Blood pressure and heart rate effect of a vasopressin antagonist in conscious normotensive rats pretreated with exogenous vasopressin

1983 ◽  
Vol 91 (1) ◽  
pp. 135-137 ◽  
Author(s):  
Bernard Waeber ◽  
Jürg Nussberger ◽  
Hans R. Brunner
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rate Effect ◽  
Vasopressin Antagonist ◽  
Heart Rate Effect

Haemodynamic Profile of Angiotensin II Antagonism in Essential Hypertensive Patients

1979 ◽  
Vol 57 (s5) ◽  
pp. 119s-121s
Author(s):  
S. N. Hunyor ◽  
H. Larkin ◽  
Janet Rowe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Salt Intake ◽  
Peripheral Resistance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
Heart Rate Effect

1. The haemodynamic response to antagonistic (10 μg min−1 kg−1) and agonistic (40 μg min−1 kg−1) doses of saralasin was studied in young essential hypertensive patients. Blood pressure behaviour alone was thought to be inadequate to describe the response pattern. 2. Pre-saralasin setting of the renin-angiotensin axis was varied with salt intake (15 and 290 mmol of Na+/day) each for 10 days. This failed to influence blood pressure or plasma volume. 3. Antagonist blockade after low salt lowered blood pressure in three patients with the highest plasma renin values. Cardiac output rose in two of these, but it dropped in all others. 4. Decreases in cardiac output occurred with both doses of saralasin and even with suppression of the renin-angiotensin axis. This response is therefore unlikely to be due to removal of myocardial or venous angiotensin effects. 5. The renin-angiotensin system played a part in maintenance of blood pressure only with severe salt restriction and in a small proportion of cases. 6. No heart rate effect was seen with saralasin. 7. Blood pressure and total peripheral resistance responses were dependent on pre-(antagonist/ agonist) setting, but heart rate and cardiac output were not influenced by this factor.

Individual-Specific QT Interval Correction for Drugs With Substantial Heart Rate Effect Using Holter ECGs Extracted Over a Wide Range of Heart Rates

2018 ◽  
Vol 58 (8) ◽  
pp. 1013-1019 ◽  
Author(s):  
Gopi Krishna Panicker ◽  
Pramod Kadam ◽  
Saikat Chakraborty ◽  
Snehal Kothari ◽  
J. Rick Turner ◽  
...  
Keyword(s):  
Heart Rate ◽  
Qt Interval ◽  
Rate Effect ◽  
Heart Rates ◽  
Wide Range ◽  
Heart Rate Effect

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.

Optimal Electrocardiographic Pulsing Windows and Heart Rate: Effect on Image Quality and Radiation Exposure at Dual-Source Coronary CT Angiography

Radiology ◽  
2008 ◽  
Vol 248 (3) ◽  
pp. 792-798 ◽  
Author(s):  
Annick C. Weustink ◽  
Nico R. Mollet ◽  
Francesca Pugliese ◽  
Willem B. Meijboom ◽  
Koen Nieman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Image Quality ◽  
Radiation Exposure ◽  
Ct Angiography ◽  
Coronary Ct Angiography ◽  
Rate Effect ◽  
Coronary Ct ◽  
Dual Source ◽  
Heart Rate Effect

Voluntary control of human heart rate: Effect on reaction to aversive stimulation.

1974 ◽  
Vol 83 (3) ◽  
pp. 261-267 ◽  
Author(s):  
Alan D. Sirota ◽  
Gary E. Schwartz ◽  
David Shapiro
Keyword(s):  
Heart Rate ◽  
Human Heart ◽  
Aversive Stimulation ◽  
Rate Effect ◽  
Voluntary Control ◽  
Heart Rate Effect

Vasopressin and angiotensin II in reflex regulation of heart rate: effect of water deprivation

1992 ◽  
Vol 263 (4) ◽  
pp. R756-R761 ◽  
Author(s):  
V. L. Brooks
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Heart Rate Response ◽  
Physiological Role ◽  
Ang Ii ◽  
Vasopressin Antagonist ◽  
Reflex Tachycardia ◽  
Vasopressin Receptors ◽  
Dose Dependent ◽  
Heart Rate Effect

This study tested the hypothesis that endogenous angiotensin II (ANG II) and vasopressin enhance baroreflex-mediated increases in heart rate in water-replete dogs and in dogs water deprived to chronically elevate plasma ANG II and vasopressin concentrations. The baroreflex was assessed by examining the heart rate response to infusion of increasing doses of nitroprusside (0.3, 0.6, 1.5, and 3.0 micrograms.kg-1.min-1). The effect on the baroreflex of pretreating the dogs with the competitive ANG II antagonist saralasin, a V1-vasopressin antagonist, or a combined V1/V2-vasopressin antagonist, alone or in combination, was determined. Nitroprusside infusion produced dose-dependent increases in heart rate, and the heart rate response was greater in water-deprived dogs in association with higher plasma levels of ANG II and vasopressin than in water-replete dogs. ANG II blockade alone depressed reflex increases in heart rate in water-deprived but not water-replete dogs. In both water-replete and water-deprived dogs, blockade of V1-vasopressin receptors reduced the heart rate response to hypotension, but this effect could be produced only when ANG II receptors were also blocked. In addition, administration of saralasin and the V1/V2-vasopressin antagonist led to a further reduction of the reflex tachycardia. These data suggest that endogenous vasopressin, acting at both V1- and V2-receptors, can amplify the increase in heart rate produced by hypotension. In addition, the results further support a physiological role for chronic elevations in endogenous ANG II in the maintenance of normal baroreflex function.

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