDT. Plasma ANP increased as much as 70% during HDT (P < 0.0001). Total variability in each of R-R interval and diastolic blood pressure was reduced during HDT (P < 0.001). Thus, at a time when plasma renin activity was decreased as much as 40% (P < 0.0001), there was in fact a decrease in the variability of R-R interval and diastolic blood pressure in contrast to the hypothesized increase such as found in previous animal experimentation. The data were compatible with tighter autonomic regulation of heart rate about the ideal mean value during HDT.

Abnormal blood pressure recovery during ganglion blockade in diabetic rats

1987 ◽  
Vol 252 (1) ◽  
pp. R102-R108 ◽  
Author(s):  
R. A. Hebden ◽  
T. Bennett ◽  
S. M. Gardiner
Keyword(s):  
Blood Pressure ◽  
Renin Angiotensin System ◽  
Diabetic Rats ◽  
Toxic Effects ◽  
Elevated Blood ◽  
Angiotensin System ◽  
Vasopressin Antagonist ◽  
Renin Angiotensin ◽  
Acute Hypotension ◽  
Per Se

The aim of the present study was to determine the extent to which vasopressin or the renin-angiotensin system contributed to the recovery of blood pressure following acute hypotension induced by treatment with pentolinium and captopril, or pentolinium and the vasopressin antagonist d(CH2)5DAVP, respectively, in conscious, free-moving rats treated 21 days previously with saline or streptozotocin (STZ) (60 mg/kg ip). Half the animals given STZ were subsequently treated with insulin (about 4.5 U/day). The STZ-treated animals demonstrated a resting bradycardia and systolic hypotension. The vasopressin-mediated recovery in blood pressure seen following administration of pentolinium, in the presence of captopril, and the renin-angiotensin-mediated recovery seen following administration of pentolinium, in the presence of d(CH2)5DAVP, were both found to be significantly (P less than 0.05) attenuated in the STZ-treated animals. These abnormalities were absent in the animals injected with STZ and treated daily with insulin, but receiving their last dose 24 h before measurement. At that time the animals had elevated blood glucoses. These results indicate that the abnormalities observed were not due to toxic effects of STZ or to hyperglycemia per se.

Blood pressure in streptozotocin-treated Brattleboro and Long-Evans rats

1990 ◽  
Vol 258 (4) ◽  
pp. R852-R859 ◽  
Author(s):  
K. C. Tomlinson ◽  
S. M. Gardiner ◽  
T. Bennett
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Insulin Treatment ◽  
Renin Angiotensin System ◽  
Brattleboro Rats ◽  
Ang Ii ◽  
Angiotensin System ◽  
Resting Blood Pressure ◽  
Long Evans

The diabetogenic agent streptozotocin (STZ) was injected intraperitoneally in Long-Evans and arginine vasopressin (AVP)-deficient Brattleboro rats. Twenty-eight days later both strains had a bradycardia and systolic hypotension; STZ-treated Brattleboro rats also had diastolic hypotension. The vasopressin (V1-receptor) antagonist, d(CH2)5[Tyr(Et)]DAVP, had no effect on resting blood pressure (BP) or heart rate (HR) in either strain of rat, indicating the relative maintenance of diastolic BP in STZ-treated Long-Evans rats was not dependent on acute vascular actions of AVP. Captopril caused a modest hypotension in all groups of rats, indicating that BP was not differentially dependent on the renin-angiotensin system in the different groups. In the presence of captopril and the ganglion blocker, pentolinium tartrate, the AVP-mediated recovery in BP was impaired in STZ-treated Long-Evans rats. During administration of d(CH2)5[Tyr(Et)]DAVP and pentolinium, the angiotensin II (ANG II)-mediated BP recovery was smaller in both groups of STZ-treated rats, indicating that this abnormality was not likely to be caused by inhibition of renin release by AVP. The abnormalities in ANG II- and AVP-mediated recovery were prevented by insulin treatment.

Pressor sensitivities to vasopressin, angiotensin II, or methoxamine in diabetic rats

1987 ◽  
Vol 253 (5) ◽  
pp. R726-R734 ◽  
Author(s):  
R. A. Hebden ◽  
T. Bennett ◽  
S. M. Gardiner
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Diabetic Rats ◽  
Significant Enhancement ◽  
Control Group ◽  
Control Groups ◽  
Angiotensin System ◽  
Significant Augmentation

We investigated the pressor sensitivities to vasopressin, angiotensin II, and methoxamine of intact and ganglion-blocked rats that had been treated 21 days earlier with streptozotocin or saline. No differences in blood pressure or heart rate responses to vasopressin or angiotensin II were found between the intact groups when these peptides were administered intravenously in equimolar doses. After ganglion blockade a significant enhancement in pressor responsiveness to both vasopressin and angiotensin II was observed in the control groups, but in the streptozotocin-treated animals no enhancement in pressor sensitivity to vasopressin was found. Furthermore, although a significant augmentation of the responses to angiotensin II was observed, it was smaller than that seen in the ganglion-blocked control group. Neither group showed enhanced pressor responsiveness to methoxamine. These results indicate that the previously observed diminished contributions from endogenous vasopressin and the renin-angiotensin system to blood pressure recovery following ganglion blockade in streptozotocin-treated rats may have been due, at least in part, to diminished pressor responsiveness.

