scholarly journals Dobutamine reverses the cardio-suppressive effects of terlipressin without improving renal function in cirrhosis and ascites: a randomized controlled trial

2020 ◽  
Vol 318 (2) ◽  
pp. G313-G321 ◽  
Author(s):  
Mads Israelsen ◽  
Emilie Kristine Dahl ◽  
Bjørn Stæhr Madsen ◽  
Signe Wiese ◽  
Flemming Bendtsen ◽  
...  
Keyword(s):  
Renal Function ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Impaired Renal Function ◽  
Combined Treatment ◽  
Suppressive Effect ◽  
Peripheral Vascular Resistance ◽  
Decompensated Cirrhosis ◽  
Peripheral Vascular ◽  
Renin Angiotensin

Acute kidney injury and hepatorenal syndrome (HRS) are frequent complications in patients with cirrhosis and ascites. First-line treatment is terlipressin, which reverses HRS in ~40% of patients but also lowers cardiac output (CO). We aimed to investigate whether reversing the cardio-suppressive effect of terlipressin with the β-adrenoceptor agonist dobutamine would increase CO and thereby increase the glomerular filtration rate (GFR). We randomized 25 patients with cirrhosis, ascites, and impaired renal function (2:2:1): group A received terlipressin followed by the addition of dobutamine; group B received dobutamine and terlipressin as monotherapies; and group C received placebo. Renal and cardiac functions were assessed during 8 clearance periods of 30 min, and concentrations of vasoactive hormones were measured. Dobutamine as a monotherapy increased CO (1.03 L/min, P < 0.01) but had no significant effects on GFR. Renin ( P < 0.05), angiotensin II ( P < 0.005), and aldosterone ( P < 0.05) increased after dobutamine infusion. Terlipressin as a monotherapy improved GFR (18.9 mL·min−1·m−2, P = 0.005) and mean arterial pressure (MAP) (14 mmHg, P = 0.001) but reduced CO (−0.92 L/min, P < 0.005) and renin ( P < .005). A combined treatment of dobutamine and terlipressin had a positive effect on CO (1.19 L/min, P < 0.05) and increased renin ( P < 0.005), angiotensin II ( P < 0.005), and aldosterone ( P < 0.05), but it had no significant effects on MAP or GFR. Dobutamine reversed the cardio-suppressive effect of terlipressin in cirrhosis, ascites, and impaired renal function. However, dobutamine reduced peripheral vascular resistance, activated renin-angiotensin-aldosterone system, and did not improve GFR compared with terlipressin as a monotherapy. Therefore, dobutamine cannot be recommended in cirrhosis and ascites. NEW & NOTEWORTHY This study shows that the cardio-suppressive effects of the vasopressin receptor agonist terlipressin can be reversed by dobutamine. This is a novel observation in patients with decompensated cirrhosis. Furthermore, we show that dobutamine reduced the peripheral vascular resistance and activated the renin-angiotensin system, whereas renal function was not further improved by terlipressin alone.

Coevolution of the rennin–angiotensin system and the nervous control of blood circulation

1984 ◽  
Vol 62 (2) ◽  
pp. 137-147 ◽  
Author(s):  
John X. Wilson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Renin Angiotensin System ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

The mammalian renin–angiotensin system appears to be involved in the maintenance of blood volume and pressure because (i) sodium depletion, hypovolemia, and hypotension increase renin levels, and (ii) administration of exogenous angiotensin II rapidly increases mineralocorticoid and antidiuretic hormone production, transepithelial ion transport, drinking behavior, and peripheral vascular resistance. Are these also the physiological properties of the renin–angiotensin system in nonmammalian species? Signals for altered levels of renin activity have yet to be conclusively identified in nonmammalian vertebrates, but circulating renin levels are elevated by hypotension in teleost fish and birds. Systemic injection of angiotensin II causes an increase in arterial blood pressure in all the vertebrates studied, suggesting that barostatic control is a universal function of this hormone. Angiotensin II alters vascular tone by direct action on arteriolar muscles in some species, but at concentrations of the hormone which probably are unphysiological. More generally, angiotensin II increases blood pressure indirectly, by acting on the sympathetic nervous system. Catecholamines, derived from chromaffin cells and (or) from peripheral adrenergic nerves, mediate some portion of the vasopressor response to angiotensin II in cyclostomes, elasmobranchs, teleosts, amphibians, reptiles, mammals, and birds. Alteration of sympathetic outflow is a prevalent mechanism through which the renin–angiotensin system may integrate blood volume, cardiac output, and peripheral vascular resistance to achieve control of blood pressure and adequate perfusion of tissues.