Effect of salt deprivation on blood pressure in rats

1989 ◽  
Vol 256 (5) ◽  
pp. H1426-H1431 ◽  
Author(s):  
C. E. Ott ◽  
W. J. Welch ◽  
J. N. Lorenz ◽  
S. A. Whitescarver ◽  
T. A. Kotchen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Salt Intake ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
The Other ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Sprague Dawley Rat ◽  
Low Salt

In most cases blood pressure (BP) is directly related to NaCl intake. In some studies, BP is increased by low salt intake. The effect of Na and Cl deprivation or selective Na deprivation on BP in the normotensive Sprague-Dawley rat was investigated. In study 1, rats were uninephrectomized and fed low NaCl, normal NaCl, or low Na-normal Cl for 3 wk. BP was higher (P less than 0.05) in rats fed low NaCl and low Na-normal Cl than normal NaCl. Plasma renin activity was stimulated by low NaCl intake but was not different between the other two groups. After captopril treatment, BP was lower in the low NaCl group (73.1 +/- 3.6 mmHg) than in the normal-NaCl (99.2 +/- 6.7 mmHg) or low Na-normal Cl (92.0 +/- 6.7 mmHg) groups. In study 2, intact rats (n = 8 per group) were fed low (less than 0.01%), normal (1%), or high NaCl (4%) for 1 wk. BP and heart rate were higher in the low-NaCl group (P less than 0.05) than in the other two groups. Plasma volumes were not different among the groups. In study 3, two groups of eight rats were given either low NaCl or 2% NaCl for 2 wk. BP (131.4 +/- 3.6 mmHg) and heart rate (402 +/- 11 beats/min) were higher in the low-NaCl group than in the 2% NaCl group (121.1 +/- 3.2 mmHg and 369 +/- 9 beats/min, respectively). In the normotensive Sprague-Dawley rat, low NaCl intake elevated BP when compared with normal or high NaCl intake. Part of the increase in the uninephrectomized, Cl-supplemented group is not dependent on the renin-angiotensin system.

scholarly journals Acute AT1-receptor blockade reverses the hemodynamic and baroreflex impairment in adult sheep exposed to antenatal betamethasone

2010 ◽  
Vol 299 (2) ◽  
pp. H541-H547 ◽  
Author(s):  
Hossam A. Shaltout ◽  
James C. Rose ◽  
Jorge P. Figueroa ◽  
Mark C. Chappell ◽  
Debra I. Diz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Low Frequency ◽  
Renin Angiotensin System ◽  
Premature Delivery ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Angiotensin Type

To accelerate lung development and protect neonates from other early developmental problems, synthetic steroids are administered maternally in the third trimester, exposing fetuses that are candidates for premature delivery to them. However, steroid exposure at this point of gestation may lead to elevated blood pressure [mean arterial pressure (MAP)] during adolescence. We hypothesize that fetal exposure to steroids activates the renin-angiotensin system, inducing an elevation in blood pressure and attenuation of baroreflex sensitivity (BRS) that is angiotensin II dependent in early adulthood. To test this hypothesis, fetal sheep were exposed to betamethasone (Beta) or vehicle (control) administered to ewes at day 80 of gestation and delivered at full term. At 1.8 yr of age, male offspring were instrumented for conscious recording of MAP, heart rate, and measurement of BRS [as low-frequency-α, high-frequency-α, sequence (seq) UP, seq DOWN, and seq TOTAL]. Beta-exposed sheep ( n = 6) had higher MAP than control sheep ( n = 5) (93 ± 2 vs. 84 ± 2 mmHg, P < 0.01). Acute blockade of angiotensin type 1 receptors with candesartan (0.3 mg/kg iv) normalized MAP in Beta-exposed sheep (85 ± 4 mmHg), with no effect in control sheep (82 ± 3 mmHg). Before angiotensin type 1 blockade, BRS maximum gain was significantly lower in Beta-exposed vs. control sheep (11 ± 3 vs. 26 ± 3 ms/mmHg, P < 0.0.01). However, 45 min after candesartan injection, BRS was increased in Beta-exposed (21 ± 5 ms/mmHg) and control (35 ± 4 ms/mmHg) sheep. Heart rate variability (HRV) and blood pressure variability (BPV) revealed lower HRV (SD of beat-to-beat interval and root mean square of successive beat-to-beat differences in R-R interval duration) and higher BPV (SD of MAP, systolic arterial pressure in low-frequency range) in Beta-exposed sheep. Candesartan partially restored HRV in Beta-exposed sheep and fully corrected BPV. Thus, in utero exposure to synthetic glucocorticoids causes long-lasting programming of the cardiovascular system via renin-angiotensin system-dependent mechanisms.

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