Cardiovascular and endocrine effects of potassium in spontaneously hypertensive rats

1985 ◽  
Vol 249 (5) ◽  
pp. H907-H913 ◽  
Author(s):  
M. L. Workman ◽  
M. S. Paller
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Peripheral Vascular Resistance ◽  
Plasma Norepinephrine ◽  
Peripheral Vascular ◽  
Baroreflex Control ◽  
Potassium Supplement ◽  
Spontaneously Hypertensive ◽  
Potassium Supplementation

Although potassium is known to lower blood pressure in a number of forms of experimental and human hypertension, the mechanism for this effect remains unclear. We studied several possible mechanisms for this effect in the spontaneously hypertensive rat (SHR). Fourteen-week-old SHR were given 0.5% KCl in the drinking water. This potassium supplement resulted in a 16-mmHg fall in mean arterial pressure and a 22% decrease in peripheral vascular resistance. Plasma potassium increased 0.4 meq/l, while muscle potassium was unchanged. Potassium supplementation resulted in no change in plasma renin activity, plasma aldosterone, or plasma norepinephrine. Urinary excretion of prostaglandin (PG) E2 and 6-keto-PGF1 alpha was also not altered by potassium supplementation. Potassium-supplemented SHR were found to have no difference in sodium excretion compared with control SHR, and plasma volume was similar in both groups. The pressor response to angiotensin II and norepinephrine was not substantially affected by potassium supplementation. Furthermore, baroreflex control of heart rate was not altered by potassium supplementation. Finally, potassium supplementation resulted in no change in mesenteric artery angiotensin II receptor number or receptor affinity. Therefore, although potassium lowers blood pressure in the SHR by decreasing peripheral vascular resistance, the mechanism of this effect on vascular resistance remains unknown.

scholarly journals Peripheral vascular resistance and angiotensin II levels during pulsatile and no-pulsatile cardiopulmonary bypass.

Thorax ◽  
1979 ◽  
Vol 34 (5) ◽  
pp. 594-598 ◽  
Author(s):  
K M Taylor ◽  
W H Bain ◽  
M Russell ◽  
J J Brannan ◽  
I J Morton
Keyword(s):  
Cardiopulmonary Bypass ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular

scholarly journals Reduction in peripheral vascular resistance predicts improvement in insulin clearance following weight loss

2015 ◽  
Vol 14 (1) ◽  
Author(s):  
Nora E. Straznicky ◽  
Mariee T. Grima ◽  
Carolina I. Sari ◽  
Elisabeth A. Lambert ◽  
Sarah E. Phillips ◽  
...  
Keyword(s):  
Weight Loss ◽  
Vascular Resistance ◽  
Insulin Clearance ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular

Euvolemic cirrhotic dogs in sodium balance maintain normal systemic hemodynamics

1988 ◽  
Vol 66 (1) ◽  
pp. 80-83 ◽  
Author(s):  
M. Levy ◽  
Elizabeth Maher ◽  
Marvin J. Wexler
Keyword(s):  
Cardiac Output ◽  
Liver Function ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Systemic Hemodynamics ◽  
Peripheral Vascular Resistance ◽  
Sodium Balance ◽  
Biliary Cirrhosis ◽  
Sodium Retention ◽  
Peripheral Vascular

Dogs with chronic biliary cirrhosis and portal hypertension commonly develop plasma volume expansion, urinary sodium retention, ascites, and perturbed systemic hemodynamics, i. e., a rise in cardiac output and a fall in peripheral vascular resistance. Our laboratory has previously demonstrated that creating a side-side portacaval anastomosis in such animals, and so venting hepatoportal pressure, will prevent sodium retention and ascites formation and will maintain the animals euvolemic. In the present study, in four cirrhotic dogs with such an anastomosis, observations made at 12 weeks postbiliary duct ligation, and in the presence of grossly disturbed liver function and morphology, failed to demonstrate any change from control conditions in arterial blood pressure, cardiac output, or peripheral vascular resistance. We conclude that venting hepatoportal pressure in cirrhotic dogs with markedly disturbed liver function prevents the advent of a hyperdynamic circulation, possibly by preventing volume expansion.

scholarly journals Thoracoabdominal asynchrony correlates with peripheral vascular resistance changes in a cohort of obese children.

2018 ◽  
pp. 169-173
Author(s):  
Marco Zaffanello ◽  
Franco Antoniazzi ◽  
Laura Tenero ◽  
Michele Piazza ◽  
Angelo Pietrobelli ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Obese Children ◽  
Thoracoabdominal Asynchrony
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